[Atypical intracerebral hemorrhage-etiology and acute management]. / Atypische intrazerebrale Blutungen ­ Ätiologie und Akutmanagement.

Acute management as well as establishing the etiology of an intracerebral hemorrhage is still a challenge for clinicians. The location of the intracerebral hemorrhage alone should not be used to determine the cause because atypically located hemorrhages can be caused by long-standing arterial hypertension and typically located hemorrhages can occur due to non-hypertensive causes. Besides discussing the classification of intracerebral hemorrhages, this article focuses on a diagnostic algorithm as well as the presentation of potential (rarer) causes of non-traumatic intracerebral hemorrhages. Furthermore, the acute treatment of intracerebral hemorrhage with respect to recent data on blood pressure management as well as the management of bleeding under oral anticoagulant treatment are described.

Microbleeds in ischemic vs hemorrhagic strokes on novel oral anticoagulants.

OBJECTIVES: To identify differences in clinical characteristics and severity of cerebral small vessel disease (CSVD) including cerebral microbleeds (CMBs), between patients suffering ischemic stroke (IS) or intracerebral hemorrhage (ICH) while taking novel (non-vitamin K antagonists) oral anticoagulants (NOACs). METHODS: Multicenter, prospective, observational cohort study performed at 38 centers between 2012 and 2015. We compared demographics, comorbidity, and functional status (before and after stroke) between NOAC-IS and NOAC-ICH patients. Extent of white matter lesions (WML), and location and counts of CMBs were analyzed in a subgroup of patients for whom MRI including hemorrhage-sensitive sequences was available. RESULTS: A total of 351 patients were included (290 NOAC-IS, 61 NOAC-ICH). Functional status was worse in NOAC-ICH patients before and after stroke. No significant differences were found for demographic variables and cardiovascular comorbidity. In the subgroup with available MRI (n = 116), the proportion of patients with at least one CMB was higher in NOAC-ICH than in NOAC-IS (15/19 [79%] vs 36/97 [37%], P < .001), as was the absolute number of CMBs (median 5 [IQR 1-24] vs 0 [0-1], P < .001). WML were more extensive in NOAC-ICH than in NOAC-IS patients. Adjusted for WML, logistic regression analysis showed higher odds of NOAC-ICH in patients with CMB than without (OR 5.60 [1.64-19.14], P = .006). CONCLUSIONS: Patients with NOAC-ICH have similar clinical characteristics but a higher prevalent burden of CSVD compared to NOAC-IS. The role of neuroimaging in selection of patients for anticoagulation with NOAC requires further investigation in longitudinal studies.

Volatile sedation with sevoflurane in intensive care patients with acute stroke or subarachnoid haemorrhage using AnaConDa®: an observational study.

BACKGROUND: The anaesthetic conserving device, AnaConDa(®), allows use of inhaled anaesthetics for sedation in the intensive care unit. We prospectively measured cerebral and cardiopulmonary parameters in patients with acute stroke or subarachnoid haemorrhage during a switch from i.v. to inhalative sedation. METHODS: 25 patients were switched from i.v. to an indefinite period of inhaled sedation with sevoflurane. Mean arterial (MAP), intracranial (ICP), and cerebral perfusion pressure (CPP), middle cerebral artery mean flow velocity (MFV) and fractional tissue oxygen extraction (FTOE), systemic cardiopulmonary parameters, and administered drugs were assessed before and after the change (-6 to +12 h). RESULTS: In 8 patients, critically reduced MAP or ICP crisis led to premature termination of sevoflurane sedation. In the other 17 patients, after the first hour, mean ICP increased [2.4 (4.5) mm Hg; P=0.046], MAP decreased [7.8 (14.1) mm Hg; P=0.036] and thus CPP decreased also [-10.2 (15.1) mm Hg; P=0.014]. MFV and FTOE did not change. Over a 12 hour post switch observational period, [Formula: see text] increased slightly [0.3 (0.8) kPa; P=0.104], ICP did not change [0.2 (3.9) mm Hg; P=0.865], but MAP [-6 (6.9) mm Hg; P=0.002] and thus CPP decreased [-6 (8.5) mm Hg; P=0.010]. CONCLUSION: Sevoflurane led to sufficient sedation, but decreased MAP and CPP in a selected cerebrovascular neurocritical care population. In about a third of these patients, severe adverse reactions, including intolerable ICP increases, were observed.