Structural Brain Injury on Brain Magnetic Resonance Imaging in Acute Respiratory Distress Syndrome.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is an acute inflammatory respiratory failure condition that may be associated with brain injury. We aimed to describe the types of structural brain injuries detected by brain magnetic resonance imaging (MRI) among patients with ARDS. METHODS: We retrospectively reviewed and collected data on brain injuries as detected by brain MRI during index hospitalization of all patients with ARDS at a single tertiary center in the United States from January 2010 to October 2018 (pre-COVID era). Structural brain injuries were classified as cerebral ischemia (ischemic infarct and hypoxic-ischemic brain injury) or cerebral hemorrhage (intraparenchymal hemorrhage, cerebral microbleeds, subarachnoid hemorrhage, and subdural hematoma). Descriptive statistics were conducted. RESULTS: Of the 678 patients with ARDS, 66 (9.7%) underwent brain MRI during their ARDS illness. The most common indication for brain MRI was encephalopathy (45.4%), and the median time from hospital admission to MRI was 10 days (interquartile range 4-17). Of 66 patients, 29 (44%) had MRI evidence of brain injury, including cerebral ischemia in 33% (22 of 66) and cerebral hemorrhage in 21% (14 of 66). Among those with cerebral ischemia, common findings were bilateral globus pallidus infarcts (n = 7, 32%), multifocal infarcts (n = 5, 23%), and diffuse hypoxic-ischemic brain injury (n = 3, 14%). Of those with cerebral hemorrhage, common findings were cerebral microbleeds (n = 12, 86%) and intraparenchymal hemorrhage (n = 2, 14%). Patients with ARDS with cerebral hemorrhage had significantly greater use of rescue therapies, including prone positioning (28.6% vs. 5.8%, p = 0.03), inhaled vasodilator (35.7% vs. 11.5%, p = 0.046), and recruitment maneuver (14.3% vs. 0%, p = 0.04). CONCLUSIONS: Structural brain injury was not uncommon among selected patients with ARDS who underwent brain MRI. The majority of brain injuries seen were bilateral globus pallidus infarcts and cerebral microbleeds.

Cerebral microbleeds in acute respiratory distress syndrome.

BACKGROUND: Cerebral microbleeds (CMB) have been observed in patients with critical illness. We sought to examine the frequency of CMB in patients with acute respiratory distress syndrome (ARDS) and association with neurologic complications including acute cerebral ischemia and seizures. METHODS: A retrospective review of patients with ARDS from January 2010 to October 2018 was performed. Patients with brain MRIs with susceptibility weighted imaging or gradient echo sequences were included. We compared neurologic complications and intensive care unit outcomes between patients with and without CMB. Cerebral small vessel disease (CSVD) was defined as the presence of CMB, lacunar infarcts, enlarged perivascular spaces, and white matter hyperintensities. RESULTS: Of 678 patients with ARDS, 61 met inclusion criteria. Median age was 54 years (IQR 42-63) and 28 were males. Of 12 (20%) with CMB, 10 had lobar CMB. Four patients had CMB in the corpus callosum, all involving the splenium. Neurologic complications were more common in those with CMB including acute cerebral ischemia (41.7% versus 10.2%, p=0.008) and seizures (33.3% versus 8.2%, p=0.021). ARDS rescue therapies were more commonly used in patients with CMB (p=0.005). There was no difference in hospital mortality (41.7% versus 34.7%, p=0.652). Patients with CMB did not have a higher CSVD score than those without CMB when accounting for the presence of CMB (median=1 versus 0, p=0.891). CONCLUSION: CMB were present in twenty percent of patients with ARDS who had MRI and were more commonly seen in patients requiring ARDS rescue therapies.

An Unusual Case of Bilateral Subperiosteal Orbital Hemorrhage.

Subperiosteal orbital hemorrhage usually occurs in the setting of facial or orbital trauma. Non-traumatic subperiosteal orbital hemorrhage (NTSOH) has rarely been reported in literature. The proposed mechanism of NTSOH is the transmission of sudden increase in cranial venous pressure to the orbital veins, which are valveless. We present a case of a 37 year old right-handed woman with a past medical history significant for type 1 diabetes, end-stage renal disease, peripheral artery disease and hypertension who developed NTSOH following an elective revision of a clotted right upper extremity arteriovenous fistula. During this procedure, she had acute eye pain, bilateral complete vision loss and emesis. CT of the orbits revealed large heterogeneously hyperdense lesions in the bilateral orbital apex extending anteriorly along the roof of the orbit, concerning for hemorrhage. Cultures obtained through nasal endoscopy were negative for a bacterial or fungal infection involving the sinuses. Ophthalmology was consulted and she underwent bilateral canthotomy and lateral cantholysis. Postoperatively, she was started on systemic and topical ocular antihypertensives, as well as prophylactic antibiotics. Visual acuity remained poor with finger counting on the right eye and lack of consistent response to light on the left eye. This case highlights periprocedural increase in systemic venous pressure secondary to a fistula repair procedure as a potential cause of NTSOH.

Assessment of Cerebral Autoregulation Using Invasive and Noninvasive Methods of Intracranial Pressure Monitoring.

BACKGROUND: Pulse amplitude index (PAx), a descriptor of cerebrovascular reactivity, correlates the changes of the pulse amplitude of the intracranial pressure (ICP) waveform (AMP) with changes in mean arterial pressure (MAP). AMP relies on cerebrovascular compliance, which is modulated by the state of the cerebrovascular reactivity. PAx can aid in prognostication after acute brain injuries as a tool for the assessment of cerebral autoregulation and could potentially tailor individual management; however, invasive measurements are required for its calculation. Our aim was to evaluate the relationship between noninvasive PAx (nPAx) derived from a novel noninvasive device for ICP monitoring and PAx derived from gold standard invasive methods. METHODS: We retrospectively analyzed invasive ICP (external ventricular drain) and non-invasive ICP (nICP), via mechanical extensometer (Brain4Care Corp.). Invasive and non-invasive ICP waveform morphology data was collected in adult patients with brain injury with arterial blood pressure monitoring. The time series from all signals were first treated to remove movement artifacts. PAx and nPAx were calculated as the moving correlation coefficients of 10-s averages of AMP or non-invasive AMP (nAMP) and MAP. AMP/nAMP was determined by calculating the fundamental frequency amplitude of the ICP/nICP signal over a 10-s window, updated every 10-s. We then evaluated the relationship between invasive PAx and noninvasive nPAx using the methods of repeated-measures analysis to generate an estimate of the correlation coefficient and its 95% confidence interval (CI). The agreement between the two methods was assessed using the Bland-Altman test. RESULTS: Twenty-four patients were identified. The median age was 53.5 years (interquartile range 40-70), and intracranial hemorrhage (84%) was the most common etiology. Twenty-one (87.5%) patients underwent mechanical ventilation, and 60% were sedated with a median Glasgow Coma Scale score of 8 (7-15). Mean PAx was 0.0296 ± 0.331, and nPAx was 0.0171 ± 0.332. The correlation between PAx and nPAx was strong (R = 0.70, p < 0.0005, 95% CI 0.687-0.717). Bland-Altman analysis showed excellent agreement, with a bias of - 0.018 (95% CI - 0.026 to - 0.01) and a localized regression trend line that did not deviate from 0. CONCLUSIONS: PAx can be calculated by conventional and noninvasive ICP monitoring in a statistically significant evaluation with strong agreement. Further study of the applications of this clinical tool is warranted, with the goal of early therapeutic intervention to improve neurologic outcomes following acute brain injuries.

Cerebral Microvascular Injury in Patients with Left Ventricular Assist Device: a Neuropathological Study.

Strokes are common among patients with left ventricular devices (LVAD). We hypothesize that there is ongoing cerebral microvascular injury with LVAD support and aim to describe this among LVAD-implanted patients through post-mortem neuropathologic evaluation. We identified and reviewed medical records of LVAD patients who underwent brain autopsy between January 2006 and December 2019 at a tertiary center. Cerebral injury was defined as both gross and microscopic injuries within the intracranial space including cerebral infarct (CI), hypoxic-ischemic brain injury (HIBI), intracranial hemorrhage (ICH), and cerebral microvascular injury. Cerebral microvascular injury was defined as microscopic brain intraparenchymal or perivascular hemorrhage, perivascular hemosiderin deposition, and perivascular inflammation. Twenty-one patients (median age = 57 years, 67% male) had autopsy after LVAD support (median LVAD support = 51 days). The median time from death to autopsy was 19 h. All 21 patients had cerebral injuries and 19 (90%) patients had cerebral microvascular injuries. Fourteen patients (78%) harbored more than one type of cerebral injury. On gross examination, 8 patients (38%) had CI, and 6 patients (29%) had ICH. On microscopic exam, 12 patients (57%) had microscopic intraparenchymal hemorrhage, 3 patients (14%) had perivascular hemorrhage, 11 patients (43%) had perivascular hemosiderin deposition, 5 patients (24%) had meningeal hemorrhage, 13 patients had chronic perivascular inflammation (62%), and 2 patients had diffuse HIBI (10%). Among patients with LVAD, there is a high prevalence of subclinical microvascular injuries and cerebral microbleeds (CMBs), which may provide some insights to the cause of frequent cerebral injury in LVAD population.

Pathophysiology of Brain Injury and Neurological Outcome in Acute Respiratory Distress Syndrome: A Scoping Review of Preclinical to Clinical Studies.

Acute respiratory distress syndrome (ARDS) has been associated with secondary acute brain injury (ABI). However, there is sparse literature on the mechanism of lung-mediated brain injury and prevalence of ARDS-associated secondary ABI. We aimed to review and elucidate potential mechanisms of ARDS-mediated ABI from preclinical models and assess the prevalence of ABI and neurological outcome in ARDS with clinical studies. We conducted a systematic search of PubMed and five other databases reporting ABI and ARDS through July 6, 2020 and included studies with ABI and neurological outcome occurring after ARDS. We found 38 studies (10 preclinical studies with 143 animals; 28 clinical studies with 1175 patients) encompassing 9 animal studies (n = 143), 1 in vitro study, 12 studies on neurocognitive outcomes (n = 797), 2 clinical observational studies (n = 126), 1 neuroimaging study (n = 15), and 13 clinical case series/reports (n = 15). Six ARDS animal studies demonstrated evidence of neuroinflammation and neuronal damage within the hippocampus. Five animal studies demonstrated altered cerebral blood flow and increased intracranial pressure with the use of lung-protective mechanical ventilation. High frequency of ARDS-associated secondary ABI or poor neurological outcome was observed ranging 82-86% in clinical observational studies. Of the clinically reported ABIs (median age 49 years, 46% men), the most common injury was hemorrhagic stroke (25%), followed by hypoxic ischemic brain injury (22%), diffuse cerebral edema (11%), and ischemic stroke (8%). Cognitive impairment in patients with ARDS (n = 797) was observed in 87% (range 73-100%) at discharge, 36% (range 32-37%) at 6 months, and 30% (range 25-45%) at 1 year. Mechanisms of ARDS-associated secondary ABI include primary hypoxic ischemic injury from hypoxic respiratory failure, secondary injury, such as lung injury induced neuroinflammation, and increased intracranial pressure from ARDS lung-protective mechanical ventilation strategy. In summary, paucity of clinical data exists on the prevalence of ABI in patients with ARDS. Hemorrhagic stroke and hypoxic ischemic brain injury were commonly observed. Persistent cognitive impairment was highly prevalent in patients with ARDS.

Neurologic aspects of coronavirus disease of 2019 infection.

PURPOSE OF REVIEW: Central and peripheral nervous system manifestations of coronavirus disease 2019 (COVID-19) have been frequently reported and may cause significant morbidity and mortality. This review details the latest evidence on the neuropathogenesis and neurologic complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. RECENT FINDINGS: Commonly reported neurologic complications include toxic-metabolic encephalopathy, acute cerebrovascular disorders, seizures, and anoxic-brain injury. These complications represent secondary injury due to COVID-19 related hypoxia, sepsis, hypercoagulability, or hyperinflammation. Postinfectious complications, such as encephalitis, postinfectious demyelination, and Guillain-Barré syndrome have been reported, but are rare. Recent reports of persistent neurocognitive symptoms highlight the possibility of lasting impairment. SUMMARY: Although some neurologic complications should be treated with standard practices, further investigations are still needed to determine the optimal treatment of COVID-related neurologic complications, such as ischemic stroke. Entering into the next phase of the pandemic, investigations into the long-term neurologic and cognitive impacts of SARS-CoV-2 infection will be needed. Clinicians must have a high clinical suspicion for both acute and chronic neurologic complications among COVID-19 patients.

Tachyarrhythmias and neurologic complications.

Tachyarrhythmias are abnormal heart rhythms with a ventricular rate of 100 or more beats per minute. These rhythms are classified as either narrow or wide-complex tachycardia with further subdivision into regular or irregular rhythm. Patients are frequently symptomatic presenting with palpitations, diaphoresis, dyspnea, chest pain, dizziness, and syncope. Sudden cardiac death may occur with certain arrhythmias. Recognizing tachyarrhythmia and understanding its management is important as a wide spectrum of neurologic complications have been associated with such arrhythmias. The purpose of this chapter is to provide a comprehensive overview on the neurologic complications of tachyarrhythmias, neurologic adverse events of antiarrhythmic interventions, and neurologic conditions that can precipitate tachyarrhythmia.

How Are We Monitoring Brain Injuries in Patients With Left Ventricular Assist Device? A Systematic Review of Literature.

Despite the common occurrence of brain injury in patients with left ventricular assist device (LVAD), optimal neuromonitoring methods are unknown. A systematic review of PubMed and six electronic databases from inception was conducted until June 5, 2019. Studies reporting methods of neuromonitoring while on LVAD were extracted. Of 5,190 records screened, 37 studies met the inclusion criteria. The neuromonitoring methods include Transcranial Doppler ultrasound for emboli monitoring (TCD-e) (n = 13) and cerebral autoregulation (n = 3), computed tomography and magnetic resonance imaging (n = 9), serum biomarkers (n = 7), carotid ultrasound (n = 3), and near-infrared spectroscopy (n = 2). Of 421 patients with TCD-e, thromboembolic events (TEs) were reported in 79 patients (20%) and microembolic signals (MES) were detected in 105 patients (27%). Ischemic stroke was more prevalent in patients with MES compared to patients without MES (43% vs.13%, p < 0.001). Carotid ultrasound for assessing carotid stenosis was unreliable after LVAD implantation. Elevated lactate dehydrogenase (LDH) levels were associated with TEs. Significant heterogeneity exists in timing, frequency, and types of neuromonitoring tools. TCD-e and serial LDH levels appeared to have potential for assessing the risk of ischemic stroke. Future prospective research incorporating protocolized TCD-e and LDH may assist in monitoring adverse events in patients with LVAD.

Neurologic complications of COVID-19.

Patients with COVID-19 have a fairly high risk of neurologic complications, including encephalopathy, stroke, central nervous system infection, seizures, and neuromuscular diseases. Many report losing their senses of smell and taste, and many survivors report lingering neurocognitive impairment. The diagnosis and treatment of these complications does not differ from that in other patients, although sophisticated testing may not be readily available for a patient in intensive care and respiratory isolation. Clinicians should therefore be alert to these complications.

Ischemic Stroke and Intracranial Hemorrhages During Impella Cardiac Support.

Impella is a percutaneously placed, ventricular assist device for short-term cardiac support. We aimed to study acute neurologic complications during short-term cardiac support with Impella. We reviewed prospectively collected data of 79 consecutive persons implanted with Impella at a single tertiary center. Acute neurologic events (ANE) were defined as ischemic strokes or intracranial hemorrhages. Among those with ANE, specific causes of ischemic and hemorrhagic events were collected and discussed. Of 79 persons with Impella with median 8 days of support (range 1-33 days), six (7.5%) developed ANE at a median of 5 days from implant (range 1-8 days). There were three ischemic strokes, two intracerebral hemorrhages, and one subdural hematoma. Hemorrhagic events were attributed to anticoagulant use and thrombocytopenia at the time of the events. Two ischemic strokes were attributed to inadequate anticoagulation with one case of pump thrombosis diagnosed at the time of ischemic stroke. Only two of the six patients survived the acute cardiogenic shock period to achieve heart transplantation. In-hospital ischemic strokes and intracranial hemorrhages are not uncommon during short-term cardiac support period with Impella. Antithrombotic intensity, duration of device support time, and thrombocytopenia might contribute to the incidence of these events.

Cerebral Microembolization in Left Ventricular Assist Device Associated Ischemic Events.

INTRODUCTION: The significance of microembolic signals (MES) detected by transcranial Doppler ultrasound emboli monitoring (TCD-e) in patients supported with left ventricular assist devices (LVAD) remains unclear. We aimed to investigate the relationship between cerebral microembolization detected by TCD-e and acute ischemic events in LVAD patients. METHODS: We reviewed consecutive patients with acute ischemic stroke or transient ischemic attack (TIA) in a prospectively collected database of LVAD patients. TCD-e exams consisted of monitoring the middle cerebral arteries for microembolic signals (MES) over 30 minutes. RESULTS: Of 515 persons with LVAD, 41 TCD-e studies were performed in 35 patients with acute ischemic stroke or transient ischemic attack (TIA) in a median of 1 day (Interquartile range [IQR]: 0-2) after the event. MES were present in 15 (44%) TCD-e studies with a median MES count of 4 (IQR: 2-15.5). Bloodstream infections were more common in patients with MES (38% versus 8%, P = .039). There were trends for lower international normalized ratio (1.39 versus 1.69, P = .214), lower activated partial thromboplastin (33.2 versus 36.6, P = .577), higher lactate dehydrogenase (531 versus 409, P = .323) and a higher frequency of pump thrombosis (13% versus 8%, P = .637) in patients with MES compared with those without MES. CONCLUSIONS: LVAD patients with acute ischemic stroke or TIA have a high prevalence of MES on TCD-e, which may serve as a marker for a prothrombotic state. Further study of MES in LVAD patients is warranted.