Endovascular and microsurgical management of blister aneurysms: a multi-centre review.

Blister aneurysms (BA) are high-risk cerebrovascular lesions accounting for 1% of intracranial aneurysms. The defective vessel wall and broad-based neck make this clinical entity difficult to treat, with high rates of re-rupture and mortality in patients presenting with acute subarachnoid haemorrhage. Blister aneurysms pose substantial challenges for both endovascular and microsurgical management. The objective of this study is to evaluate endovascular and microsurgical outcomes in intracranial blister aneurysm management across two tertiary hospitals. A review of two tertiary hospitals with a systematic imaging database search for term of "blister" in modalities from January 2010 to October 2022 was conducted. Operation reports were screened for the 5-year period since cerebral angiogram reports transitioned to surgical database. Identified reports were screened and reviewed for confirmed diagnosis by consultant neuroradiologist. A total of 21 cases of blister aneurysms managed at respective facilities were included. Sixteen cases (76%) were managed endovascularly. Four cases (19%) were managed surgically-2 with primary clipping, and 2 wrap and clipping. One case was managed conservatively (5%). Clinical outcomes were discharge disposition, aneurysm exclusion and post-operative complications. BAs have challenging considerations with high mortality and morbidity. Endovascular treatment offers a less invasive modality with lower rates of intraoperative rupture and morbidity. Mortality rates and patients discharged home were comparable. Commencement of dual anti-platelet therapy was safe in patients with flow diversion stents despite sub-arachnoid blood volume. Management of blister aneurysms is complex. Endovascular treatment shows promise for acute management but careful collaborative consideration of antithrombotic regime and requirement for further surgery should be considered.

The incidence of cerebral arterial vasospasm following aneurysmal subarachnoid haemorrhage: a systematic review and meta-analysis.

PURPOSE: To describe a pooled estimated incidence of cerebral arterial vasospasm (aVSP) following aneurysmal subarachnoid haemorrhage (aSAH) and to describe sources of variation in the reported incidence. METHODS: We performed a systematic review and meta-analysis of randomised clinical trials (RCTs) and cohort studies. The primary outcome was the proportion of study participants diagnosed with aVSP. We assessed for heterogeneity based on mode of imaging, indication for imaging, study design and clinical characteristics at a study level. RESULTS: We identified 120 studies, including 19,171 participants. More than 40 different criteria were used to diagnose aVSP. The pooled estimate of the proportion of patients diagnosed with aVSP was 0.42 (95% CI 0.39 to 0.46, I2 = 96.5%). There was no evidence that the incidence aVSP was different, nor that heterogeneity was reduced, when the estimate was assessed by study type, imaging modalities, the proportion of participants with high grade CT scores or poor grade clinical scores. The pooled estimate of the proportion of study participants diagnosed with aVSP was higher in studies with routine imaging (0.47, 95% CI 0.43 to 0.52, I2 = 96.5%) compared to those when imaging was performed when indicated (0.30, 95% CI 0.25 to 0.36, I2 = 94.0%, p for between-group difference < 0.0005). CONCLUSION: The incidence of cerebral arterial vasospasm following aSAH varies widely from 9 to 93% of study participants. Heterogeneity in the reported incidence may be due to variation in the criteria used to diagnose aVSP. A standard set of diagnostic criteria is necessary to resolve the role that aVSP plays in delayed neurological deterioration following aSAH. PROSPERO REGISTRATION: CRD42020191895.

The association between hyponatraemia and long-term functional outcome in patients with aneurysmal subarachnoid haemorrhage: A single centre prospective cohort study.

To assess the association between hyponatraemia and long-term functional outcome and other relevant outcomes in patients with aneurysmal subarachnoid haemorrhage (aSAH) we conducted a prospective cohort study in a Neurosciences Intensive Care Unit (ICU) in Sydney, Australia. The primary exposure variable was hyponatraemia (Na+ <135 mmol/L). The primary outcome was favourable outcome, a score of 5-8 on the extended Glasgow Outcome Score (GOSe) at 12 months. We also measured mortality, the incidence of delayed cerebral ischaemia (DCI) and cerebral arterial vasospasm and duration of ICU and hospital admission. There were 200 participants, 111 (56%) developed hyponatraemia. Hyponatraemia was not associated with favourable outcome at 12 months (unadjusted odds ratio [OR] OR 1.31, 95% confidence interval [CI] 0.65-2.65, p = 0.56). The result was similar after adjustment for baseline covariates (adjusted OR 0.60, 95% CI 0.16-1.99, p = 0.43). There was no association between hyponatraemia and the incidence of DCI (OR 0.95, 95% CI 0.46 to 2.0, p > 0.99) nor cerebral arterial vasospasm (OR 1.4, 95% CI 0.8 to 2.5, p = 0.27). Those who developed hyponatraemia had a longer median duration of ICU admission (17 days, interquartile range [IQR] 12 to 20, compared to 13 days, IQR 8-21, p = 0.02) and longer median duration of hospital admission (24 days, IQR 21-30, compared to 22 days IQR 14-31, p = 0.05). While hyponatraemia is common following aSAH, it is not associated with worse long-term functional outcome, increased rate of DCI, nor cerebral arterial vasospasm. Hyponatraemia in patients with aSAH was associated with longer duration of ICU and hospital admission.

Syrinx to Subarachnoid Shunting for Syringomyelia.

OBJECTIVE: Surgery for syringomyelia generally aims to treat the underlying cause, if it is known. Optimal management is unclear for idiopathic syringomyelia, or when treatment of the putative cause has failed or is high risk. Syrinx to subarachnoid shunting is an option for these cases; a series is reported to assess the outcomes of this approach. METHODS: We retrospectively analyzed the clinical and radiologic features of a consecutive series of patients with syringomyelia treated with syrinx to subarachnoid shunting. RESULTS: Forty-one patients (19 male, 4-79 years old) were treated from 2000 to 2016, including 15 patients with idiopathic syringomyelia, 13 with spinal trauma, 5 with Chiari malformation, 4 with arachnoiditis, 3 with tethered cord, and 1 with arachnoid bands. The patients were treated with a syrinx to subarachnoid shunt, and a subset also underwent expansile duraplasty. At follow-up (3-108 months, mean 36 months) syrinx size was reduced in 37 patients, and there was improvement or stabilization of symptoms in all but 1 patient. Three patients had temporary lower limb sensory symptoms after surgery. Other complications were 2 transient cerebrospinal fluid leaks, a pseudomeningocoele, and 1 postoperative myocardial infarction. Two cases of shunt dislodgement required reoperation, and a third case required early reoperation for an enlarging syrinx. There were no cases of shunt blockage or infection. CONCLUSIONS: Syrinx to subarachnoid shunting is a safe and effective treatment for idiopathic syringomyelia and for patients who are not suitable for, or have not responded to, other treatment.

Comparative analysis of caspase activation and apoptosis in renal tubular epithelial cells and renal cell carcinomas.

BACKGROUND/AIMS: Treatment of renal cell carcinoma (RCC) is limited by its resistance to conventional chemotherapies. This may occur, in part, from resistance to apoptosis. The role of caspase activation in apoptosis resistance in treated RCCs was investigated. METHODS: Two human RCC cell lines (ACHN and SN12K1) and renal tubular epithelial cells (HK2) were treated with 5-fluorouracil (0.2-20 microg/ml) or cisplatin (1-100 microM). Activation of caspase-3 and -2 was analysed and compared with levels of apoptosis. Caspase function was analysed using pan-caspase inhibition (z-VAD-fmk) and caspase-2 inhibition (z-VDVAD-fmk). RESULTS: RCC apoptosis was significantly lower (p < 0.05) than in HK2s after treatment, confirming their chemoresistance. Pro-caspase-3 (32 kDa) was detected in all cell lines. Cleaved caspase-3 (19 kDa) was not detected by Western immunoblots in treated RCCs and only minimal activated caspase-3 was detected in treated RCCs using immunohistochemistry. All cells had pro-caspase-2 (48 kDa) and the activated form (33 kDa) appeared in all treated cells. Caspase inhibition caused a reduction in, but not negation of, therapy-induced apoptosis in HK2s and RCCs (p < 0.05 for HK2s and ACHN cells), indicating that a caspase activation pathway must occur in RCC apoptosis but this pathway does not act via caspase-3 cleavage. Inhibition of caspase-2 reduced apoptosis only in HK2s, indicating that the activated caspase-2, identified in treated RCCs, was not responsible for their apoptosis induction. CONCLUSION: Specific differences in caspase-3 and -2 activation were identified in renal tubular epithelium and RCCs after chemotherapy. Identification of RCC-specific caspase inactivation or redundancy may explain, in part, the resistance of RCCs to cancer therapies and may be useful in targeting apoptotic pathways to overcome RCC resistance to treatment.