Terson Syndrome: a prospective analysis of 45 consecutive patients

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Presentation transcript:

Terson Syndrome: a prospective analysis of 45 consecutive patients George Hadjigeorgiou Department of Neurosurgery Red Cross Hospital Athens, Greece

Introduction First described in 1900 by Albert Terson, as the presence of vitreous hemorrhage in patients with SAH

Introduction Castren, 1963: modification in order to include other forms of intraocular hemorrhage (retinal, subhyaloid) Manschot, 1944: associated TS with increased mortality

Material & Methods Prospective, non-randomized case series study 45 consecutive patients, who were admitted to our clinic with the diagnosis of aneurysmal SAH All patients underwent a 4-vessel DSA Indirect opthalmoscopy under mydriasis was performed in all patients upon admission and on the 7th day Exclusion criteria: causes of SAH other than aneurysmal rupture (e.g. AVM), death of the patient before the opthalmological examination, traumatic SAH Classification according to the GCS, Hunt&Hess and Fischer grade on admission and according to GOS on discharge

Results 45 pt with aSAH: 14 males (31%), 31 females (69%) Mean age 52.1 yo Endovascular treatment 37 pt – clipping 8 pt TS in 6/45 pt (13,3%)  2 males , 4 females All cases of TS-group were related to aneurysms localized in the anterior circulation

Results GCS w/o TS TS 15 16 12-14 11 9-11 6 1 6-8 2 3 3-5 4 H & H 12-14 11 9-11 6 1 6-8 2 3 3-5 4 H & H w/o TS TS I 5 II 12 III 16 1 IV 4 V 2 Fisher w/o TS TS I 1 II 15 III 18 5 IV

Results GOS Pt w/o TS Pt with TS 1 6 2 4 3 12 10 5 7

Discussion TS is a common phenomenon Studies have estimated that 12-16% of patients with SAH do not reach hospital to be clinically assessed (Pobereskin, 2001) Prospective Study No of Patients with SAH % with TS Garfinkle et al (1992) 22 27 % Pfausler et al (1996) 60 17% Frizzeli et al (1997) 99 8% Fountas et al (2008) 174 12,1% He et al (2011) 101 14,8% Watanabe et al (2011) 47 29% Stienen et al (2012) 18,3% Current Study 45 13,3%

Discussion Pathogenesis of TS proposed mechanisms: Increased ICP may force blood into the subarachnoid space and along the optic nerve sheath into the preretinal space (Muller, 1974) Compression of the central retinal vein and retinochoroidal anastomoses by elevated CSF pressure causing venous hypertension and disruption of retinal veins (Garfinkle, 1992)

Discussion A higher frequency of TS was demonstrated in patients with low GCS, high H&H and Fisher grade TS-group displayed a significantly worse outcome (GOS: 1,8 vs 3,2) and a higher mortality rate than the non-TS group (33,3% vs 15,4%) All patients with TS in our study had conservative treatment for the ocular hemorrhage; however it is described that in some cases opthalmic surgery (eg. vitrectomy) may be required (Garweg, 2009)

Discussion In our study, all the cases of the TS-group were related to aneurysms localized in the anterior circulation However, neither our study nor previous ones in the literature could find a statistical significance correlation between the aneurysm localization and incidence of TS

Discussion For the diagnosis of TS a precise fundoscopy remains the most sensitive method Fundoscopy may be limited in an acutely ill patient; need for pupil’s size examination CT: may identify up to 66,7% of TS cases  thickening, nodularity or crescent-shaped increased density of the retinal surface (Swallow, 1998) Ocular U/S: confirm diagnosis and detection of secondary complications (eg. retinal detachment)

Conclusions TS is a relatively common phenomenon in patients with SAH and is an underdiagnosed complication in the daily hospital routine TS is an indicator of poor prognosis An early recognition of TS is important since a permanent impairment of vision may occur For the accurate assessment of TS and whether intraocular hemorrhage is an independent prognostic variable in patients with SAH, larger and ideally population based prospective studies are required

Thank you!