Neurocritical care
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The magnitude of the COVID-19 pandemic will result in substantial neurological disease, whether through direct infection (rare), para-infectious complications (less rare), or critical illness more generally (common). Here, we raise the importance of stringent diagnosis and data collection regarding neurological complications of COVID-19; we urge caution in the over-diagnosis of neurological disease where it does not exist, but equally strongly encourage the concerted surveillance for such conditions. ⋯ We therefore also outline the specific management of patients with neuroinflammatory diseases in the context of the pandemic. This article describes the implications of COVID-19 on neurological disease and advertises the Neurocritical Care Society's international data collection collaborative that seeks to align data elements.
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Antithrombotic therapy is administered after left ventricular assist device (LVAD) implantation to prevent thromboembolic events. Intracranial hemorrhage (ICH) is a life-threatening adverse event requiring immediate discontinuation of antithrombotics. We investigated the timing of antithrombotic resumption after ICH in patients with LVADs and the association between timing and risk of recurrent hemorrhage and thrombotic events. ⋯ Despite timing of resumption of antithrombotic therapy after ICH, recurrent hemorrhagic events can be expected in one-quarter of these patients over the subsequent year.
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A relationship between intracranial and abdominal aortic aneurysms (AAA) has been appreciated through genome-wide association studies suggesting a shared pathophysiology. However, the actual prevalence of AAA in patients presenting with ruptured intracranial aneurysms is not known. Our aim was to estimate the prevalence of previously undiagnosed AAA in patients presenting with aneurysmal subarachnoid hemorrhage (aSAH) to see if it may be high enough to justify formally testing the utility of screening. ⋯ The co-prevalence of AAA in patients presenting with ruptured brain aneurysms may be sufficiently high such that screening for AAA among likely survivors of aSAH might be appropriate. Larger studies would be needed to establish a net clinical benefit from screening AAA and then treating newly identified large AAAs in this morbid population.
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A clinical history leads to an examination, tests and a diagnosis. This time-honored sequence in medicine remains valid in critical illness, but in the heat of the moment there is a quickly appearing inevitable sketchiness. Intensivists should never be too unquestioning, too comfortable with incomplete information, or too unwilling to start over if information is muddled or contradictory. ⋯ I review the essentials of history taking in a neurocritically ill patient. Examples of the value of a good medical history are shown but also the familiar biases when asking questions. There are obstacles, errors of commission and omission, and the importance of recognition of a clinical trajectory.
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Attenuation of neuronal apoptosis helps maintain neurological function in patients after cardiac arrest. After ischemia-reperfusion, both cyclosporin A (CsA) and ischemic postconditioning independently protect mitochondria and thus reduce nerve injury. This study employed a rat model to evaluate the neuroprotective effect of combining ischemic postconditioning with CsA after cardiopulmonary resuscitation (CPR). ⋯ Ischemic postconditioning combined with CsA exerted a better neuroprotective effect after CPR than did either postconditioning or CsA alone. Inhibiting the opening of the mPTP is not the only neuroprotective mechanism.