ABSTRACT
BACKGROUND: Hospital length of stay (HLOS) is a commonly used measure of hospital quality and is influenced by clinical and non-clinical factors. To reduce HLOS, it is key to identify factors placing patients at increased risk of lengthy HLOS and discharge delays. METHODS: This was a retrospective cohort study of patients age ≥ 18 admitted to four level 1 trauma centers between 1/1/2015 and 3/31/2018 with traumatic brain injury (TBI). The primary outcome was discharge delay, defined as discharge ≥24 h after case management notes indicated the patient was ready for discharge. The independent variables of interest were primary insurance provider and discharge destination. Chi-square, Fisher exact, and unadjusted and adjusted logistic regression analyses were used to assess associations between discharge delay and the two primary independent variables, as well as other patient demographic and clinical characteristics. Complications developing during the delay period were also examined. RESULTS: A total of 1543 patients with TBI were included. The median age was 61 years, and the median HLOS was 5 days. Approximately half of patients were discharged home (54%). The most common insurance providers were Medicare (35%) and commercial/private (35%). Two-hundred ten (14%) patients experienced a discharge delay. The median delay period was 3 days, and the most common reasons for delay were insurance authorization (52%) and lack of accepting bed (41%). Compared to being discharged home, patients discharged to a skilled nursing facility (adjusted odds ratio (AOR) = 10.35) or intermediate care facility (AOR = 10.64) had the highest odds of discharge delay. Compared to Medicare patients, uninsured/self-pay patients (AOR = 2.98) and those with Medicaid (AOR = 2.83) or commercial/private insurance (AOR = 2.22) had higher odds of delay. Thirty-two patients (15% of those delayed) experienced at least one complication during the delay, some of which were clinically severe. CONCLUSIONS: A substantial portion of TBI patients in this study experienced discharge delays, and discharge destination and primary insurance provider were significant drivers of these delays. Evaluation of a facility's quality of care should consider the specific causes of these delays.
ABSTRACT
Current surgical management of volume overload-induced heart failure (HF) leads to variable recovery of left ventricular (LV) function despite a return of LV geometry. The mechanisms that prevent restoration of function are unknown but may be related to the timing of intervention and the degree of LV contractile impairment. This study determined whether reduction of aortocaval fistula (ACF)-induced LV volume overload during the compensatory stage of HF results in beneficial LV structural remodeling and restoration of pump function. Rats were subjected to ACF for 4 wk; a subset then received a load-reversal procedure by closing the shunt using a custom-made stent graft approach. Echocardiography or in vivo pressure-volume analysis was used to assess LV morphology and function in sham rats; rats subjected to 4-, 8-, or 15-wk ACF; and rats subjected to 4-wk ACF followed by 4- or 11-wk reversal. Structural and functional changes were correlated to LV collagen content, extracellular matrix (ECM) proteins, and hypertrophic markers. ACF-induced volume overload led to progressive LV chamber dilation and contractile dysfunction. Rats subjected to short-term reversal (4-wk ACF + 4-wk reversal) exhibited improved chamber dimensions (LV diastolic dimension) and LV compliance that were associated with ECM remodeling and normalization of atrial and brain natriuretic peptides. Load-independent parameters indicated LV systolic (preload recruitable stroke work, Ees) and diastolic dysfunction (tau, arterial elastance). These changes were associated with an altered α/ß-myosin heavy chain ratio. However, these changes were normalized to sham levels in long-term reversal rats (4-wk ACF + 11-wk reversal). Acute hemodynamic changes following ACF reversal improve LV geometry, but LV dysfunction persists. Gradual restoration of function was related to normalization of eccentric hypertrophy, LV wall stress, and ECM remodeling. These results suggest that mild to moderate LV systolic dysfunction may be an important indicator of the ability of the myocardium to remodel following the reversal of hemodynamic overload.
