Factors related to acute hydrocephalus after subarachnoid hemorrhage

Jartti, P.; Karttunen, Ari; Jartti, Airi; Ukkola, V.; Sajanti, Juha; Pyhtinen, J.

doi:10.1080/02841850410004274

Cited by 25 publications

(19 citation statements)

References 13 publications

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“…Clinical studies have shown that amount of blood in the subarachnoid space and the presence of intraventricular hemorrhage increase the risk of acute hydrocephalus. 9, 10 Similar to these reports, ventricular volume was correlated with the severity of SAH and all animals with hydrocephalus had intraventricular blood in our study. Our results suggest that the amount of subarachnoid blood or presence of intraventricular blood may cause obstruction of CSF flow.…”

Section: Discussionsupporting

confidence: 89%

Subarachnoid Hemorrhage-Induced Hydrocephalus in Rats

Okubo

Strahle

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et al. 2013

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Background and Purpose Hydrocephalus is an important complication of subarachnoid hemorrhage (SAH). We investigated the occurrence of acute hydrocephalus in a rat SAH model. Methods SAH was induced by endovascular perforation in adult male Sprague-Dawley rats (n=36). Sham rats (n=8) underwent the same procedure without perforation. MRI was performed 24 hours after SAH and the volume of the ventricular system and extent of T2* hypointensity lesions were measured. We defined hydrocephalus as ventricular volume greater than +3 standard deviations above the mean in sham animals. SAH grade was determined and brains were used for histology, immunohistochemistry, Perls’ staining and Western blot analysis. Ventricular wall damage was defined as percentage of ependymal surface disruption. Results All surviving rats (n=27) after SAH had ventricular enlargement (33.6±4.7 vs. 13.5±1.4 mm3 in sham animals, p<0.01). Ventricular volume correlated with SAH severity (r=0.48, p<0.05). 12 of 27 SAH rats demonstrated hydrocephalus and all had intraventricular blood accumulation. Rats with hydrocephalus had more severe ventricular wall damage (7.4±1.2%) than the sham animals (0.6±0.2%, p<0.01) and rats without hydrocephalus (1.1±0.2%, p<0.01). Periventricular iron deposition was observed and HO-1 and Iba-1 expression were markedly increased in hydrocephalus rats. Conclusions SAH causes ventricular enlargement in a rat endovascular perforation model, with hydrocephalus occurring in 44% of animals at 24 hours. Rats with hydrocephalus had more severe SAH, intraventricular hemorrhage and greater ventricular wall damage.

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Section: Discussionsupporting

confidence: 89%

Subarachnoid Hemorrhage-Induced Hydrocephalus in Rats

Okubo

Strahle

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et al. 2013

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“…The multivariate analysis identified hydrocephalus (OR 3.7), elderly patients (OR 5.8), and Fi3 NASAH (OR 2.3) as independent risk factors for an unfavorable outcome after NASAH. For aneurysmal SAH, previous data have shown that a diffuse bleeding pattern (Fi3) is associated with significantly higher hydrocephalus rates and CVS 17 27. This point is also supported for the Fi3 blood distribution in NASAH by the significantly higher rates of hydrocephalus, CVS and DCI compared with NASAH without Fi3 bleeding pattern (table 3).…”

Section: Discussionsupporting

confidence: 57%

“…For aneurysmal SAH it is known that hydrocephalus, CVS, and DCI are related to the pattern of hemorrhage (with highest rates for Fi3 and Fi4) 17 27. It seems to be clear that the pattern of hemorrhage should also be an important factor for hydrocephalus, CVS, and DCI in NASAH.…”

Section: Discussionmentioning

confidence: 99%

Cerebral vasospasm and delayed cerebral infarctions in 225 patients with non-aneurysmal subarachnoid hemorrhage: the underestimated risk of Fisher 3 blood distribution

Konczalla

Kashefiolasl

Brawanski

et al. 2016

J NeuroIntervent Surg

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Patients with NASAH without a Fi3 bleeding pattern had a similar excellent outcome to patients with PM-SAH. Patients with Fi3 had a high risk for early hydrocephalus, CVS, DCI, and an unfavorable outcome, similar to patients with aneurysmal SAH. After multivariate analysis, early hydrocephalus, elderly patients, and Fi3 were identified as negative prognostic factors. Therefore, patients with Fi3 are at risk and need careful clinical observation.

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“…This hypothesis is in line with Hasan 5 report that acute HC could occur in the absence of ventricular bleeding as long as there was blood in the perimesencephalic subarachnoid spaces. According to Jartti, 25 the incidence of acute HC in a 180‐patient series was higher in subjects with blood throughout the anterior, lateral, and basal regions than in subjects with no blood distributed across these three areas ( P = .010).…”

Section: Discussionmentioning

confidence: 95%