Increase in the fluid content of blood, resulting in diminution of the concentration of formed elements.


see Triple H therapy.

Hemodilution is used to lower hematocrit.

Consider for Emergency carotid endarterectomy with acute neuro deficit.

High hemoglobin (HGB) level was associated with increased risk of postsurgical cerebral ischemiapulmonary embolism and lower-limb DVT and poor prognosis in poor grade aneurysmal subarachnoid hemorrhage patients. Preoperative hemodilution therapy might be beneficial in reducing operative complications, reducing hospital stay and improving short-term prognosis for neurological functional recovery in aSAH patients with high hemoglobin concentration, but further detailed research is needed 1).



Anqi X, Ruiqi C, Yanming R, Chao Y. Elevated hemoglobin is associated with poor prognosis in Tibetans with poor-grade aneurysmal subarachnoid hemorrhage after clipping: A Retrospective Case-Control Study. Neurochirurgie. 2019 Jul 10. pii: S0028-3770(19)30186-9. doi: 10.1016/j.neuchi.2019.06.005. [Epub ahead of print] PubMed PMID: 31301387.



The neurotoxic aldehyde 3-aminopropanal (3-AP) contributes to brain injury following cerebral ischemia. Tiopronin (N-2-mercaptopropionyl-glycine[N-2-MPG]) is a US Food and Drug Administration (FDA)-approved drug for the treatment of cystinuria and a putative neuroprotective agent that has been shown to bind and neutralize 3-AP and reduce infarct volumes.

The objective of a trial was to establish the safety of tiopronin administration in patients with aneurysmal subarachnoid hemorrhage (aSAH) in preparation for further trials of its efficacy as a neuroprotective agent in this disease process.

This Phase I dose-escalation trial enrolled three-patient cohorts using a conventional “3+3” study design. Tiopronin dose began at 1 g/d until aSAH Day 14. Each subsequent cohort received a dose of tiopronin based on predetermined guidelines. A maximum dose of 3 g/d was selected, because this is the maximum FDA-approved dose for long-term cystinuria treatment. Subjects were monitored for known side effects of tiopronin.

Nine patients were enrolled, the minimum number required based on the study design. None of these patients experienced serious side effects attributable to tiopronin, and no adverse events were noted that could not be attributed to the pathophysiology of aSAH.

The administration of 3 g/d of tiopronin following aSAH for up to 14 days appears to be safe and without the side effects associated with long-term use. Plans for a randomized, placebo-controlled Phase II trial of tiopronin for neuroprotection following aSAH are underway 1).

A phase II clinical trial evaluated the efficacy of tiopronin in reducing CSF 3-AMINOPROPANAL levels in patients with aSAH.

In a prospectiverandomizeddouble blindplacebo controlled, multicenter clinical trial, 60 patients were assigned to receive tiopronin or placebo in a 1:1 ratio. Treatment was commenced within 96 hours after aSAH onset, administered at a dose of 3 g daily, and continued until 14 days after aSAH or hospital discharge, whichever occurred earlier. The primary efficacy outcome was the CSF 3-AP level at 7 ± 1 days after aSAH.

Of the 60 enrolled patients, 29 (97%) and 27 (93%) in the tiopronin and placebo arms, respectively, received more than one dose of the study drug or placebo. At post-aSAH day 7 ± 1, CSF samples were available in 41% (n = 12/29) and 48% (n = 13/27) of patients in the tiopronin and placebo arms, respectively. No difference in CSF 3-AP levels at post-aSAH day 7 ± 1 was observed between the study arms (11 ± 12 nmol/mL vs 13 ± 18 nmol/mL; p = 0.766). Prespecified adverse events led to early treatment cessation for 4 patients in the tiopronin arm and 2 in the placebo arm.

The power of this study was affected by missing data. Therefore, the authors could not establish or refute an effect of tiopronin on CSF 3-AP levels. Additional observational studies investigating the role of 3-AP as a biomarker for DCI may be warranted prior to its use as a molecular target in future clinical trials.Clinical trial registration no.: NCT01095731 (ClinicalTrials.gov) 2).



Kim GH, Kellner CP, Hickman ZL, Zacharia BE, Starke RM, Hwang BY, Ducruet AF, Fernandez L, Mayer SA, Tracey KJ, Connolly ES Jr. A phase I clinical trial of tiopronin, a putative neuroprotective agent, in aneurysmal subarachnoid hemorrhage. Neurosurgery. 2010 Jul;67(1):182-5; discussion 186. doi: 10.1227/01.NEU.0000370919.93259.3C. PubMed PMID: 20559104; PubMed Central PMCID: PMC4540229.

Ironside N, Christophe B, Bruce S, Carpenter AM, Robison T, Yoh N, Cremers S, Landry D, Frey HP, Chen CJ, Hoh BL, Kim LJ, Claassen J, Connolly ES. A phase II randomized controlled trial of tiopronin for aneurysmal subarachnoid hemorrhage. J Neurosurg. 2019 Jul 12:1-9. doi: 10.3171/2019.4.JNS19478. [Epub ahead of print] PubMed PMID: 31299655.

Woven EndoBridge (WEB)

Woven EndoBridge (WEB)

The Woven EndoBridge (WEB) (Sequent Medical, Aliso Viejo, California), is a ellipsoid braided-wire embolization device designed to provide flow disruption along the aneurysm neck 1).

Placed in the aneurysm, the device will modify the blood flow at the level of the neck and induce aneurysmal thrombosis. The WEB shape was designed to treat wide necked aneurysm. The device has been developed progressively from a dual-layer version (WEB DL) to single-layer versions (WEB SL and WEB SLS [single-layer spherical]).

This device does not require long-term antiplatelet use.


For the treatment of both ruptured and unruptured aneurysms. The WEB has received the CE mark and to date has been used to treat a wide variety of more than 1,400 aneurysms in Europe, Latin America and New Zealand. The WEB is not available for sale or use in the United States.

The WEB is a self-expanding, oblate, braided nitinol mesh.

The device is composed of an inner and outer braid held together by proximal, middle, and distal radiopaque markers, creating 2 compartments: 1 distal and 1 proximal. Depending on the device diame- ter, the inner and outer braids are 108 wires or 144 wires. Therefore, blood flow into a WEB-embolized aneurysm initially encounters 2 layers of wires comprising 216 or 288 wires, with the largest interwire distance ranging from 106 to 181 􏰅m, respectively, depending on the device size. The WEB implant is deployed—or retrieved before de- tachment—in a manner similar to that in endovascular coil systems, through microcatheters with an internal diameter 􏰆0.027 inch. For devices with a diameter of 􏰇7 mm, microcatheters with an internal diameter of 0.027 inch are used; and for devices with a diameter 􏰁7 mm, microcatheters with an internal diameter 0.032 inch are used. The detachment system is electrothermal and instantaneous. 2).

In a study, there was no difference in the early clinical course between those treated with WEB embolization, coil embolization, or neurosurgical clipping. Since WEB embolization is a valuable treatment alternative to coiling, it seems not justified to exclude this procedure from upcoming clinical SAH trials, yet the clinical long-term outcome, aneurysm occlusion, and retreatment rates have to be analyzed in further studies 3).


The WEB Clinical Assessment of Intrasaccular Aneurysm Therapy (WEBCAST) trial is a prospective European trial evaluating the safety and efficacy of WEB in wide necked aneurysm of the bifurcation.



It does not immediately secure the aneurysm in most subarachnoid hemorrhage cases. Second, it may not be suitable for embolization of wide-neck aneurysms with an unfavorable aspect ratio. To overcome these limitations, Zanaty et al., used the WEB device in conjunction with stenting and/or coiling.

They presented a technical note with an illustrated case-series, and provide a detailed step-by-step description on how the WEB device can be used in adjunct to coiling and/or stenting to achieve successful angiographic results. Accurate sizing of the WEB device before deployment is critical. Larger case-series are required to further assess the safety and success of these combined techniques 4).

Case series



Ding YH, Lewis DA, Kadirvel R, Dai D, Kallmes DF. The Woven EndoBridge: a new aneurysm occlusion device. AJNR Am J Neuroradiol. 2011 Mar;32(3):607-11. doi: 10.3174/ajnr.A2399. Epub 2011 Feb 17. PubMed PMID: 21330397.

Pierot L, Liebig T, Sychra V, Kadziolka K, Dorn F, Strasilla C, Kabbasch C, Klisch J. Intrasaccular flow-disruption treatment of intracranial aneurysms: preliminary results of a multicenter clinical study. AJNR Am J Neuroradiol. 2012 Aug;33(7):1232-8. doi: 10.3174/ajnr.A3191. Epub 2012 Jun 7. PubMed PMID: 22678844.

Sauvigny T, Nawka MT, Schweingruber N, Mader MM, Regelsberger J, Schmidt NO, Westphal M, Czorlich P. Early clinical course after aneurysmal subarachnoid hemorrhage: comparison of patients treated with Woven EndoBridge, microsurgical clipping, or endovascular coiling. Acta Neurochir (Wien). 2019 Jul 6. doi: 10.1007/s00701-019-03992-4. [Epub ahead of print] PubMed PMID: 31280480.

Zanaty M, Roa JA, Dandapat S, Samaniego EA, Jabbour P, Hasan D. Diverse Use of the WEB Device: A Technical Note on WEB Stenting and WEB Coiling of Complex Aneurysms. World Neurosurg. 2019 Jul 10. pii: S1878-8750(19)31933-3. doi: 10.1016/j.wneu.2019.07.027. [Epub ahead of print] PubMed PMID: 31301439.
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