intracranial hemorrhage

They had an objective of evaluating the effect of Sigamidex on change in GCS and analgo-sedation requirements in the emergency department.

They had the goal of filling gaps in literature by being a multi-state and system multi-center study, including a larger sample size of patients and refocusing on traumatic brain injury or TBI and spontaneous intracranial hemorrhage or ICH.

Being a multicenter retrospective observational court study, as I mentioned earlier, and it included patients with a primary diagnosis of TBI or spontaneous ICH that received rocuronium either in the emergency department or pre-hospital.

And all patients also received Sigamidex in the emergency department for neurologic evaluation.

By including pre-hospital administration of rocuronium, this makes the results more generalizable and reflective of real practices in states where emergency medical services can do rapid sequence intubation.

The focus was on TBI and spontaneous ICH and specifically excluded status epilepticus and ischemic stroke patients because lack of neurologic exam and those may not change acute or initial management.

Patients also had to have a GCS score documented at baseline and within 30 minutes after SIGAMIDEX administration.

The primary outcome assessed was a increase in GCS of at least one point within 30 minutes post-Sigamidex administration.

We'll examine what their different results tell us about symptoms, rhythm burden, and beta blockers.

Then we'll turn to dual energy ablation, structured exercise, individualized substrate ablation, and edoxaban after intracranial hemorrhage.

The central question isn't simply whether an intervention changes a rhythm recording.

It's whether that change produces additional benefit that matters to the patient and at what cost in treatment burden and risk.

The EP Edge take, a feasible dual energy strategy with useful procedural data, not evidence of superiority over another platform.

The next step is prospective lesion guidance and controlled comparisons using comparable monitoring.

Our final trial asks a difficult question: After intracranial hemorrhage, does anticoagulation improve the overall outcome for a patient with AF? This is ENRICH-AF, presented by Ashkan Shamanesh at the August 2026 European Cardiology Society Congress.

Nine hundred forty-eight patients were randomized.

We have Dr. Andy Webb.

And we are going to be talking about an article that came out in Neurocritical Care Journal, which is titled "Effect of Desmopressin on Attaining Therapeutic Hypernatremia with Hypertonic Saline Continuous Infusion in Intracranial Hemorrhage," which was authored by Villegas et al.

Now, Dr. Webb, you're very well-known to the Neurocritical Care Society, to the Neurocritical Care podcast as well, having been featured in multiple episodes.

I still remember fondly that episode about the Indexa trial when it had come out.

Now, that dose cap of twenty micrograms is actually somewhat common.

It actually comes from Canadian package labeling, where that dose came from studies that were done in the hemophilia population that's oftentimes extrapolated to this population.

Essentially, what they wanted to look at is in patients with general intracranial hemorrhage, so spontaneous and traumatic, who received the DDAVP dose and were also started on this institution sort of hypertonic three percent, uh, saline sliding scale targeting a goal of, uh, one-fifty to one-fifty-five, whether or not patients achieved that hypertonic, you know, sodium goal less often if they had received desmopressin versus those who had not received desmopressin.

They excluded, you know, their exclusion criteria were relatively straightforward, you know, patients who were baseline hyponatremic, pa- patients who had baseline SIADH, those with burns or those with ESRD where you might have a little bit harder time managing their electrolytes.

Plasmin can also indirectly affect platelet function, so there may be a dysfunction of platelet as well that may additionally contribute to some hemorrhage.

The reason why some patients develop post-thrombolytic ICH and some don't, there are certain risk factors.

Generally, patients who are older may be more likely to develop post-thrombolytic ICH.

Those studies have not definitively shown that patients who have coagulopathy for unknown reason, low platelet counts, atrial fibrillation, small vessel disease, or amyloid angiopathy may be more at risk for developing hemorrhage.

Another thing to mention would be uncontrolled hypertension.

In order to administer thrombolytics, you have to have a systolic blood pressure less than one eighty-five.

And then once thrombolytics have been administered, the blood pressure goal is further lowered and is to be maintained at less than one eighty for the next twenty-four hours.

So if you have a patient who has received thrombolysis but has uncontrolled hypertension, those patients are at higher risk for developing post-thrombolytic ICH.

Today, we are looking at the paper by Enjitama and colleagues.

It was published in Open Heart in August 2026, and it’s titled Walking a Tightrope: The Safety and Efficacy of Oral Anticoagulants in Atrial Fibrillation Patients With Prior Intracranial Hemorrhage, a Systematic Review and Meta-Analysis.

It is a fundamentally important paper for our field.

I, I agree.

And before we get into the weeds, we need to provide our initial practical summary for neurologists who are pressed for time.

I mean, that’s crucial.

So in patients with atrial fibrillation and a history of intracranial hemorrhage, direct oral anticoagulants are associated with a significantly lower risk of recurrent intracranial hemorrhage compared to vitamin K antagonists.

Mm.