The risk of intracerebral hemorrhage (ICH) hematoma expansion (HE) is highest in the first hours after onset, and coagulopathy is believed to further increase this risk. However, there is a paucity of data comparing the risk of HE over time for various antithrombotic agents. We conducted a retrospective study of spontaneous ICH patients enrolled at a comprehensive stroke center between December 2016 and May 2022, excluding those who underwent surgical evacuation. ICH volumes were calculated using ABC/2 methodology and HE was coded for a ≥ 33

Objective: Disorders of consciousness (DoC) are known to correlate with worse functional outcome after hemorrhagic stroke. Here we evaluate factors associated low Glasgow Coma Scale [GCS] score at time of admission in patients with hemorrhagic stroke. Methods: We performed a prospective cohort study of patients enrolled in the Neurological Emergencies Outcomes Study between January 2014 and June 2023 of patients with primary intracranial hemorrhage (intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH)). The primary outcome was coma (GCS ≤ 8) at time of admission. Univariable analysis with chi-squared test and Mann Whitney U test followed by adjusted logistic regression were used to assess the relationship between admission factors and DoC. We then confirmed the association with admission GCS and discharge modified Rankin score (mRS). Results: We included 314 patients admitted with intracranial hemorrhage, 51 (16%) of whom had GCS ≤ 8 at time of admission, 51% female and median [interquartile (IQR)] age of 63 [51-73]. The median [IQR] ICH volume was 9.3 ml [2.5-27.2] for ICH patients and the median [IQR] modified Fisher score was 3 [3-4] for SAH patients. Female gender, Asian race, hematoma size, hydrocephalus, peak temperature, lowest hemoglobin, and peak glucose in the first 24 hours were all associated with DoC (p<0.05 for all). Controlling for age, disease process (ICH vs SAH), and all factors with p < 0.05, we found female gender (OR 4.7, 95% CI 1.7-13.4), highest temperature (OR 3.8, 95% CI 1.9-7.3), lowest hemoglobin (OR 0.8, 95% CI 0.6-0.99), and highest glucose OR 1.01, 95% CI 1.00-1.02) remained significantly associated with coma at time of admission. Premorbid dependency as measured by Barthel Index was not a predictor of coma. However, coma at time of admission was associated with a worse discharge mRS (median discharge mRS [IQR] for patients with coma 5 [4-6] vs without 3 [2-4], p < 0.001). Conclusions: We found that female gender, low hemoglobin, high body temperature, and elevated glucose at time of admission were all associated with coma. Low admission GSC (≤ 8) was associated with higher mRS at time of discharge. These modifiable risk factors are an important therapeutic target for improving outcomes for patients with DoC.

Introduction: Patients who have had hemorrhagic strokes experience psychological and functional deficits after hospital discharge. Social Determinants of Health (SDoH) can also impact outcomes. The relationship between SDoH and psychological outcomes following hemorrhagic stroke has not been well studied. Methods: This is a prospective cohort study including patients ≥18-years-old hospitalized in Manhattan for non-traumatic hemorrhagic stroke, including intracerebral hemorrhage (ICH) and subarachnoid hemorrhage, between 2015 and 2022, aiming to determine the relationship between SDoH, functional and psychological outcomes. SDoH were reported on admission by patients or their surrogate, and included education level, occupation, insurance, marriage status, median household income (MHI) by zip code, and race/ethnicity. Questionnaires for the Barthel Index and Quality of Life in Neurological Disorders (T-score >50 abnormal) were completed at 3 and 12 months. Pearson’s Chi-Square and Mann Whitney U test were used to explore the relationship between SDoH and abnormal psychological outcomes. Results: We identified 120 patients with hemorrhagic stroke that had follow up psychological outcome testing. The median age [interquartile range (IQR)] was 64 [51-75], 46% female, median ICH score [IQR] was 1 [0-2], median Hunt-Hess scale [IQR] was 2[1-3]. Patients whose highest level of education was high school or below (21% of the cohort) were more likely to be dependent than independent with activities of daily living (33% vs 8%, p≤0.01) at 3 months. The median MHI by zip code [IQR] was $90,306 [$68,220-$131,038]. Patients with impaired communication were more likely to be from areas with lower MHI ($57,770 [$56,572-$68,221] vs. $90,871 [$72,895-$129,705], p=0.01) at 3 months. Employed patients (49% of cohort) were more likely to have cognitive executive dysfunction at both 3 (71% vs 39%) and 12 months (70% vs 34%, p<0.01 for both). Employed patients were also less likely to report overall good well-being (61% vs 29% at 3 months, 61% vs 20% at 12 months, p<0.01 for both). Conclusion: Psychological and functional outcomes for patients with hemorrhagic strokes are associated with SDoH. Interventions specifically addressing SDoH should be considered.

The utility of head computed tomography (CT) in predicting elevated intracranial pressure (ICP) is known to be limited in traumatic brain injury; however, few data exist in patients with spontaneous intracranial hemorrhage. We conducted a retrospective review of prospectively collected data in patients with nontraumatic intracranial hemorrhage (subarachnoid hemorrhage [SAH] or intraparenchymal hemorrhage [IPH]) who underwent external ventricular drain (EVD) placement. Head CT scans performed immediately prior to EVD placement were quantitatively reviewed for features suggestive of elevated ICP, including temporal horn diameter, bicaudate index, basal cistern effacement, midline shift, and global cerebral edema. The modified Fisher score (mFS), intraventricular hemorrhage score, and IPH volume were also measured, as applicable. We calculated the accuracy, positive predictive value (PPV), and negative predictive value (NPV) of these radiographic features for the coprimary outcomes of elevated ICP (> 20 mm Hg) at the time of EVD placement and at any time during the hospital stay. Multivariable backward stepwise logistic regression analysis was performed to identify significant radiographic factors associated with elevated ICP. Of 608 patients with intracranial hemorrhages enrolled during the study time frame, 243 (40

Kahn, D. Ethan1; Lord, Aaron2; Zhou, Ting3; Scher, Erica4; Frontera, Jennifer5; Bhatt, Prachi6; Agarwal, Shashank7 Author Information

Introduction: While the thrombotic complications of COVID-19 have been described, there are limited data on its implications in hemorrhagic stroke. The clinical characteristics, underlying stroke mechanism, and outcomes in this group of patients are especially salient as empiric therapeutic anticoagulation becomes increasingly common in the treatment and prevention of thrombotic complications of COVID-19. Methods: We conducted a retrospective cohort study of patients with hemorrhagic stroke (both non-traumatic intracerebral hemorrhage and spontaneous non-aneurysmal subarachnoid hemorrhage) who were hospitalized between 3/1/20-5/15/20 at a NYC hospital system, during the coronavirus pandemic. We compared the demographic and clinical characteristics of patients with hemorrhagic stroke and COVID-19 to those without COVID-19 admitted to our hospital between 3/1/20-5/15/20 (contemporary controls) and 3/1/19-5/15/19 (historical controls), using Fischer’s exact test and non-parametric testing. We adjusted for multiple comparisons using the Bonferroni method. Results: During the study period, 19 out of 4071 (0.5%) patients who were hospitalized with COVID-19 had hemorrhagic stroke on imaging. Of all COVID-19 with hemorrhagic stroke, only 3 had non-aneurysmal SAH without intraparenchymal hemorrhage. Among hemorrhagic stroke and COVID-19 patients, coagulopathy was the most common etiology (73.7%); empiric anticoagulation was started in 89.5% vs 4.2% of contemporary and 10.0% of historical controls (both with p =<0.001). Compared to contemporary and historical controls, COVID-19 patients had higher initial NIHSS scores, INR, PTT and fibrinogen levels. These patients also had higher rates of in-hospital mortality [84.6% vs. 4.6%, p =<0.001]. Sensitivity analyses excluding patients with strictly subarachnoid hemorrhage yielded similar results. Conclusion: We observed an overall low rate of imaging-confirmed hemorrhagic stroke among patients hospitalized with COVID-19. Most hemorrhages in COVID-19 patients occurred in the setting of therapeutic anticoagulation and were associated with increased mortality. Further studies are needed to evaluate the safety and efficacy of therapeutic anticoagulation in COVID-19 patients.

ABSTRACTBackgroundLittle is known regarding long-term outcomes of patients hospitalized with COVID-19.MethodsWe conducted a prospective study of 6-month outcomes of hospitalized COVID-19 patients. Patients with new neurological complications during hospitalization who survived were propensity score-matched to COVID-19 survivors without neurological complications hospitalized during the same period. The primary 6-month outcome was multivariable ordinal analysis of the modified Rankin Scale(mRS) comparing patients with or without neurological complications. Secondary outcomes included: activities of daily living (ADLs;Barthel Index), telephone Montreal Cognitive Assessment and Neuro-QoL batteries for anxiety, depression, fatigue and sleep.ResultsOf 606 COVID-19 patients with neurological complications, 395 survived hospitalization and were matched to 395 controls; N=196 neurological patients and N=186 controls completed follow-up. Overall, 346/382 (91%) patients had at least one abnormal outcome: 56% had limited ADLs, 50% impaired cognition, 47% could not return to work and 62% scored worse than average on ≥1 Neuro-QoL scale (worse anxiety 46%, sleep 38%, fatigue 36%, and depression 25%). In multivariable analysis, patients with neurological complications had worse 6-month mRS (median 4 vs. 3 among controls, adjusted OR 2.03, 95%CI 1.22-3.40, P=0.01), worse ADLs (aOR 0.38, 95%CI 0.29-0.74, P=0.01) and were less likely to return to work than controls (41% versus 64%, P=0.04). Cognitive and Neuro-QOL metrics were similar between groups.ConclusionsAbnormalities in functional outcomes, ADLs, anxiety, depression and sleep occurred in over 90% of patients 6-months after hospitalization for COVID-19. In multivariable analysis, patients with neurological complications during index hospitalization had significantly worse 6-month functional outcomes than those without.

We appreciate the comments by Kumar et al. on our article.1 The referenced Kremer study2 was a retrospective case series and included patients with positive MRI findings only. It is unclear whether the patients with the diagnosis of "encephalitis" met diagnostic or causal criteria outlined by the International Encephalitis Consortium3 and others.4 Indeed, CSF SARS-CoV-2 RT-PCR was negative in 20 patients. In 2 of 3 with CSF pleocytosis (>5 cell/mm3), imaging was performed >2 weeks from symptom onset, possibly representing postinfectious autoimmune encephalitis and not infectious encephalitis. Many of the MRI findings described are nonspecific and can be seen in hypoxic/ischemic brain injury, metabolic encephalopathy, or postseizure. Notably, 100% of "encephalitis" patients required oxygen and 75% had ARDS, suggesting that a proportion of the MRI changes may represent hypoxic/ischemic injury (defined as a global insult due to hypoxemia, hypotension, or cardiac arrest). Although we detected elevated CSF protein in some patients,1 this is nonspecific and can be found in stroke, hemorrhage (or traumatic tap), hypoxic/ischemic injury, diabetes, uremia, tumor, neuropathy, and many other conditions. Because the implications of SARS-CoV-2 neurotropism are far reaching, we believe that it is critical to follow the most rigorous standards and criteria when ascribing encephalitis/meningitis/myelitis to SARS-CoV-2 infection.

Toxic metabolic encephalopathy (TME) has been reported in 7–31% of hospitalized patients with coronavirus disease 2019 (COVID-19); however, some reports include sedation-related delirium and few data exist on the etiology of TME. We aimed to identify the prevalence, etiologies, and mortality rates associated with TME in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-positive patients. We conducted a retrospective, multicenter, observational cohort study among patients with reverse transcriptase–polymerase chain reaction-confirmed SARS-CoV-2 infection hospitalized at four New York City hospitals in the same health network between March 1, 2020, and May 20, 2020. TME was diagnosed in patients with altered mental status off sedation or after an adequate sedation washout. Patients with structural brain disease, seizures, or primary neurological diagnoses were excluded. The coprimary outcomes were the prevalence of TME stratified by etiology and in-hospital mortality (excluding comfort care only patients) assessed by using a multivariable time-dependent Cox proportional hazards models with adjustment for age, race, sex, intubation, intensive care unit requirement, Sequential Organ Failure Assessment scores, hospital location, and date of admission. Among 4491 patients with COVID-19, 559 (12%) were diagnosed with TME, of whom 435 of 559 (78%) developed encephalopathy immediately prior to hospital admission. The most common etiologies were septic encephalopathy (n = 247 of 559 [62%]), hypoxic-ischemic encephalopathy (HIE) (n = 331 of 559 [59%]), and uremia (n = 156 of 559 [28%]). Multiple etiologies were present in 435 (78%) patients. Compared with those without TME (n = 3932), patients with TME were older (76 vs. 62 years), had dementia (27% vs. 3%) or psychiatric history (20% vs. 10%), were more often intubated (37% vs. 20%), had a longer hospital length of stay (7.9 vs. 6.0 days), and were less often discharged home (25% vs. 66% [all P < 0.001]). Excluding comfort care patients (n = 267 of 4491 [6%]) and after adjustment for confounders, TME remained associated with increased risk of in-hospital death (n = 128 of 425 [30%] patients with TME died, compared with n = 600 of 3799 [16%] patients without TME; adjusted hazard ratio [aHR] 1.24, 95% confidence interval [CI] 1.02–1.52, P = 0.031), and TME due to hypoxemia conferred the highest risk (n = 97 of 233 [42%] patients with HIE died, compared with n = 631 of 3991 [16%] patients without HIE; aHR 1.56, 95% CI 1.21–2.00, P = 0.001). TME occurred in one in eight hospitalized patients with COVID-19, was typically multifactorial, and was most often due to hypoxemia, sepsis, and uremia. After we adjustment for confounding factors, TME was associated with a 24% increased risk of in-hospital mortality.

The COVID-19 pandemic dramatically affected the operations of New York City hospitals during March and April of 2020. This article describes the transformation of a neurology division at a 450-bed tertiary care hospital in a multi-ethnic community in Brooklyn during this initial wave of COVID-19. In lieu of a mass redeployment of staff to internal medicine teams, we report a novel method for a neurology division to participate in a hospital's expansion of care for patients with COVID-19 while maintaining existing team structures and their inherent supervisory and interpersonal support mechanisms.

Objectives: Hyponatremia occurs in up to 30% of patients with pneumonia and is associated with increased morbidity and mortality. The prevalence of hyponatremia associated with coronavirus disease 2019 and the impact on outcome is unknown. We aimed to identify the prevalence, predictors, and impact on outcome of mild, moderate, and severe admission hyponatremia compared with normonatremia among coronavirus disease 2019 patients. Design: Retrospective, multicenter, observational cohort study. Setting: Four New York City hospitals that are part of the same health network. Patients: Hospitalized, laboratory-confirmed adult coronavirus disease 2019 patients admitted between March 1, 2020, and May 13, 2020. Interventions: None. Measurements and Main Results: Hyponatremia was categorized as mild (sodium: 130-134 mmol/L), moderate (sodium: 121-129 mmol/L), or severe (sodium: <= 120 mmol/L) versus normonatremia (135-145 mmol/L). The primary outcome was the association of increasing severity of hyponatremia and in-hospital mortality assessed using multivariable logistic regression analysis. Secondary outcomes included encephalopathy, acute renal failure, mechanical ventilation, and discharge home compared across sodium levels using Kruskal-Wallis and chi-square tests. In exploratory analysis, the association of sodium levels and interleukin-6 levels (which has been linked to nonosmotic release of vasopressin) was assessed. Among 4,645 patient encounters, hyponatremia (sodium < 135 mmol/L) occurred in 1,373 (30%) and 374 of 1,373 (27%) required invasive mechanical ventilation. Mild, moderate, and severe hyponatremia occurred in 1,032 (22%), 305 (7%), and 36 (1%) patients, respectively. Each level of worsening hyponatremia conferred 43% increased odds of in-hospital death after adjusting for age, gender, race, body mass index, past medical history, admission laboratory abnormalities, admission Sequential Organ Failure Assessment score, renal failure, encephalopathy, and mechanical ventilation (adjusted odds ratio, 1.43; 95% CI, 1.08-1.88; p = 0.012). Increasing severity of hyponatremia was associated with encephalopathy, mechanical ventilation, and decreased probability of discharge home (all p < 0.001). Higher interleukin-6 levels correlated with lower sodium levels (p = 0.017). Conclusions: Hyponatremia occurred in nearly a third of coronavirus disease 2019 patients, was an independent predictor of in-hospital mortality, and was associated with increased risk of encephalopathy and mechanical ventilation.

While the thrombotic complications of COVID-19 have been well described, there are limited data on clinically significant bleeding complications including hemorrhagic stroke. The clinical characteristics, underlying stroke mechanism, and outcomes in this particular subset of patients are especially salient as therapeutic anticoagulation becomes increasingly common in the treatment and prevention of thrombotic complications of COVID-19. We conducted a retrospective cohort study of patients with hemorrhagic stroke (both non-traumatic intracerebral hemorrhage and spontaneous non-aneurysmal subarachnoid hemorrhage) who were hospitalized between March 1, 2020, and May 15, 2020, within a major healthcare system in New York, during the coronavirus pandemic. Patients with hemorrhagic stroke on admission and who developed hemorrhage during hospitalization were both included. We compared the clinical characteristics of patients with hemorrhagic stroke and COVID-19 to those without COVID-19 admitted to our hospital system between March 1, 2020, and May 15, 2020 (contemporary controls), and March 1, 2019, and May 15, 2019 (historical controls). Demographic variables and clinical characteristics between the individual groups were compared using Fischer’s exact test for categorical variables and nonparametric test for continuous variables. We adjusted for multiple comparisons using the Bonferroni method. During the study period in 2020, out of 4071 patients who were hospitalized with COVID-19, we identified 19 (0.5%) with hemorrhagic stroke. Of all COVID-19 with hemorrhagic stroke, only three had isolated non-aneurysmal SAH with no associated intraparenchymal hemorrhage. Among hemorrhagic stroke in patients with COVID-19, coagulopathy was the most common etiology (73.7%); empiric anticoagulation was started in 89.5% of these patients versus 4.2% in contemporary controls (p ≤ .001) and 10.0% in historical controls (p ≤ .001). Compared to contemporary and historical controls, patients with COVID-19 had higher initial NIHSS scores, INR, PTT, and fibrinogen levels. Patients with COVID-19 also had higher rates of in-hospital mortality (84.6% vs. 4.6%, p ≤ 0.001). Sensitivity analyses excluding patients with strictly subarachnoid hemorrhage yielded similar results. We observed an overall low rate of imaging-confirmed hemorrhagic stroke among patients hospitalized with COVID-19. Most hemorrhages in patients with COVID-19 infection occurred in the setting of therapeutic anticoagulation and were associated with increased mortality. Further studies are needed to evaluate the safety and efficacy of therapeutic anticoagulation in patients with COVID-19.

Background. Standard urine sampling and testing techniques do not mitigate against detection of colonization, resulting in false positive catheter-associated urinary tract infections (CAUTI). We aimed to evaluate whether a novel protocol for urine sampling and testing reduces rates of CAUTI. Methods. A preintervention and postintervention study with a contemporaneous control group was conducted at 2 campuses (test and control) of the same academic medical center. The test campus implemented a protocol requiring urinary catheter removal prior to urine sampling from a new catheter or sterile straight catheterization, along with urine bacteria and pyuria screening prior to culture. Primary outcomes were test campus CAUTI rates, compared between each 9-month pre- and postintervention epoch. Secondary outcomes included the percent reductions in CAUTI rates, compared between the test campus and a propensity score-matched cohort at the control campus. Results. A total of 7991 patients from the test campus were included in the primary analysis, and 4264 were included in the propensity score-matched secondary analysis. In the primary analysis, the number of CAUTI cases per 1000 patients was reduced by 77% (6.6 to 1.5), the number of CAUTI cases per 1000 catheter days was reduced by 63% (5.9 to 2.2), and the number of urinary catheter days per patient was reduced by 37% (1.1 to 0.69; all P values <= .001). In the propensity score-matched analysis, the number of CAUTI cases per 1000 patients was reduced by 82% at the test campus, versus 57% at the control campus; the number of CAUTI cases per 1000 catheter days declined by 68% versus 57%, respectively; and the number of urinary catheter days per patient decreased by 44% versus 1%, respectively (all P values <.001). Conclusions. Protocolized urine sampling and testing aimed at minimizing contamination by colonization was associated with significantly reduced CAUTI infection rates and urinary catheter days.

Coronavirus disease 2019 (COVID-19) can cause diffuse leukoencephalopathy. cAlthough the pathophysiology of leukoencephalopathy due to COVID-19 is unclear, there are myriad possible mechanisms for this finding, including hypoxic-ischemic injury, microvascular thrombosis secondary to hypercoagulability, and endothelial damage. Oy-sters cDo not assume that critically ill patients with COVID-19 who are on sedation for a protracted period will be neurologically intact when sedation is discontinued and wears off.cIn critically ill patients with COVID-19 who have encephalopathy, before attributing prolonged coma to infection and toxic-metabolic conditions, obtain an MRI.The neurologic manifestations of coronavirus disease 2019 (COVID-19) have been increasingly documented. 1 However, severe encephalopathy with white matter changes on imaging has not been well-described.We present 4 patients with leukoencephalopathy following COVID-19 infection who were evaluated by the neurology team at New York University Langone Health-associated hospitals between April 2 and April 29, 2020.Select clinical data and laboratory values are found in table 1 and table e-1 (links.lww.com/WNL/B187),respectively.All 4 cases were positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nasopharyngeal PCR on admission.