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BACKGROUND AND PURPOSE: To explore the prevalence, risk factors, time correlation, characteristics and clinical outcome of dural arteriovenous fistulas (dAVFs) in a cerebral venous thrombosis (CVT) population. METHODS: We included patients from the International CVT Consortium registries. Diagnosis of dAVF was confirmed centrally. We assessed the prevalence and risk factors for dAVF among consecutive CVT patients and investigated its impact on clinical outcome using logistic regression analysis. We defined poor outcome as modified Rankin Scale score 3-6 at last follow-up. RESULTS: dAVF was confirmed in 29/1218 (2.4%) consecutive CVT patients. The median (interquartile range [IQR]) follow-up time was 8 (5-23) months. Patients with dAVF were older (median [IQR] 53 [44-61] vs. 41 [29-53] years; p < 0.001), more frequently male (69% vs. 33%; p < 0.001), more often had chronic clinical CVT onset (>30 days: 39% vs. 7%; p < 0.001) and sigmoid sinus thrombosis (86% vs. 51%; p < 0.001), and less frequently had parenchymal lesions (31% vs. 55%; p = 0.013) at baseline imaging. Clinical outcome at last follow-up did not differ between patients with and without dAVF. Additionally, five patients were confirmed with dAVF from non-consecutive CVT cohorts. Among all patients with CVT and dAVF, 17/34 (50%) had multiple fistulas and 23/34 (68%) had cortical venous drainage. Of 34 patients with dAVF with 36 separate CVT events, 3/36 fistulas (8%) were diagnosed prior to, 20/36 (56%) simultaneously and 13/36 after (36%, median 115 [IQR 38-337] days) diagnosis of CVT. CONCLUSIONS: Dural arteriovenous fistulas occur in at least 2% of CVT patients and are associated with chronic CVT onset, older age and male sex. Most CVT-related dAVFs are detected simultaneously or subsequently to diagnosis of CVT.

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Simultaneous bilateral acute angle closure crisis (AACC) is a sight-threatening ocular emergency. Many "cold and flu" preparations contain compounds with sympathomimetic or anticholinergic qualities that confer a risk of inducing AACC. We present a review of cold and flu preparation-induced AACC, and present a case of simultaneous bilateral AACC triggered by a single oral dose of pseudoephedrine. The challenges facing the clinician in recognizing simultaneous bilateral AACC in the context of an upper respiratory tract infection are addressed. An awareness of this uncommon clinical entity, its pertinent clinical features, risk factors, and the drug classes that may precipitate an attack is critical for the timely diagnosis and management of this ocular emergency. Notably, clinicians must be aware that even a single dose of an implicated medication may trigger an attack of AACC.

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BACKGROUND: Ischaemic stroke is reportedly preceded by transient ischaemic attack (TIA) in 15-30% of all cases. The risk of stroke following TIA is highest in the presence of unstable atherosclerotic plaques in large arteries. The recent population-based Adelaide Stroke Incidence Study describes a population with a low proportion (16%) of stroke attributable to large artery atherosclerosis (LAA). We hypothesized that this population-based ischaemic stroke cohort would have a lower rate of preceding TIA than previously reported. METHODS: This paper is a prospective ascertainment of all suspected TIAs and strokes in a 12-month period from 2009 to 2010. Ischaemic stroke pathogenesis was classified by the TOAST criteria. Details of preceding TIA events were scrutinised. RESULTS: In this 12-month period, 318 stroke events in 301 individuals were recorded. Of the total 258 ischaemic strokes, 16% (95% confidence interval [CI] 12-22) were from LAA. Of 258 ischaemic stroke patients, only 11 (4%; 95% CI 2-7) reported symptoms in the preceding 90 days consistent with TIA. Nine (82%) sought medical attention. The median ABCD2 score in this group was 4.5 (IQR: 3-7), and the median time of event prior to stroke was 20 days (IQR: 4-32). CONCLUSION: In our population-based cohort, rates of TIA preceding ischaemic stroke were much lower than previously reported, probably reflective of effective secondary prevention (active TIA clinics) and primary prevention (limiting LAA prevalence). In our population, further enhancements in TIA care will be of limited yield.

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AIM: Indigenous Australians with asthma have higher morbidity and mortality compared with non-Indigenous Australians. In children hospitalised with acute asthma, we aimed to (i) determine if acute severity, risk factors and management differed between Indigenous and non-Indigenous children; and (ii) identify intervention points to reduce morbidity and mortality of asthma. METHODS: Retrospective review of 200 children hospitalised to Royal Darwin Hospital with asthma. We compared admission characteristics, severity indices, treatment, discharge plans and readmissions in Indigenous and non-Indigenous children. RESULTS: Median age was 3.6 years (interquartile range 2.2, 6.8). A significantly higher proportion of Indigenous children (95.2%) were exposed to tobacco smoke compared with non-Indigenous children (45.7%). The difference in proportions was -0.41 (95% confidence interval (CI) -0.60, -0.22). Other risk factors, asthma severity (moderate 83.9% vs. 83.3%; severe 16% vs. 16.1%), length of stay (1.9 vs. 1.3 days) and readmission rate (27.4% vs. 27.5%) were similar between Indigenous and non-Indigenous children. Indigenous children were significantly more likely to be followed up in a community clinic (difference in proportions = 0.10, 95% CI 0.1, 0.17) and less likely by a paediatrician. Only 62.5% of all children had an asthma action plan on discharge. CONCLUSION: Unlike other common respiratory diseases requiring hospitalisation, biological factors are unlikely major contributors to the known gap in asthma outcomes between Indigenous and non-Indigenous children. Intervention points include better identification, documentation and management of tobacco smoke exposure, delivery of salbutamol and discharge planning (including education and utilisation of asthma action plans).

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