[Update on Intensive Care Unit Management of Stroke]. / Aktuelle Aspekte in der Intensivtherapie des Schlaganfalls.

In this review, we provide an update on the intensive care unit (ICU) management of ischemic stroke. Over the last decade, new evidence has led to rapid changes in the early management of patients admitted with acute ischemic stroke. Nevertheless, stroke remains a leading cause of disability. Consequently, a significant number of patients with acute ischemic stroke require ICU level care. The most frequent reasons for ICU admissions are large infarction with potential swelling, reduced level of consciousness, secondary hemorrhagic transformation, acute symptomatic seizures or respiratory failure and stroke-related disorders of the brain-heart interaction. Moreover, there is an increasing number of patients receiving intravenous thrombolysis or mechanical thrombectomy with a subsequent need of ICU monitoring. Several studies have shown that the implementation of specialized neuro-intensive care teams help to improve functional outcome after acute ischemic stroke. The main goal in the ICU management of stroke patients is to prevent secondary brain injury. To this end, a comprehensive approach to optimize systemic physiological homeostasis, control intracranial pressure, cerebral perfusion, hemodynamic and respiratory parameters is needed. Here, we summarize recent advances in invasive and non-invasive neuro-monitoring, decision making in decompressive neurosurgery for large supratentorial or cerebellar infarction, specific cardiorespiratory management, nutrition, temperature management and mobilization strategies in ischemic stroke.

Loss of cerebral blood flow and cerebral perfusion pressure in brain death: A transcranial Duplex ultrasonography study.

PURPOSE: We investigated cerebral perfusion pressure (CPP) at the time loss of cerebral blood flow (CBF) occurred during brain death (BD). We hypothesized that a critical closing pressure (CrCP) may be reached before CPP drops to 0 mmHg. MATERIALS AND METHODS: 14 patients with increasing intracranial pressure (ICP) leading to BD were included. Transcranial Duplex (TCD) ultrasonography was used to investigate CBF. Starting at a CPP of 30 mmHg, TCD was repeated until waveforms indicated loss of CBF. We then analyzed CPP by the time TCD indicated absent CBF and clinical BD was established. RESULTS: In 12 patients, CPP was positive when clinical BD was manifest and TCD illustrated absent CBF. Across all patients, mean CPP at clinical BD manifestation was 10.0 mmHg (range 0-20 mmHg); mean CPP by the time CBF stopped was 7.5 mmHg (0-20 mmHg). In four patients, clinical BD preceded loss of CBF. Here, the mean CPP difference from clinical BD to loss of CBF was 8.8 mmHg (5-15 mmHg). CONCLUSIONS: CrCP may be reached although CPP is still positive, resulting in complete loss of CBF and BD. By including bedside TCD, neuromonitoring may contribute to early identification of patients at risk to experience loss of CBF and subsequent BD.