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Colum P. Nolan and R. Loch Macdonald

✓ The authors tested the null hypothesis that published literature with a high level of evidence does not support the assertion that subarachnoid hemorrhage (SAH) causes cerebral vasospasm, which in turn causes cerebral infarction and poor outcome after aneurysmal SAH. The medical literature on SAH was searched in MEDLINE. The author's personal files of all published literature on SAH were reviewed. References cited in Cochrane reviews as well as the published papers that were reviewed were also retrieved.

There is no question that SAH causes what the authors have chosen to call “angiographic vasospasm.” However, the incidence and severity of vasospasm in recent series of patients is not well defined. There is reasonable evidence that vasospasm causes infarction, but again, accurate data on how severe and how diffuse vasospasm has to be to cause infarction and how often vasospasm is the primary cause of infarction are not available. There are good data on the incidence of cerebral infarction after SAH, and these data indicate that it is highly associated with poor outcome. The link between angiographic vasospasm and poor outcome is particularly poorly described in terms of what would be considered data of a high level of evidence.

The question as to whether there is a clear pathway from SAH to vasospasm to cerebral infarction to poor outcome seems so obvious to neurosurgeons as to make it one not worth asking. Nevertheless, the obvious is not always true or accurate, so it is important to note that published literature only weakly supports the causative association of vasospasm with infarction and poor outcome after SAH. It behooves neurosurgeons to document this seemingly straightforward pathway with high-quality evidence acceptable to the proponents of evidence-based medicine.

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George W. Weyer, Colum P. Nolan, and R. Loch Macdonald

✓Cerebral vasospasm and delayed cerebral ischemia remain common complications of aneurysmal subarachnoid hemorrhage (SAH), and yet therapies for cerebral vasospasm are limited. Despite a large number of clinical trials, only calcium antagonists have strong evidence supporting their effectiveness. The purpose of this work was to perform a systematic review of the literature on the treatment of cerebral vasospasm.

A literature search for randomized controlled trials of therapies used for prevention or treatment of cerebral vasospasm and/or delayed cerebral ischemia was conducted, and 41 articles meeting the review criteria were found. Study characteristics and primary results of these articles are reviewed.

Key indicators of quality were poor when averaged across all studies, but have improved greatly over time. The only proven therapy for vasospasm is nimodipine. Tirilazad is not effective, and studies of hemodynamic maneuvers, magnesium, statin medications, endothelin antagonists, steroid drugs, anticoagulant/antiplatelet agents, and intrathecal fibrinolytic drugs have yielded inconclusive results.

The following conclusions were made: nimodipine is indicated after SAH and tirilazad is not effective. More study of hemodynamic maneuvers, the effectiveness of other calcium channel antagonists such as nicardipine delivered by other routes (for example intrathecally), magnesium, statin drugs, endothelin antagonists, and intrathecal fibrinolytic therapy is warranted. There is less enthusiasm for the study of steroid drugs and anticoagulant/antiplatelet agents because they entail more risks and investigations so far have shown little evidence of efficacy. The study of rescue therapy such as balloon angioplasty and intraarterial vasodilating agents will be difficult. The quality of clinical trials should be improved.

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Lester Lee, Sharon Low, David Low, Lee Ping Ng, Colum Nolan, and Wan Tew Seow

OBJECTIVE

The introduction of ventriculoperitoneal shunts changed the way hydrocephalus was treated. Whereas much is known about the causes of shunt failure in the first few years, there is a paucity of data in the literature regarding the cause of late shunt failures. The authors conducted a study to find out the different causes of late shunt failures in their institution.

METHODS

A 10-year retrospective study of all the patients who were treated in the authors' hospital between 2006 and 2015 was conducted. Late shunt failures included those in patients who had to undergo shunt revision more than 5 years after their initial shunt insertion. The patient's notes and scans were reviewed to obtain the age and sex of the patient, the time it took for the shunt to fail, the reason for failure, and the patient's follow-up.

RESULTS

Forty-six patients in the authors' institution experienced 48 late shunt failures in the last 10 years. Their ages ranged from 7 to 26 years (12.23 ± 4.459 years [mean ± SD]). The time it took for the shunts to fail was between 6 and 24 years (mean 10.25 ± 3.77 years). Reasons for failure resulting in shunt revision include shunt fracture in 24 patients (50%), shunt blockage in 14 patients (29.2%), tract fibrosis in 6 patients (12.5%), shunt dislodgement in 2 patients (4.2%), and shunt erosion in 2 patients (4.2%). Postoperative follow-up for the patients ranged from 6 to 138 months (mean 45.15 ± 33.26 months).

CONCLUSIONS

Late shunt failure is caused by the effects of aging on the shunt, and the complications are different from early shunt failure. A large proportion are complications associated with shunt calcification. The authors advocate a long follow-up for pediatric patients with shunts in situ to monitor them for various causes of late shunt failure.