Increasing resources are devoted to osteoarthritis surgical care in Australia annually, with significant expenditure attributed to hip and knee arthroplasties. Safe, efficient, and sustainable models of care are required. This study aimed to determine the impact on healthcare costs of implementing an enhanced short-stay model of care (ESS-MOC) for arthroplasty at a national level.

Budget impact analysis was conducted for hospitals providing arthroplasty surgery over the years 2023 to 2030. Population-based sample projections obtained from clinical registry and administrative datasets of individuals receiving hip or knee arthroplasty for osteoarthritis were applied. The ESS-MOC assigned 30 percent of eligible patients to a shortened acute-ward-stay pathway and outpatient rehabilitation. The remaining 70 percent received a current practice pathway. The primary outcome was total healthcare cost savings post-implementation of the ESS-MOC, with return on investment (ROI) ratio and hospital bed-days utilized also estimated. Costs are presented in Australian dollars (AUD) and United States dollars (USD), at 2023 prices.

Estimated hospital cost savings for the years 2023 to 2030 from implementing the ESS-MOC were AUD641 million (USD427 million) (95% CI: AUD99 million [USD66 million] to AUD1,250 million) [USD834 million]). This corresponds to a ROI ratio of 8.88 (1.3 to 17.9) dollars returned for each dollar invested in implementing the care model. For the period 2023 to 2030, an estimated 337,000 (261,000 to 412,000) acute surgical ward bed-days, and 721,000 (471,000 to 1,028,000) rehabilitation bed-days could be saved. Total implementation costs for the ESS-MOC were estimated at AUD72 million (USD46 million) over eight years.

Implementation of an ESS-MOC for eligible arthroplasty patients in Australia would generate significant cost and healthcare resource savings. This budget impact analysis demonstrates a best practice approach to comprehensively assessing value, at a national level, of implementing sustainable models of care in high-burden healthcare contexts. Findings are relevant to other settings where hospital stay following joint arthroplasty remains excessively long.

Deficiency in contextual and enhanced responding in cued fear learning may contribute to the development of posttraumatic stress disorder (PTSD). We examined the responses to aversive Pavlovian conditioning with an unpredictable spatial context as conditioned stimulus compared to a predictable context. We hypothesized that the PTSD group would demonstrate less hippocampal and ventromedial prefrontal cortex (vmPFC) activation during acquisition and extinction of unpredictable contexts and an over-reactive amygdala response in the predictable contexts compared to controls.

A novel combined differential cue-context conditioning paradigm was applied using virtual reality with spatial contexts that required configural and cue processing. We assessed 20 patients with PTSD, 21 healthy trauma-exposed (TC) and 22 non-trauma-exposed (HC) participants using functional magnetic resonance imaging, skin conductance responses, and self-report measures.

During fear acquisition, patients with PTSD compared to TC showed lower activity in the hippocampi in the unpredictable and higher activity in the amygdalae in the predictable context. During fear extinction, TC compared to patients and HC showed higher brain activity in the vmPFC in the predictable context. There were no significant differences in self-report or skin conductance responses.

Our results suggest that patients with PTSD differ in brain activation from controls in regions such as the hippocampus, the amygdala, and the vmPFC in the processing of unpredictable and predictable contexts. Deficient encoding of more complex configurations might lead to a preponderance of cue-based predictions in PTSD. Exposure-based treatments need to focus on improving predictability of contextual processing and reducing enhanced cue reactivity.

To characterize bacterial infections and antibiotic utilization in hospitalized cancer patients with coronavirus disease 2019 (COVID-19).

Retrospective cohort study.

Tertiary cancer center in New York City.

Hospitalized cancer patients ≥18 years with COVID-19 between March 1, 2020, and May 31, 2020.

Patients were classified with mild COVID-19 (ie, with room air), moderate COVID-19 (ie, using nasal cannula oxygen), or severe COVID-19 (ie, using high-flow oxygen or mechanical ventilation). The primary outcome was bacterial infection rate within 30 days of COVID-19 onset. Secondary outcomes included the proportion of patients receiving antibiotics and antibiotic length of therapy (LOT).

Of 358 study patients, 133 had mild COVID-19, 97 had moderate COVID-19, and 128 had severe COVID-19. Of 358 patients, 234 (65%) had a solid tumor. Also, 200 patients (56%) had 245 bacterial infections, of which 67 (27%) were microbiologically confirmed. The proportion of patients with bacterial infection increased with COVID-19 severity: mild (n = 47, 35%) versus moderate (n = 49, 51%) versus severe (n = 104, 81%) (P < .0001). Also, 274 (77%) received antibiotics for a median of 4 days. The median antibiotic LOTs were 7 days with 1 infection and 20 days with multiple infections (P < .0001). Antibiotic durations were 1 day for patients with mild COVID-19, 4 days for patients with moderate COVID-19, and 8 days for patients with severe COVID-19 (P < .0001).

Hospitalized cancer patients with COVID-19 had a high rate of bacterial infection. As COVID-19 severity increased, the proportion of patients diagnosed with bacterial infection and given antibiotics increased. In mild COVID-19 cases, antibiotic LOT was short, suggesting that empiric antibiotics can be safely avoided or discontinued in this group.

Ghrelin showed antidepressant-like effects in mice. Furthermore, ghrelin influences sleep and the activity of hypothalamic-pituitary-adrenal (HPA) and somatotropic axis in healthy humans as indicated by increased cortisol and growth hormone (GH) plasma levels. Both sleep and the activity of these endocrine axes are disturbed in depression.

To study the effect of ghrelin on psychopathology, sleep and secretion of cortisol and GH in patients with major depression.

Depressive symptoms as assessed by a validated self rating scale (’Befindlichkeits-Skala’, [well-being scale]), secretion profiles of cortisol and GH and sleep-EEGs were determined in 14 unmedicated patients with major depression (7 women) twice, receiving 50 μg ghrelin or placebo at 2200, 2300, 0000, and 0100 hours.

Overall, depressive symptoms did not change significantly after ghrelin administration (placebo: 37 ± 8; ghrelin: 33 ± 10, p = 0.178). However, there was an improvement at trend level in men (placebo: 36 ± 9 to ghrelin: 30 ± 9, p = 0.093) but not in women. In men, ghrelin was associated with less time awake (placebo: 149.0 ± 11.1; ghrelin: 88.0±12.2 min, p = 0.029) and more non-REM sleep (placebo: 263.2 ± 24.1; ghrelin: 304.9 ± 14.1 min, p = 0.027), in women with less REM sleep (placebo: 108.6 ± 15.7; ghrelin: 74.1 ± 13.8 min, p = 0.031) and longer REM latency (placebo: 49.9 ± 6.5; ghrelin: 85.6 ± 14.1 min, p = 0.019). In both sexes, ghrelin caused strong transient increases of GH and cortisol.

Our study may provide an initial indication that ghrelin can exert antidepressant effects in patients with major depression. Ghrelin strongly affected sleep and secretion of GH and cortisol in a partly different way as previously reported in healthy subjects.

Sleep studies in patients with major depression receiving the new selective norepinephrine and serotonin reuptake inhibitor (SNRI) duloxetine are lacking.

Polysomnography in 10 patients with major depression (7 males, 39.9 ± 7.6 years, HAMD-21 score: 23.6 ± 5.6) was recorded twice, before and after 7-14 days of treatment with duloxetine.

A significant (p < 0.01) increase from baseline to endpoint was found for amount of stage 3 sleep (21.0 ± 10.7 to 37.4 ± 20.1 minutes) and REM latency (58.5 ± 31.1 to 193.6 ± 72.6 minutes). Amount of REM sleep significantly (p < 0.01) decreased from 94.8 ± 34.5 to 51.5 ± 42.5 minutes.

These results partly differ from those in healthy subjects receiving duloxetine.