====== Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage ======

Delayed [[cerebral ischemia]] (DCI) is the most consequential secondary insult after [[aneurysmal subarachnoid hemorrhage]] (SAH). It is a multifactorial process caused by a combination of the large artery [[vasospasm]] and microcirculatory dysregulation. Despite numerous efforts, no effective therapeutic strategies are available to prevent DCI.
Follows some cases of SAH (usually), trauma, or other insults

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For decades, [[cerebral vasospasm]] triggered by the amount of [[blood]] in the [[basal cistern]]s was regarded as causal for delayed [[cerebral ischemia]]
((Macdonald  RL.  Origins of the concept of vasospasm.   Stroke. 2016;47(1):e11-e15. doi:10.1161/STROKEAHA.114.006498))

===== Risk factors =====


Failure of cerebral autoregulation has been shown in patients with aSAH even before vasospasm sets in and contributes to [[delayed ischemic neurological deficit]]s (DIND) along with vasospasm
((Sriganesh K, Venkataramaiah S. Concerns and challenges during anesthetic
management of aneurysmal subarachnoid hemorrhage. Saudi J Anaesth. 2015
Jul-Sep;9(3):306-13. doi: 10.4103/1658-354X.154733. Review. PubMed PMID:
26240552; PubMed Central PMCID: PMC4478826.
)).




[[Delayed ischemic neurological deficit]] (DIND) due to symptomatic [[vasospasm]] is a major cause of morbidity and mortality after [[aneurysmal subarachnoid hemorrhage]]  (aSAH), most likely because of a decreased availability of [[nitric oxide]] (NO) in the cerebral [[microcirculation]]
((Ehlert A, Schmidt C, Wölfer J, Manthei G, Jacobs AH, Brüning R, Heindel W,
Ringelstein EB, Stummer W, Pluta RM, Hesselmann V. Molsidomine for the prevention
of vasospasm-related delayed ischemic neurological deficits and delayed brain
infarction and the improvement of clinical outcome after subarachnoid hemorrhage:
a single-center clinical observational study. J Neurosurg. 2016 Jan;124(1):51-8. 
doi: 10.3171/2014.12.JNS13846. Epub 2015 Jul 10. PubMed PMID: 26162034.
)).


The [[VASOGRADE]]: is a Simple Grading Scale for Prediction of Delayed Cerebral Ischemia After Subarachnoid Hemorrhage
((de Oliveira Manoel AL, Jaja BN, Germans MR, Yan H, Qian W, Kouzmina E, Marotta
TR, Turkel-Parrella D, Schweizer TA, Macdonald RL; SAHIT collaborators. The
VASOGRADE: A Simple Grading Scale for Prediction of Delayed Cerebral Ischemia
After Subarachnoid Hemorrhage. Stroke. 2015 Jul;46(7):1826-31. doi:
10.1161/STROKEAHA.115.008728. Epub 2015 May 14. PubMed PMID: 25977276.)).

[[Intracerebral hematoma]] (ICH) was associated with an increased risk of DCI. Furthermore, adding the presence or absence of ICH to the [[modified Fisher Scale]] (mFS) improved the identification of patients at the highest risk for the development of DCI. Thus, a simple adjustment of the mFS might help to identify patients at high risk for DCI
((Platz J, Güresir E, Wagner M, Seifert V, Konczalla J. Increased risk of
delayed cerebral ischemia in subarachnoid hemorrhage patients with additional
intracerebral hematoma. J Neurosurg. 2017 Feb;126(2):504-510. doi:
10.3171/2015.12.JNS151563. PubMed PMID: 26967776.
)).

===== Pathogenesis =====

[[Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage pathogenesis]].

===== Pathophysiology =====

see [[Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage pathophysiology]].

===== Diagnosis =====
see [[Delayed cerebral ischemia diagnosis]].



===== Prevention =====

 
[[Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage prevention]]


===== Treatment =====

[[Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage treatment]]


===== Outcome =====

[[Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage outcome]].



===== Case series =====
Fifty-seven of 176 prospectively studied patients with aneurysmal subarachnoid hemorrhage (SAH) developed delayed cerebral ischemia. Clinical features included hemispheric focal signs (13), decrease in level of consciousness (14), or both (30), and mutism (15). Forty-seven patients showed hypodense lesions on CT in one (19) or multiple vascular territories (22), or diffusely in one or both hemispheres (6). Twenty-eight had symmetric decrease in ventricular size. Of 18 autopsied patients, only 1 had a purely univascular lesion. The clinical, CT, and pathologic features suggest that delayed cerebral ischemia after SAH is a multivascular or diffuse process in most patients
((Hijdra A, Van Gijn J, Stefanko S, Van Dongen KJ, Vermeulen M, Van Crevel H. Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage: clinicoanatomic correlations. Neurology. 1986 Mar;36(3):329-33. doi: 10.1212/wnl.36.3.329. PMID: 3951698.)).