Dataset Information

Readmission following hypoxic ischemic brain injury: a population-based cohort study.

ABSTRACT:

Background

Readmission to acute care is common and is associated with indicators of suboptimal care and health system inefficiencies. The objective of this study was to identify independent determinants of readmission following survival of hypoxic ischemic brain injury.

Methods

We conducted a population-based retrospective cohort study using Ontario's administrative health data. Survivors of hypoxic ischemic brain injury aged 20 years or more discharged from acute care between fiscal years 2002/03 and 2010/11 were included. Multivariable negative binomial regression was used to identify independent determinants of both number of readmissions and cumulative duration of hospital stay(s) within 1 year after the index discharge.

Results

Of the 593 patients with hypoxic ischemic brain injury, 233 (39.3%) were readmitted within 1 year of the index acute care discharge. The number of readmissions was associated with age (35-49 yr v. 65-79 yr: rate ratio [RR] 0.57, 95% confidence interval [CI] 0.38-0.85; ? 80 yr v. 65-79 yr: RR 0.58, 95% CI 0.34-0.97) and higher comorbidity score (Johns Hopkins Aggregated Diagnosis Groups score > 30 v. < 10: RR 1.60, 95% CI 1.11-2.31). Cumulative readmission stay was associated with increased index acute care length of stay (31-90 d v. ? 90 d: RR 4.17, 95% CI 1.38-12.64), prior use of health care services (minimal v. very high: RR 0.15, 95% CI 0.05-0.49) and discharge disposition (home v. continuing/long-term care: RR 0.44, 95% CI 0.21-0.91).

Interpretation

The findings indicate a high readmission rate in the first year after the index acute care admission for survivors of hypoxic ischemic brain injury, reflecting care gaps and system inefficiencies. This suggests that bolstered discharge and home care planning and support are needed to address the specific needs of those with hypoxic ischemic brain injury.

SUBMITTER: Chan V

PROVIDER: S-EPMC6263420 | biostudies-literature | 2018 Oct-Dec

REPOSITORIES: biostudies-literature

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Publications

Readmission following hypoxic ischemic brain injury: a population-based cohort study.

Chan Vincy V Stock David D Jacob Binu B Cullen Nora N Colantonio Angela A

CMAJ open 20181001 4

<h4>Background</h4>Readmission to acute care is common and is associated with indicators of suboptimal care and health system inefficiencies. The objective of this study was to identify independent determinants of readmission following survival of hypoxic ischemic brain injury.<h4>Methods</h4>We conducted a population-based retrospective cohort study using Ontario's administrative health data. Survivors of hypoxic ischemic brain injury aged 20 years or more discharged from acute care between fis ...[more]

PMID: 30482758

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Project description:BackgroundDelayed discharge, captured as alternate-level-of-care days, represents inefficient use of high-demand acute care resources and results in potentially poorer patient outcomes. We performed a study to determine the extent of alternate-level-of-care days among patients who survived hypoxic-ischemic brain injury in inpatient hospital care in Ontario and to identify predictors of alternate-level-of-care use in this population.MethodsA population-based cohort of acute care survivors of hypoxic-ischemic brain injury aged 20 years or more from 2002/03 through 2011/12 was identified. We used 2 case definitions, the more specific identifying patients with a most responsible diagnosis of "anoxic brain damage," and the more sensitive capturing additional likely causative conditions as the most responsible diagnosis. Multivariable zero-inflated negative binomial regression was used to estimate independent effects on the relative incidence of alternate-level-of-care days.ResultsWe identified 491 patients using the specific case definition and 669 patients using the extended case definition. After deaths were excluded, 232 patients (47.2%) and 278 patients (41.6%), respectively, had at least 1 alternate-level-of-care day (median 20 and 19 d, respectively). In both cohorts, decreasing age, no special care unit hours and acute care episode earlier in the study period were predictive of increased alternate-level-of-care days relative to length of stay. Discharge disposition and psychiatric/behavioural comorbidity were most predictive of having any alternate-level-of-care days.InterpretationPatients with hypoxic-ischemic brain injury had a greater proportion of alternate-level-of-care days than has been reported for patients with other types of acquired brain injury. This finding suggests that substantial barriers to appropriate discharge exist for this population. Predictors of increased alternate-level-of-care days were also shown to be unique. Further study of care deficits among patients with hypoxic-ischemic brain injury is warranted.

Project description:Hypoxic-ischemic encephalopathy (HIE) is a major cause of mortality and morbidity in neonates, with an estimated global incidence of 3/1,000 live births. HIE brain damage is associated with an inflammatory response and oxidative stress, resulting in the activation of cell death pathways. At present, therapeutic hypothermia is the only clinically approved treatment available for HIE. This approach, however, is only partially effective. Therefore, there is an unmet clinical need for the development of novel therapeutic interventions for the treatment of HIE. Curcumin is an antioxidant reactive oxygen species scavenger, with reported anti-tumor and anti-inflammatory activity. Curcumin has been shown to attenuate mitochondrial dysfunction, stabilize the cell membrane, stimulate proliferation, and reduce injury severity in adult models of spinal cord injury, cancer, and cardiovascular disease. The role of curcumin in neonatal HIE has not been widely studied due to its low bioavailability and limited aqueous solubility. The aim of this study was to investigate the effect of curcumin treatment in neonatal HIE, including time of administration and dose-dependent effects. Our results indicate that curcumin administration prior to HIE in neonatal mice elevated cell and tissue loss, as well as glial activation compared to HI alone. However, immediate post-treatment with curcumin was significantly neuroprotective, reducing grey and white matter tissue loss, TUNEL+ cell death, microglia activation, reactive astrogliosis, and iNOS oxidative stress when compared to vehicle-treated littermates. This effect was dose-dependent, with 200 μg/g body weight as the optimal dose-regimen, and was maintained when curcumin treatment was delayed by 60 or 120 min post-HI. Cell proliferation measurements showed no changes between curcumin and HI alone, suggesting that the protective effects of curcumin on the neonatal brain following HI are most likely due to curcumin's anti-inflammatory and antioxidant properties, as seen in the reduced glial and iNOS activity. In conclusion, this study suggests curcumin as a potent neuroprotective agent with potential for the treatment of HIE. The delayed application of curcumin further increases its clinical relevance.

Project description:Neuroinflammation is a hallmark of hypoxic-ischemic injury and can be characterized by the activation of glial cells and the expression of inflammatory cytokines and chemokines. Interleukin (IL)-1β and tumor necrosis factor (TNF)α are among the best-characterized early response cytokines and are often expressed concurrently. Several types of central nervous system cells secrete IL-1β and TNFα, including microglia, astrocytes, and neurons, and these cytokines convey potent pro-inflammatory actions. Chemokines also play a central role in neuroinflammation by controlling inflammatory cell trafficking. Our aim was to characterise the evolution of early neuroinflammation in the neonatal piglet model of hypoxic-ischemic encephalopathy (HIE). Piglets (< 24 h old) were exposed to HI insult, and recovered to 2, 4, 8, 12 or 24H post-insult. Brain tissue from the frontal cortex and basal ganglia was harvested for assessment of glial cell activation profiles and transcription levels of inflammatory markers in HI piglets with comparison to a control group of newborn piglets. Fluorescence microscopy was used to observe microglia, astrocytes, neurons, degenerating neurons and possibly apoptotic cells, and quantitative polymerase chain reaction was used to measure gene expression of several cytokines and chemokines. HI injury was associated with microglial activation and morphological changes to astrocytes at all time points examined. Gene expression analyses of inflammation-related markers revealed significantly higher expression of pro-inflammatory cytokines tumor necrosis factor-α (TNFα) and interleukin 1 beta (IL-1β), chemokines cxc-chemokine motif ligand (CXCL)8 and CXCL10, and anti-inflammatory cytokine transforming growth factor (TGF)β in every HI group, with some region-specific differences noted. No significant difference was observed in the level of C-X-C chemokine receptor (CCR)5 over time. This high degree of neuroinflammation was associated with a reduction in the number of neurons in piglets at 12H and 24H in the frontal cortex, and the putamen at 12H. This reduction of neurons was not associated with increased numbers of degenerating neurons or potentially apoptotic cells. HI injury triggered a robust early neuroinflammatory response associated with a reduction in neurons in cortical and subcortical regions in our piglet model of HIE. This neuroinflammatory response may be targeted using novel therapeutics to reduce neuropathology in our piglet model of neonatal HIE.

Dataset Information

Readmission following hypoxic ischemic brain injury: a population-based cohort study.

Background

Methods

Results

Interpretation

Publications

Readmission following hypoxic ischemic brain injury: a population-based cohort study.

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