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The risk of death from venous thromboembolism (VTE) is high in intensive care unit patients with neurological diagnoses. This is due to an increased risk of venous stasis secondary to paralysis as well as an increased prevalence of underlying pathologies that cause endothelial activation and create an increased risk of embolus formation. In many of these diseases, there is an associated risk from bleeding because of standard VTE prophylaxis. There is a paucity of prospective studies examining different VTE prophylaxis strategies in the neurologically ill. The lack of a solid evidentiary base has posed challenges for the establishment of consistent and evidence-based clinical practice standards. In response to this need for guidance, the Neurocritical Care Society set out to develop and evidence-based guideline using GRADE to safely reduce VTE and its associated complications.

Over a median follow-up period of 47 months, 10% of UIA enlarged. Larger aneurysms had a significantly increased risk of enlargement. The likelihood of enlargement was highest in aneurysms with diameters >or=8 mm. However, a clinically significant proportion of small aneurysms grow, and this growth can be detected by serial MRA.

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CPM can develop in the setting of hyperosmolar hyperglycemia without abnormalities of sodium homeostasis. This supports the theory that the pathogenesis of CPM is dependent on a relatively hypertonic insult, which may occur independently of sodium abnormalities. CPM can present as isolated gait ataxia. Clinical manifestations of the disorder may show significant improvement despite a dramatic initial presentation.

Isoflurane is an alternative treatment for refractory status epilepticus. Little is known regarding human toxicities caused by isoflurane. We present 2 patients with prolonged refractory status epilepticus treated with high concentrations of isoflurane who developed signal abnormalities on magnetic resonance imaging. Patient 1 was treated with isoflurane for 85 days with 1975.2% concentration-hours. Patient 2 was treated with isoflurane for 34 days with 1382.4% concentration-hours. Serial brain magnetic resonance images in both showed progressive T2 signal hyperintensity involving thalamus and cerebellum, which improved after discontinuation of isoflurane. These cases suggest that isoflurane may be neurotoxic when used in high doses for long time periods.

Background Coronary artery disease is the leading cause of death after transient ischemic attack (TIA). Reliable estimates of the risk of myocardial infarction (MI) after TIA, however, are lacking. Purpose To determine the incidence of and risk factors for MI after TIA Methods We cross-referenced pre-existing incidence cohorts from the Rochester Epidemiology Project for TIA (1985–1994) and MI (1979–2006) to identify all community residents with incident MI after incident TIA. Incidence of MI after TIA was determined using Kaplan-Meier life-table methods. This was compared to the age-, sex-, and period-specific MI incidence in the general population. Proportional hazards regression analysis was used to examine associations between clinical variables and the occurrence of MI after TIA. Results Average annual incidence of MI after TIA was 0.95%. Relative risk for incident MI in the TIA cohort compared to the general population was 2.09 (95% CI 1.52–2.81). This was highest in patients under 60 years old (relative risk 15.1; 95% CI 4.11–38.6). Increasing age (HR 1.51 per 10 years, 95% CI 1.14–2.01), male sex (HR 2.19, 95% CI 1.18–4.06), and the use of lipid lowering therapy at the time of TIA (HR 3.10, 95% CI 1.20–8.00) were independent risk factors for MI after TIA. Conclusions Average annual incidence of MI after TIA is approximately 1%, about double that of the general population. The relative risk increase is especially high in patients under 60 years old. These data are useful for identifying subgroups of patients with TIA at highest risk for subsequent MI.

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