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To assess the risk of hematoma expansion in patients with acute intracranial hemorrhage (ICH) requiring therapeutic anticoagulation for the treatment of venous thromboembolism.We retrospectively reviewed all patients at our institution between 2014 and 2019 who were therapeutically anticoagulated for venous thromboembolism within 4 weeks after ICH. We included subtypes of traumatic ICH and spontaneous intraparenchymal hemorrhage. Our main outcome was the incidence of hematoma expansion within 14 days from initiating therapeutic anticoagulation. Hematoma expansion was defined as (1) radiographically proven expansion leading to cessation of therapeutic anticoagulation or (2) death due to hematoma expansion. Secondary outcomes included mortality due to hematoma expansion and characteristics associated with hematoma expansion.Fifty patients met inclusion criteria (mean age: 54 years, 80% male, 76% Caucasian); 24% had undergone a neurosurgical procedure prior to therapeutic anticoagulation. Median time from ICH to therapeutic anticoagulation initiation was 9.5 days (IQR 4-17), 40% received therapeutic anticoagulation in 7 days after ICH. Six patients (12%) developed hematoma expansion, of whom two (4%) died. While not statistically significant, patients with hematoma expansion tended to be older (57.8 vs. 53.5 years), were anticoagulated sooner (4 vs. 10 days), presented with lower GCS (50% vs. 39% with GCS8), higher hematoma volume (50% vs. 42%30 cc), and higher SDH diameter (16 mm vs. 8.35 mm). There was a trend towards greater risk of hematoma expansion for patients undergoing endoscopic ICH evacuation (16% vs. 2%,Our study is among the first to explore characteristics associated with hematoma expansion in patients undergoing therapeutic anticoagulation after acute ICH. Larger studies in different ICH subtypes are needed to identify determinants of hematoma expansion in this high-acuity population.

This qualitative study assessed the experience of patients with chronic rhinosinusitis with nasal polyposis (NP) to inform the development of a novel symptom diary for clinical study use.Concept elicitation and cognitive interviews were conducted with patients who had a physician-verified diagnosis of NP and a history of intranasal corticosteroid use. Concepts were identified via open-ended and follow-up questions. Relative symptom/impact disturbance level was assessed using a scale of 0 (not at all disturbing) to 10 (extremely disturbing).Patients (n = 30) attributed numerous symptoms and impacts to NP; the most prevalent and disturbing were nasal congestion (identified by 100% of patients; average disturbance rating = 7.9), nasal blockage/obstruction (97%; 8.2), difficulty with sense of smell (97%; 7.6), facial pressure (90%; 6.2), postnasal drip (87%; 6.5), runny nose (87%; 6.2), facial pain (80%; 6.3), and headache (77%; 6.5). These symptoms, along with the impact of NP on sleep and daily activities, were included in the Nasal Polyposis Symptom Diary (NPSD). Cognitive interviews confirmed that patients understood the NPSD items and could select a response reflective of their experience at its worst over the past 24 hours using a four-point scale (none, mild, moderate, or severe).The most relevant and disturbing symptoms, according to patients with NP, were included in the NPSD. Interviews confirmed the suitability of NPSD in capturing the daily experience of patients. These findings support the content validity of the NPSD as a suitable tool for capturing NP symptoms and impacts.

To summarize pathophysiology, key conflicts, and therapeutic approaches in managing concomitant severe acute brain injury (SABI) and acute respiratory distress syndrome (ARDS).ARDS is common in SABI and independently associated with worse outcomes in all SABI subtypes. Most landmark ARDS trials excluded patients with SABI, and evidence to guide decisions is limited in this population. Potential areas of conflict in the management of patients with both SABI and ARDS are (1) risk of intracranial pressure (ICP) elevation with high levels of positive end-expiratory pressure (PEEP), permissive hypercapnia due to lung protective ventilation (LPV), or prone ventilation; (2) balancing a conservative fluid management strategy with ensuring adequate cerebral perfusion, particularly in patients with symptomatic vasospasm or impaired cerebrovascular blood flow; and (3) uncertainty about the benefit and harm of corticosteroids in this population, with a mortality benefit in ARDS, increased mortality shown in TBI, and conflicting data in other SABI subtypes. Also, the widely adapted partial pressure of oxygen (PThe management of SABI with ARDS is highly complex, and conventional ARDS management strategies may result in increased ICP and decreased cerebral perfusion. A crucial aspect of concurrent management is to recognize the risk of secondary brain injury in the individual patient, monitor with vigilance, and adjust management during critical time windows. The care of these patients requires meticulous attention to oxygenation and ventilation, hemodynamics, temperature management, and the neurological exam. LPV and prone ventilation should be utilized, and supplemented with invasive ICP monitoring if there is concern for cerebral edema and increased ICP. PEEP titration should be deliberate, involving measures of hemodynamic, pulmonary, and brain physiology. Serial volume status assessments should be performed in SABI and ARDS, and fluid management should be individualized based on measures of brain perfusion, the neurological exam, and cardiopulmonary status. More research is needed to define risks and benefits in corticosteroids in this population.

Antiplatelet therapy remains the standard of care in secondary stroke prevention for non-cardioembolic ischemic stroke and transient ischemic attack. We aim to examine the use of antiplatelet agents in secondary prevention through highlighting relevant clinical trials and meta-analyses as well as providing commentary regarding our practice. In the POINT and CHANCE trials, dual antiplatelet therapy reduced recurrent stroke compared to aspirin monotherapy. Sub-analyses of these trials suggest that genetic polymorphisms could play a role in diminishing the effectiveness of clopidogrel. Similarly, THALES demonstrated better outcomes with ticagrelor-aspirin combination therapy over aspirin monotherapy. Combination antiplatelet therapy with aspirin and the P2Y12 inhibitors, clopidogrel and ticagrelor, reduced stroke recurrence in those presenting with mild ischemic stroke or high risk TIA. Genetic polymorphisms may play a role in determining the appropriate regimen. Questions remain regarding the optimal duration of combination antiplatelet therapy for various stroke etiologies.