Comparative analysis of financial toxicity between SARS-CoV-2 infection and common comorbidities.

Financial toxicity is common in individuals with COVID-19 and Long COVID. However, the extent of financial toxicity experienced, in comparison to other common comorbidities, is uncertain. Contributing factors exacerbating financial challenges in Long COVID are also unclear. These knowledge gaps are addressed via a cross-sectional analysis utilizing data from the 2022 National Health Interview Survey (NHIS), a representative sample drawn from the United States. COVID-19 cases were identified through self-reported positive testing or physician diagnoses. Long COVID was defined as experiencing COVID-19-related symptoms for more than three months. Comorbidity was assessed based on self-reported diagnoses of ten doctor-diagnosed conditions (Yes/No). Financial toxicity was defined as having difficulty paying medical bills, cost-related medication nonadherence, delaying healthcare due to cost, and/or not obtained healthcare due to cost. A total of 27,492 NHIS 2022 respondents were included in our analysis, representing 253 million U.S. adults. In multivariable logistic regression models, adults with Long COVID (excluding respondents with COVID-19 but not Long COVID), showed increased financial toxicity compared to those with other comorbidities, such as epilepsy (OR [95% CI]: 1.69 [1.22, 2.33]), dementia (1.51 [1.01, 2.25]), cancer (1.43 [1.19, 1.71]) or respiratory/cardiovascular conditions (1.18 [1.00, 1.40]/1.23 [1.02, 1.47]). Long COVID-related financial toxicity was associated with female sex, age <65 years, lack of medical insurance, current paid employment, residence region, food insecurity, fatigue, mild to severe depression symptoms experienced during the survey completion, visits to hospital emergency rooms, presence of arthritis, cardiovascular or respiratory conditions, and social activity limitations. In conclusion, American adults with Long COVID, but not those who had prior COVID-19 infection without Long COVID, exhibited a higher prevalence of financial toxicity compared to individuals with common comorbidities. Vulnerable populations were at greater risk for financial toxicity. These findings emphasize the importance of evaluating strategies to reduce economic burden and increase awareness of the effect of Long COVID-related financial toxicity on patient's healthcare and health status.

Fatigue, Toll-Like Receptor 4, and Pro-Inflammatory Cytokines in Adults With Subarachnoid Hemorrhage: A 6-Month Longitudinal Study.

BACKGROUND: Fatigue is prevalent in subarachnoid hemorrhage (SAH) survivors. Biological mechanisms underlying fatigue post-SAH are not clear. Inflammation may contribute to the development of fatigue. This study aimed to examine the associations between inflammatory markers and fatigue during the first 6 months post-SAH. Specific biomarkers examined included both early and concurrent expression of Toll-Like Receptor 4 (TLR4) messenger RNA (mRNA) and plasma concentrations of pro-inflammatory cytokines, Tumor Necrosis Factor-alpha (TNF-α), Interleukin (IL)1ß, and IL6. METHODS: We conducted a 6-month longitudinal study with a convenience sample of 43 SAH survivors. We collected blood samples on days 2, 3, and 7 and 2, 3, and 6 months post-SAH to assess biomarkers. Fatigue was assessed by the PROMIS Fatigue Scale at 2, 3, and 6 months. Linear mixed models were used to test the associations between early (days 2, 3, and 7) and concurrent (2, 3, and 6 months) TLR4 mRNA expression (TagMan gene expression assays) and TNF-α, IL1ß, and IL6 plasma concentrations (multiplex assays) and concurrent fatigue. RESULTS: 28% of SAH survivors experienced fatigue during the first 6 months post-SAH. Fatigue levels in SAH survivors were higher than those of the U.S. population and consistent during the 6 months. Experience of fatigue during the 6 months post-SAH was associated with higher IL1ß plasma concentrations on day 7 and IL1ß, IL6, and TNF-α plasma concentrations during the 6 months post-SAH. CONCLUSION: Inflammation appears to underlie the development of fatigue in SAH survivors.

Impact of Age on Plasma Inflammatory Biomarkers in the 6 Months Following Mild Traumatic Brain Injury.

OBJECTIVE: To compare plasma inflammatory biomarker concentrations to 6 months in young and older adults with and without mild traumatic brain injury (TBI). SETTING: Level 1 trauma center. PARTICIPANTS: Younger (21-54 years) and older (55+) adults diagnosed with mild TBI along with age-/sex-matched noninjured controls (n = 313). DESIGN: Prospective cohort study. MAIN MEASURES: Multiplex assays were used to quantify concentrations of selected plasma inflammatory markers at day 0, months 1 and 6. RESULTS: Persistent aging-related differences were found between control groups in concentrations of 4 cytokines up to 6 months. At day 0, interleukin-6 (IL-6), IL-8, and fractalkine were higher in the older TBI compared with older control as well as the younger TBI groups, while IL-10 was higher in older TBI compared with controls. At month 1, significantly higher concentrations of IL-8, fractalkine, and tumor necrosis factor-α (TNF-α) were seen. At 6 months postinjury, significantly higher concentrations of IL-6 and IL-8 were seen, while a lower concentration of IL-7 was found in older versus younger TBI groups. CONCLUSION: The neuroinflammatory signature that accompanies mild TBI in older adults differs from that of younger adults. The differences seen are notable for their roles in neutrophil attraction (IL-8), neuronal-microglial-immune cell interactions (fractalkine), and chronic inflammation (IL-6).

Orthopaedic nurses' knowledge of delirium in older hospitalized patients.

BACKGROUND: Delirium is a serious health issue experienced by many hospitalized older adults following orthopaedic surgery. Nurses often do not recognize delirium, attributing symptoms to normal changes associated with aging or dementia. OBJECTIVES: To (a) describe orthopaedic nurses' baseline knowledge about delirium in orthopaedic patients, particularly those aged 65 years, (b) test the effectiveness of an educational intervention based on nationally recommended guidelines, and (c) describe factors associated with differences in (1) nurses' baseline knowledge about delirium and (2) the effectiveness of the educational intervention. METHODS: A pretest-posttest study design, using an educational evidence-based intervention. RESULTS: Regardless of education, years of experience, or shift worked, orthopaedic RNs had difficulty with questions related to recognition of delirium, predisposing, and precipitating risk factors, and medications that can contribute to delirium. The educational intervention was effective and scores significantly improved from baseline following the intervention. CONCLUSIONS: Baseline knowledge assessment confirmed orthopaedic nurses' lack of understanding of delirium. The 1-hr educational intervention, based on nationally recommended standards, improved the nurses' knowledge and could be useful in orthopaedic nursing continuing education.

Development and validation of the mortality risk for trauma comorbidity index.

OBJECTIVE: The aim of this study was to develop and validate a comorbidity index to predict the risk of mortality associated with chronic health conditions following a traumatic injury. SUMMARY BACKGROUND DATA: Currently available comorbidity adjustment tools do not account for certain chronic conditions, which may influence outcome following traumatic injury or they have not been fully validated for trauma. Controlling for comorbidity in trauma patients is becoming increasingly important as the population ages and elderly patients are more active, as well as to adjust for bias in trauma mortality studies. METHODS: Cohort study using data from the National Study on the Costs and Outcome of Trauma. Subject pool (N = 4644/Weighted Number = 14,069) was randomly divided in half; the first half of subjects was used to derive the risk scale, the second to validate the instrument. To construct the Mortality Risk Score for Trauma (MoRT), univariate analysis and odds ratios were performed to determine relative risk of mortality at hospital discharge comparing those persons with a comorbid condition to those without. Conditions significantly associated with mortality (P < 0.05) were included in the multivariate model. The variables in the final model were used to build the MoRT. The predictive ability of the MoRT and the Charlson Comorbidity Index (CCI) for discharge and 1-year mortality were estimated using the c-statistic in the validation sample. RESULTS: Six comorbidity factors were independently associated with the risk of mortality and formed the basis for the MoRT: severe liver disease, myocardial infarction, cerebrovascular disease, cardiac arrhythmias, dementia, and depression. The MoRT had a similar overall discrimination as the CCI for mortality at hospital discharge in injured adults (c-statistic: 0.56 vs. 0.56) although neither by itself performed well. The addition of age and gender improved the predictive ability of the MoRT (0.59; 95% CI: 0.56, 0.62) and the CCI (0.59; 0.56, 0.62). Similar results were seen at 1-year postinjury. The further addition of Injury Severity Score significantly improved the predictive ability of the MoRT (0.77, 95% CI: 0.74, 0.79) and the CCI (0.77, 95% CI: 0.75, 0.80). CONCLUSIONS: The MoRTs primary advantage over current instruments is its parsimony, containing only 6 items. In the present study, the comorbid conditions found to be predictive of mortality had some overlap with the CCI, but this study identified 2 novel predictors: cardiac arrhythmias and depression. Inclusion and reporting of these items within trauma registries would therefore be an important step to allow further validation and use of the MoRT.

Health-and disease-related biomarkers in aging research.

This article focuses on a synthesis of knowledge about healthy aging research in human beings and then synthesized nurse-led research in gerontology and geriatrics that use biomarkers. Healthy aging research has attracted considerable attention in the biomedical and basic sciences within the context of four major areas: (a) genetic variations as an expression of successful or unsuccessful aging; (b) caloric restriction as an intervention to slow the progression of aging; (c) immunological aging; (d) neurobiology of the aging brain. A systematic review of the literature was performed to identify nurse-led geriatric-related biomarker research. Nurse researchers who have chosen to integrate biomarkers as part of their research studies have been working in six focal areas, which are reviewed: health promotion within risk populations, cancer, vascular disease, Alzheimer's disease, caregiving, and complementary therapies. The article provides a discussion of contributions to date, identifying existing gaps and future research opportunities.

Traumatic brain injury induces adipokine gene expression in rat brain.

UNLABELLED: Traumatic brain injury (TBI) induces cachexia and neuroinflammation which profoundly impact patient recovery. Adipokine genes such as leptin (ob), resistin (rstn) and fasting-induced adipose factor (fiaf) are implicated in energy metabolism and body weight control and are also associated with chronic low grade inflammation. Since central rstn and fiaf expression was increased following hypoxic/ischemic brain injury, we hypothesized that these genes would also be induced in the rat brain following TBI. Realtime RT-PCR detected a 2-2.5-fold increase in ob mRNA in the ipsilateral cortex and thalamus 12h following lateral fluid percussion (FP)-induced brain injury. Fiaf mRNA was elevated 5-7.5-fold in cortex, hippocampus and thalamus, and modest increases were also detectable in the contralateral brain. Remarkably, rstn mRNA was elevated in ipsilateral (150-fold) and in contralateral (50-fold) hippocampus. To test whether these changes were part of an inflammatory response to TBI we also examined the effects of an intracerebral injection of lipopolysaccharide (LPS). We determined that central injection of LPS produced some, but not all, of the changes seen after TBI. For example, in contrast to the stimulatory influence of TBI, LPS had no effect on ob expression in any brain region, though fiaf and rstn mRNA levels were significantly elevated in both ipsi- and contralateral cortex. IN CONCLUSION: (a) brain-derived adipokines could be involved in the acute pathology of traumatic brain injury partly through modulation of central inflammatory responses, but also via leptin-mediated neuroprotective effects and (b) TBI-induced brain adipokines may induce the metabolic changes observed following neurotrauma.

A feasibility study of methodological issues and short-term outcomes in seriously injured older adults.

BACKGROUND: For any given traumatic injury, older adults experience a longer hospitalization, more complications, and higher mortality than do younger patients. OBJECTIVES: To prospectively identify problems in designing follow-up studies in seriously injured older adults without head injury and to examine outcomes after serious trauma in older adults who were sent to a level I trauma center. METHODS: A short-term descriptive follow-up design was used in which each patient served as his or her baseline. Eligible patients had injuries that required admission to an intensive care unit, a hospital length of stay longer than 72 hours, or surgery. Patients with isolated hip fractures, central nervous system injuries, and burn injuries were excluded. Data were collected by using standardized instruments during the acute hospital stay and 3 months after discharge from the hospital. RESULTS: During a representative 2-month period, 21% of a potential 77 subjects died in the hospital, 44% had cognitive impairment that precluded participation, and 17% declined to participate. Twenty older adults (mean age 73.5 years) who were injured in motor vehicle crashes (45%), falls (35%), or pedestrian accidents (15%) or who had gunshot wounds (5%) were enrolled. Ten percent died after discharge. Levels of physical disability at 3 months after discharge were higher than those before the injury (score on Sickness Impact Profile physical subscale 24.5 vs 10.9, P = .02), and psychological distress (Impact of Event Scale score 20.9) remained elevated. CONCLUSION: Mortality, disability, and posttraumatic psychological distress after discharge are problems in seriously injured older adults.

Acute, transient hemorrhagic hypotension does not aggravate structural damage or neurologic motor deficits but delays the long-term cognitive recovery following mild to moderate traumatic brain injury.

OBJECTIVES: Posttraumatic hypotension is believed to increase morbidity and mortality in traumatically brain-injured patients. Using a clinically relevant model of combined traumatic brain injury with superimposed hemorrhagic hypotension in rats, the present study evaluated whether a reduction in mean arterial blood pressure aggravates regional brain edema formation, regional cell death, and neurologic motor/cognitive deficits associated with traumatic brain injury. DESIGN: Experimental prospective, randomized study in rodents. SETTING: Experimental laboratory at a university hospital. SUBJECTS: One hundred nineteen male Sprague-Dawley rats weighing 350-385 g. INTERVENTIONS: Experimental traumatic brain injury of mild to moderate severity was induced using the lateral fluid percussion brain injury model in anesthetized rats (n = 89). Following traumatic brain injury, in surviving animals one group of animals was subjected to pressure-controlled hemorrhagic hypotension, maintaining the mean arterial blood pressure at 50-60 mm Hg for 30 mins (n = 47). The animals were subsequently either resuscitated with lactated Ringer's solution (three times shed blood volume, n = 18) or left uncompensated (n = 29). Other groups of animals included those with isolated traumatic brain injury (n = 34), those with isolated hemorrhagic hypotension (n = 8), and sham-injured control animals receiving anesthesia and surgery alone (n = 22). MEASUREMENTS AND MAIN RESULTS: The withdrawal of 6-7 mL of arterial blood significantly reduced mean arterial blood pressure by 50% without decreasing arterial oxygen saturation or Pao2. Brain injury induced significant cerebral edema (p < .001) in vulnerable brain regions and cortical tissue loss (p < .01) compared with sham-injured animals. Neither regional brain edema formation at 24 hrs postinjury nor the extent of cortical tissue loss assessed at 7 days postinjury was significantly aggravated by superimposed hemorrhagic hypotension. Brain injury-induced neurologic deficits persisted up to 20 wks after injury and were also not aggravated by the hemorrhagic hypotension. Cognitive dysfunction persisted for up to 16 wks postinjury. The superimposition of hemorrhagic hypotension significantly delayed the time course of cognitive recovery. CONCLUSIONS: A single, acute hypotensive event lasting 30 mins did not aggravate the short- and long-term structural and motor deficits but delayed the speed of recovery of cognitive function associated with experimental traumatic brain injury.

Not your "typical patient": cryptococcal meningitis in an immunocompetent patient.

Meningitis, when caused by the fungal mycoses Cryptococcus neoformans, is normally seen in immuno-compromised hosts. However, immunocompetent patients are also susceptible to cryptococcal meningitis (CM). In patients with an intact immune system, CM usually presents with the typical signs and symptoms of meningitis: fever, stiff neck, and headache. Major implications for the primary and advanced practice nursing plans of care for CM patients include a thorough history and physical exam, early diagnosis and treatment, and an individualized plan of care focused on minimizing sequelae and side effects of treatment and maximizing functional recovery.