Economic Evaluation of a Hospital-Based Palliative Care Program.

PURPOSE: Establish costs of an inpatient palliative care unit (PCU) and conduct a threshold analysis to estimate the maximum possible costs for the PCU to be considered cost effective. METHODS: We used a hospital perspective to determine costs on the basis of claims from administrative data from Johns Hopkins PCU between March 2013 and March 2014. Using existing literature, we estimated the number of quality-adjusted life years (QALYs) that the PCU could generate. We conducted a threshold analysis to assess the maximum costs for the PCU to be considered cost effective, incorporating willingness to pay ($180,000 per QALY). Three types of costs were considered, which included variable costs alone, contribution margin (ie, revenue minus variable costs), and PCU cost savings compared with usual care (from a separate publication). RESULTS: The data showed that there were 153 patient encounters (PEs), variable costs of $1,050,031 ($1,343 per PE per day), a contribution margin of $318,413 ($407 per PE per day), and savings compared with usual care of $353,645 ($452 savings per PE per day). On the basis of the literature, the program could generate 3.11 QALYs from PEs (0.05 QALY) and caregivers (3.06 QALYs). The threshold analysis determined that the maximum variable cost required to be cost effective was $559,800 (an additional $716 per PE per day could be spent). CONCLUSION: According to variable costs, the PCU was not cost effective; however, when considering savings of the PCU compared with usual care, the PCU was cost saving. The contribution margin showed that the PCU was cost saving. This study supports efforts to expand PCUs, which enhance care for patients and their caregivers and can generate hospital savings. Future research should prospectively explore the cost utility of PCUs.

Impact of a New Palliative Care Program on Health System Finances: An Analysis of the Palliative Care Program Inpatient Unit and Consultations at Johns Hopkins Medical Institutions.

PURPOSE: Palliative care inpatient units (PCUs) can improve symptoms, family perception of care, and lower per-diem costs compared with usual care. In March 2013, Johns Hopkins Medical Institutions (JHMI) added a PCU to the palliative care (PC) program. We studied the financial impact of the PC program on JHMI from March 2013 to March 2014. METHODS: This study considered three components of the PC program: PCU, PC consultations, and professional fees. Using 13 months of admissions data, the team calculated the per-day variable cost pre-PCU (ie, in another hospital unit) and after transfer to the PCU. These fees were multiplied by the number of patients transferred to the PCU and by the average length of stay in the PCU. Consultation savings were estimated using established methods. Professional fees assumed a collection rate of 50%. RESULTS: The total positive financial impact of the PC program was $3,488,863.17. There were 153 transfers to the PCU, 60% with cancer, and an average length of stay of 5.11 days. The daily loss pretransfer to the PCU of $1,797.67 was reduced to $1,345.34 in the PCU (-25%). The PCU saved JHMI $353,645.17 in variable costs, or $452.33 per transfer. Cost savings for PC consultations in the hospital, 60% with cancer, were estimated at $2,765,218. $370,000 was collected in professional fees savings. CONCLUSION: The PCU and PC program had a favorable impact on JHMI while providing expert patient-centered care. As JHMI moves to an accountable care organization model, value-based patient-centered care and increased intensive care unit availability are desirable.

Role for dopamine-3 receptor in the hyperphagia of an unanticipated high-fat meal in rats.

Behavioral studies have indicated that midbrain dopamine projections arising in the ventral tegmental area and substantia nigra play a central role in integrating violations of expectancy in reward-related paradigms. The present study was designed to assess violations of dietary expectation and the role the dopamine-3 receptor plays in integrating reward-related food intake in violations of expectancy. Two groups of rats were conditioned to a meal-feeding schedule (3 h of access to food per day) in which they received either standard rodent chow or a preferable, high-fat diet. Animals either received the diet they had access to during the training period (no contrast) or the opposite diet (negative and positive contrast). As predicted, animals in the positive contrast condition were hyperphagic compared to no contrast animals. Animals in the negative contrast (high fat to chow) condition were hypophagic compared to no contrast animals. A dopamine agonist specific to the dopamine three receptor, ((+/-)-7-Hydroxy-dipropylaminotetralin HBr) and the dopamine-2 receptor antagonist raclopride were administered in equimolar doses peripherally to assess the involvement of the dopamine receptor subtypes in the violation of expectancy food intake effects. 7-Hydroxy-dipropylaminotetralin HBr blocked the hyperphagia associated with positive contrast and did not disrupt intake in the negative contrast or no contrast paradigm. Raclopride was ineffective at disrupting food intake. These results support the hypothesis that the dopamine-3 receptor is involved in the hyperphagia of an unexpected high fat meal.

High-fat diet induced adiposity in mice with targeted disruption of the dopamine-3 receptor gene.

Dopamine (DA) signaling has been implicated in the control of energy balance and ingestive behavior. In the present study, we sought to characterize body weight, body fat and food intake regulation in a mouse with a targeted disruption of the dopamine-3 receptor gene (Drd3). In the first set of experiments male and female wild-type and mutant (Drd3-/-) mice were given access to two different diets varying in fat content. Body weight, food intake, carcass analysis and plasma levels of leptin and insulin were measured. Male Drd3-/- mice have increased body weight and body fat when given access to high fat (HF) diet but not standard rodent chow. The female Drd3-/- mice did not demonstrate increased body weight when given access to either diet, but did have increased body fat on both diets. Plasma leptin and insulin levels reflected the increased adiposity demonstrated in each genotype and gender. These findings suggest the D3-R signaling is involved in the regulation of body weight and body fat when mice are given access to diets differing in palatability and fat content.

7-OH-DPAT selectively reduces intake of both chow and high fat diets in different food intake regimens.

Mesolimbic dopaminergic system activation correlates with ingestive behavior in numerous feeding regimens. DA release is enhanced by food intake following deprivation, amount of food consumed, and the palatability of the food consumed. The dopamine-3 receptor (D3-R) has a limited expression pattern that is restricted largely to the mesolimbic dopaminergic system. The D3-R has been hypothesized to inhibit DA-mediated reward, locomotion and motivation. To test the potential for an inhibitory role of the D3-R on food intake, we administered the D3-R agonist 7-OH-DPAT (5, 10 and 50 microg/kg ip) to rats that had ad libitum access to standard rodent chow (3.41 kcal/gm, 0.51 kcal/gm from fat) or a preferable, high fat (HF) (4.4 kcal/gm, 1.71 kcal/gm from fat). In the second set of experiments we administered 7-OH-DPAT (10, 50 and 100 microg/kg) to rats that had access to chow or HF diet for only 3 h per day (meal fed). In the third set of experiments we administered 7-OH-DPAT (10 and 50 microg/kg) to rats that had access to chow or HF diet after a 21-h food restriction. The 10 and 50 microg/kg doses significantly, but equally reduced intake of chow and HF diet in animals that were ad libitum fed. In animals that were meal-fed the dose response was effectively shifted to the right and the 10 microg/kg dose was ineffective at reducing intake. The 50 and 100 microg/kg doses significantly but equally reduced intake of both diets. In animals that were 21-h restricted and had access to chow both the 10 and 50 microg/kg doses were ineffective at reducing intake. However, in animals that had access to HF diet, 7-OH-DPAT dose-dependently reduced intake. These results support a potential role for the D3-R in ingestive behavior particularly in situations that involve a significant learned component.

Ethanol consumption in mice with a targeted disruption of the dopamine-3 receptor gene.

Considerable evidence suggests that the mesolimbic dopaminergic system is an important substrate for the rewarding effects of ethanol consumption. Previous data have demonstrated that pharmacological agents that alter dopamine signaling also influence the self-administration of ethanol. The present experiments were designed to assess the role of the dopamine-3 receptor (D3-R) on voluntary ethanol consumption in C57BL/6 mice. Mice with targeted disruption of the D3-R gene (D3-R - /-) were compared to wild-type controls in an ethanol intake paradigm. In Experiment 1, mice had 24-hour access to ethanol each day in a two-bottle choice paradigm for a period of 7 days per concentration. The concentrations tested were 3, 6, 10 and 15%. In Experiment 2, mice had I hour of access to ethanol each day in a two-bottle paradigm for a period of 7 days per concentration. The same concentrations in Experiment I were compared in Experiment 2. In Experiment 3 we sought to test the development of a conditioned taste aversion (CTA) after receiving an intraperitoneal (ip.) injection of 2.0 g/kg ethanol. In Experiment 4, blood ethanol levels where assessed following a 2.0 g/kg ip.injection of ethanol. Experiment 5 assessed taste preference for saccharine and quinine in wild-type and D3-R -/- mice. Contrary to our predictions, both D3-R -/- and wild-types on a CS57BL/6 background had similar intakes of ethanol, at all concentrations tested, in the 24-hour and 1-hour intake paradigms. Wild-type and D3-R -/- mice respond to injected ethanol similarly by developing a conditioned taste aversion. Metabolic analysis revealed mutant mice are slower in metabolizing a bolus injection of ethanol. Lastly, wild-type and D3-R -/- mice showed similar consumption to increasing concentration of both sweet and bitter tastes. These data suggest that deletion of the D3-R gene does not increase ethanol consumption above that found on the C57BL/6 genetic background. Furthermore, the D3-R -/- mice adequately learn a CTA to ethanol and do not ham differing taste reactivity to saccharin or quinine. However, D3-R -/- mice do appear to have a slower rate of ethanol metabolism.

Altered feeding responses in mice with targeted disruption of the dopamine-3 receptor gene.

Dopamine signaling has been implicated in the control of food intake and body weight. In particular, dopamine is important in the control of meal size and number and is thought to mediate the response to metabolic deprivation states. In the present experiments, the authors assessed the role of the dopamine-3 receptor (D3R) in the feeding responses to 2-deoxy-D-glucose, mercaptoacetate, and peripheral insulin. All 3 compounds increased food intake in wild-type mice, but the hyperphagic responses were blunted in D3R-/- mice. In other experiments, D3R-/- mice were hyperresponsive to the administration of amylin and leptin relative to wild-type mice. These results support the hypothesis that D3Rs chronically inhibit the effects of adiposity hormones, thereby contributing to a net anabolic state.