Faculty Bibliography

BACKGROUND:Persistent cognitive symptoms have been reported following COVID-19 hospitalization. We investigated the relationship between demographics, social determinants of health (SDOH) and cognitive outcomes 6-months after hospitalization for COVID-19. METHODS:We analyzed 6-month follow-up data collected from a multi-center, prospective study of hospitalized COVID-19 patients. Demographic and SDOH variables (age, race/ethnicity, education, employment, health insurance status, median income, primary language, living arrangements, and pre-COVID disability) were compared between patients with normal versus abnormal telephone Montreal Cognitive Assessments (t-MOCA; scores<18/22). Multivariable logistic regression models were constructed to evaluate predictors of t-MoCA. RESULTS:Of 382 patients available for 6-month follow-up, 215 (56%) completed the t-MoCA (n = 109/215 [51%] had normal and n = 106/215 [49%] abnormal results). 14/215 (7%) patients had a prior history of dementia/cognitive impairment. Significant univariate predictors of abnormal t-MoCA included older age, ≤12 years of education, unemployment pre-COVID, Black race, and a pre-COVID history of cognitive impairment (all p < 0.05). In multivariable analyses, education ≤12 years (adjusted OR 5.21, 95%CI 2.25-12.09), Black race (aOR 5.54, 95%CI 2.25-13.66), and the interaction of baseline functional status and unemployment prior to hospitalization (aOR 3.98, 95%CI 1.23-12.92) were significantly associated with abnormal t-MoCA scores after adjusting for age, history of dementia, language, neurological complications, income and discharge disposition. CONCLUSIONS:Fewer years of education, Black race and unemployment with baseline disability were associated with abnormal t-MoCA scores 6-months post-hospitalization for COVID-19. These associations may be due to undiagnosed baseline cognitive dysfunction, implicit biases of the t-MoCA, other unmeasured SDOH or biological effects of SARS-CoV-2.

INTRODUCTION: Subarachnoid Hemorrhage (SAH) associated headaches are severe and challenging to manage. The use of sedating, high-dose opioids can cloud neurological assessments, leading to unnecessary testing and potentially increase the risk of dependence. We hypothesized that a tiered opioid sparing pain management protocol favoring NSAIDs and gabapentin for low grade SAH patients would decrease opioid use without adversely affecting headache severity scores.
METHOD(S): We performed a retrospective cohort study pre- and post-implementation of the opioid sparing protocol. Inclusion criteria included admission to NYU Langone-Brooklyn Hospital with Hunt Hess Grade 1 or 2 aneurysmal SAH on Day 3 of hospital admission as most patients received periprocedural sedation and analgesia during the first 2 days. The pre-implementation group (pre) was admitted from 8/2016 to 8/2017 and the post-implementation group (post) was admitted from 4/2019 to 4/2020. The two-year washout period was included because newly hired intensivists integrated elements of opioid-sparing protocols as part of their practice prior to the go-live date. We collected demographics, baseline admission characteristics, hospital complications, and past history of headaches and opioid use. From day 3-7, we tracked total use of morphine milligram equivalents (MME) of all opioids, acetaminophen, NSAIDS, barbiturates, and gabapentin. We recorded the highest (HP) and lowest (LP) visual analogue pain assessment scores in daily quartiles. Data analysis was completed with SPSS.
RESULT(S): 55 patients (n=24 pre and n=31 post) were eligible and enrolled in the study. 85 patients were excluded. Aneurysm location, surgical method, symptomatic vasospasm, and EVD placement were similar between groups. Hydrocephalus was more common in pre; EVD complications were more common in post. There were no documented stress ulcers nor re-hemorrhage attributed to medications. The protocol resulted in a 19% decrease in total average MME compared to baseline use ((21.7 vs 26.9, p=0.77), a 12% decrease in average HP (2.60 vs. 2.96, p=0.41), and a 30% decrease in average LP (0.63 vs. 0.90, p=0.16), although not statistically significant. 14 pre received barbiturates; 0 post.
CONCLUSION(S): Pain control with reduced opioid usage can be achieved with a tiered opioid sparing pain protocol

BACKGROUND:Post-acute sequelae of COVID-19 (PASC) includes a heterogeneous group of patients with variable symptomatology, who may respond to different therapeutic interventions. Identifying phenotypes of PASC and therapeutic strategies for different subgroups would be a major step forward in management. METHODS:In a prospective cohort study of patients hospitalized with COVID-19, 12-month symptoms and quantitative outcome metrics were collected. Unsupervised hierarchical cluster analyses were performed to identify patients with: (1) similar symptoms lasting ≥4 weeks after acute SARS-CoV-2 infection, and (2) similar therapeutic interventions. Logistic regression analyses were used to evaluate the association of these symptom and therapy clusters with quantitative 12-month outcome metrics (modified Rankin Scale, Barthel Index, NIH NeuroQoL). RESULTS:Among 242 patients, 122 (50%) reported ≥1 PASC symptom (median 3, IQR 1-5) lasting a median of 12-months (range 1-15) post-COVID diagnosis. Cluster analysis generated three symptom groups: Cluster1 had few symptoms (most commonly headache); Cluster2 had many symptoms including high levels of anxiety and depression; and Cluster3 primarily included shortness of breath, headache and cognitive symptoms. Cluster1 received few therapeutic interventions (OR 2.6, 95% CI 1.1-5.9), Cluster2 received several interventions, including antidepressants, anti-anxiety medications and psychological therapy (OR 15.7, 95% CI 4.1-59.7) and Cluster3 primarily received physical and occupational therapy (OR 3.1, 95%CI 1.3-7.1). The most severely affected patients (Symptom Cluster 2) had higher rates of disability (worse modified Rankin scores), worse NeuroQoL measures of anxiety, depression, fatigue and sleep disorder, and a higher number of stressors (all P<0.05). 100% of those who received a treatment strategy that included psychiatric therapies reported symptom improvement, compared to 97% who received primarily physical/occupational therapy, and 83% who received few interventions (P = 0.042). CONCLUSIONS:We identified three clinically relevant PASC symptom-based phenotypes, which received different therapeutic interventions with varying response rates. These data may be helpful in tailoring individual treatment programs.

BACKGROUND: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. METHODS: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. RESULTS: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). CONCLUSIONS: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.

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 aim to evaluate if a novel protocol for urine sampling and testing reduces rates of CAUTI. METHODS:A pre-intervention and post-intervention study with a contemporaneous control group was conducted at two 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 post-intervention 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 7,991 patients from the test campus were included in the primary analysis, and 4,264 were included in the propensity-score matched secondary analysis. In primary analysis, CAUTI/1000-patients was reduced by 77% (6.6 to 1.5), CAUTI/1000-catheter days by 63% (5.9 to 2.2) and urinary catheter days/patient by 37% (1.1 to 0.69, all P≤0.001). In propensity score-matched analysis, CAUTI/1000-patients was reduced by 82% at the test campus versus 57% at the control campus, CAUTI/1000 catheter-days declined by 68% versus 57% and catheter-days/patient decreased by 44% versus 1% (all P<0.001). CONCLUSIONS: Protocolized urine sampling and testing aimed at minimizing contamination by colonization was associated with significantly reduced CAUTI infection rates and urinary catheter days.

Since the onset of the COVID-19 pandemic, a substantial proportion of COVID-19 patients had documented thrombotic complications and ischemic stroke. Several mechanisms related to immune mediated thrombosis, the renin angiotensin system, and the effect of SARS-CoV-2 in cardiac and brain tissue may contribute to the pathogenesis of ischemic stroke in patients with COVID-19. Simultaneously, significant strains on global healthcare delivery, including ischemic stroke management, have made treatment of stroke in the setting of COVID-19 particularly challenging. In this review we summarize the current knowledge on epidemiology, clinical manifestation and pathophysiology of ischemic stroke in patients with COVID-19 to bridge the gap from bench to bedside and clinical practice during the most challenging global health crisis of the last decades.

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