Technology management: case study of an integrated health system.

Technology management has assumed a role of vital importance in today's health care environment. Capital reserves and operating income have been stretched by pervasive and expensive technologies, while overall reimbursement has been reduced. It is imperative for hospitals to develop and consistently use technology management processes that begin prior to a technology's introduction in the hospital and continue throughout its life cycle. At Samaritan Health System (SHS), an integrated health care delivery system based in Phoenix, technology management provides tools to improve decision making and assist in the system's integration strategy as well as control expenses. SHS uses a systemwide technology-specific plan to guide acquisition and/or funding decisions. This plan describes how particular technologies can help achieve SHS' organizational goals such as promoting system integration and/or improving patient outcomes while providing good economic value. After technologies are targeted in this systemwide plan they are prioritized using a two-stage capital prioritization process. The first stage of the capital prioritization process considers the quantitative and qualitative factors critical for equitable capital distribution across the system. The second stage develops a sense of ownership among the parties that affect and are affected by the allocation at a facility level. This process promotes an efficient, effective, equitable, and defensible approach to resource allocation and technology decision making. Minimizing equipment maintenance expenditures is also an integral part of technology management at SHS. The keys to reducing maintenance expenditures are having a process in place that supports a routine fiscal evaluation of maintenance coverage options and ensuring that manufacturers are obligated to provide critical maintenance resources at the time of equipment purchase. Maintenance service options under consideration in this report include full-service contracts with the manufacturer, insurance coverage, time and materials, and independent service vendors/in-house support. Careful consideration of all the ramifications of each option is warranted because there are substantial cost differences among these methods. At SHS, technology management efforts resulted in equipment purchases and maintenance negotiations representing savings of more than $1.5 million in a single year. SHS undertakes an intensive review of purchases and maintenance expenditures, using the techniques described in this report, with the objective of reducing expenses by 10% per year. This report describes the technology management methods that SHS uses to achieve these results.

Sustained seizures cause circumscribed cerebral changes in glial fibrillary acidic protein, neurofilament and laminin immunofluorescence.

Sustained experimental seizures in rats have previously been shown to cause an extensive necrosis in pars reticulata of substantia nigra (SNPR) and globus pallidus (GP). In the present paper we have studied the effects of hexafluorodiethyl ether-induced seizures on the immunoreactivity seen with antibodies directed against glial fibrillary acidic protein, GFA, used to visualize astrocytes, antibodies to the glycoprotein laminin as a marker for blood vessel walls and neurofilament (NF) antibodies to monitor neuronal disturbances. Already 12 h after a 20-min seizure period a reduction in GFA immunofluorescence intensity was observed in SNPR. After 3 days, marked lesions were noted in SNPR and GP as seen with cresyl violet staining. The lesions contained almost no GFA-positive structures. In the proximity of the lesions, an increase in GFA-immunoreactivity was noted. Such an increase, although less pronounced, was also seen in the major projection areas of SNPR. Two months post-seizure, the gliotic reaction had disappeared, and only a thin and elongated gliotic scar was observed. In spite of the development of a profound central necrosis especially evident in SNPR, both laminin- and NF-immunoreactivity was slightly increased within the lesioned areas. NF-immunoreactivity was also increased in the superior colliculus and in the reticular formation. Two months post-experiment NF-immunofluorescence was normalized but the former lesion sites showed signs of hypervascularization. We conclude that hexafluorodiethyl ether-induced 20-min seizures lead to rapid, localized glial and neuronal changes in the rat brain as evidenced by GFA and NF immunohistochemistry, while the vascular network remains intact.

Short- and long-term consequences of intracranial injections of the excitotoxin, quinolinic acid, as evidenced by GFA immunohistochemistry of astrocytes.

Astroglial reactions to intrastriatal and intrahypothalamic injections of the endogenous excitotoxin quinolinic acid (50 micrograms in 1 microliter) were studied in adult rats, using immunohistochemistry with antiserum to glial fibrillary acidic protein. Animals were sacrificed 6 h, 24 h, 3, 7 and 30 days or 1 year after the injection. Six and 24 h after quinolinic acid, the amount of glial fibrillary acidic protein-like immunoreactivity in the injected striatum was lower than in controls but returned to a normal level at 3 days. Not until 7 days was a clear striatal gliosis apparent, as evidenced by an increased density of glial fibrillary acidic protein-positive structures and brightly fluorescent, clearly hypertrophic cells. This gliosis was even more developed in animals sacrificed 30 days postoperatively. A weak astrocytic reaction was also observed in the ipsilateral corpus callosum at 6 h after quinolinic acid. By 3 days, a marked gliosis restricted to the injected hemisphere was present throughout corpus callosum and cortex cerebri. In animals sacrificed 30 days after quinolinic acid the extrastriatal astrocytic reaction was clearly diminished, although the striatal gliosis was still prominent. One year postinjection, no obvious gliosis could be observed in cortex cerebri or corpus callosum while striatal tissue, now markedly reduced in volume, was clearly gliotic. Using neurofilament antiserum, increased fluorescence intensity was noted in striatal nerve bundles during the first day after an intrastriatal quinolinic acid injection and persisted 1 year postoperatively. Controls were similarly injected with an equimolar amount of nicotinic acid, the non-excitatory, non-neurotoxic decarboxylation product of quinolinic acid. No changes in immunoreactivity of glial fibrillary acidic protein or neurofilament were found in these animals. In animals treated intrahypothalamically, a spherical central area almost devoid of glial fibrillary acidic protein-immunoreactivity was noted around the injection site 7 days after quinolinic acid administration. Around this area, gliosis was observed. Apart from a very restricted gliotic reaction around the needle tract, no astrocytic reaction was observed in nicotinic acid-injected control animals. We conclude that quinolinic acid causes both reversible and long-lasting gliosis when injected into the rat striatum. As a natural brain metabolite, quinolinic acid may constitute a particularly valuable tool for the elucidation of a possible role of glia in neurodegenerative disorders.

Cells in neonatal rat hypothalamus primary culture--an immunofluorescence study.

Hypothalami from 1 day neonatal rats were dissociated and cultured for 4-16 days. Using immunofluorescence and antisera against neurofilament (NF) peptides, glial fibrillary acidic protein (GFAP), galactocerebroside and fibronectin we have distinguished neurons, astrocytes, oligodendrocytes and fibroblast-like cells in culture. Astrocytes initially grew as islets of 15-30 cells which dispersed as the culture aged. These cells, together with fibronectin-reactive flat cells, formed a monolayer upon which ovoid and process-bearing cells grew after 4 days in culture. Neurofilament-positive neurons constituted 5-10% of the total cell population. In maturing cultures the number of neurons decreased and fibroblasts increased. Oligodendrocytes represented less than 1% of total cell population. These studies emphasize the necessity of using the complementary techniques of morphology and immunocytochemistry for the characterization of hypothalamic neural cells in vitro.

Neonatal rat hypothalamus cell culture: neuron subpopulations secrete immunoreactive beta-endorphin but not immunoreactive ACTH.

Primary cultures of dissociated hypothalamic cells were prepared from 1-day-old rat neonates. Studies with cell-specific antisera revealed the presence of neurons, glial cells, oligodendrocytes and fibroblast-like cells. By immunohistochemistry, two morphologically distinct cells in culture were positive for immunoreactive beta-endorphin (IR-beta-EP). The medium derived from these cultures contained radioimmunoassayable IR-beta-EP, but not IR-ACTH. These data suggest that, in rat neonatal hypothalamic cultures, two subpopulations of cells exist which store and secrete IR-beta-EP, but not IR-ACTH.

[On the effect of hyperbaric oxygen (OHP) at the guinea pig's cochlea insulted by hypoxia (author's transl)]. / Die Wirkung von hyperbarem Sauerstoff (OHP) auf die hypoxisch geschädigte Cochlea des Meerschweinchens.

The effect of OHP (oxygen under high pressure) by examining 17 CO-intoxicated guinea pigs. The following effects have been observed: The microphonics recovered significantly faster after hypoxia caused by CO than under air. Hyperbaric oxygen has a protecting effect on the inner ear. If OHP is applicated before CO, the microphonics decrease less than under normal breathing. The postmortal microphonics increased to a level above the known postmortal slope, suggesting a diffusion of oxygen through the round window.