Clinical outcomes of point-of-care testing in the interventional radiology and invasive cardiology setting.

BACKGROUND: Point-of-care testing (POCT) can provide rapid test results, but its impact on patient care is not well documented. We investigated the ability of POCT to decrease inpatient and outpatient waiting times for cardiovascular procedures. METHODS: We prospectively studied, over a 7-month period, 216 patients requiring diagnostic laboratory testing for coagulation (prothrombin time/activated partial thromboplastin time) and/or renal function (urea nitrogen, creatinine, sodium, and potassium) before elective invasive cardiac and radiologic procedures. Overall patient management and workflow were examined in the initial phase. In phase 2, we implemented POCT but utilized central laboratory results for patient management. In phase 3, therapeutic decisions were based on POCT results. The final phase, phase 4, sought to optimize workflow around the availability of POCT. Patient wait and timing of phlebotomy, availability of laboratory results, and therapeutic action were monitored. Split sampling allowed comparability of POCT and central laboratory results throughout the study. RESULTS: In phase 1, 44% of central laboratory results were not available before the scheduled time for procedure (n = 135). Mean waiting times (arrival to procedure) were 188 +/- 54 min for patients who needed renal testing (phase 2; n = 14) and 171 +/- 76 min for those needing coagulation testing (n = 24). For patients needing renal testing, POCT decreased patient wait times (phases 3 and 4 combined, 141 +/- 52 min; n = 18; P = 0.02). For patients needing coagulation testing, wait times improved only when systematic changes were made in workflow (phase 4, 109 +/- 41 min; n = 12; P = 0.01). CONCLUSIONS: Although POCT has the potential to provide beneficial patient outcomes, merely moving testing from a central laboratory to the medical unit does not guarantee improved outcomes. Systematic changes in patient management may be required.

Local control of oligodendrocyte development in isolated dorsal mouse spinal cord.

The earliest oligodendrocyte precursors have been proposed to arise in the ventral ventricular zone of the embryonic thoraco-lumbar spinal cord and subsequently migrate to populate dorsal spinal cord. Using the expression of O4 immunoreactivity to define cells of the oligodendrocyte lineage, the development of oligodendrocytes in different regions of the mouse spinal cord was assayed. Consistent with earlier studies in other species, isolated explants of E11 ventral but not dorsal mouse spinal cord developed oligodendrocytes after 7 days in vitro. In contrast, in cultures derived from E13 embryos O4(+) oligodendrocytes developed in both ventral and dorsal cultures after 5 days in vitro. These data are consistent with a ventral to dorsal migration of committed oligodendrocyte progenitors occurring between E11 and E13. Although isolated early embryonic dorsal spinal cord does not give rise to oligodendrocytes in short term cultures, in long term cultures O4(+) cells develop in a subset of dorsal explants. After 10 days in vitro approximately 25% of both cervical and thoraco-lumbar E11 derived dorsal explants contained significant numbers of O4(+) cells. The molecular requirements for the dorsally-derived oligodendrocytes was similar to that in ventral cord. The appearance of O4(+) cells was dependent on sonic hedgehog and enhanced by neuregulin. These data suggest that early embryonic dorsal mouse spinal cord has an independent potential to generate oligodendrocytes under appropriate conditions. Whether this potential is realized during normal spinal cord development is currently unknown.

Sonic hedgehog signaling is required during the appearance of spinal cord oligodendrocyte precursors.

Spinal cord oligodendrocyte precursors arise in the ventral ventricular zone as a result of local signals. Ectopic oligodendrocyte precursors can be induced by sonic hedgehog (Shh) in explants of chick dorsal spinal cord over an extended developmental period. The role of Shh during normal oligodendrocyte development is, however, unclear. Here we demonstrate that Shh is localized to the ventral spinal cord immediately prior to, and during the appearance of oligodendrocyte precursors. Continued expression of Shh is required for the appearance of spinal cord oligodendrocyte precursors as neutralization of Shh signaling both in vivo and in vitro during a defined developmental period blocked their emergence. The inhibition of oligodendrocyte precursor emergence in the absence of Shh signaling was not the result of inhibiting precursor cell proliferation, and the neutralization of Shh signaling after the emergence of oligodendrocyte precursors had no effect on the appearance of additional cells or their subsequent differentiation. Similar concentrations of Shh induce motor neurons and oligodendrocytes in dorsal spinal cord explants. However, in explants from early embryos the motor neuron lineage is preferentially expanded while in explants from older embryos the oligodendrocyte lineage is preferentially expanded.

Technical evaluation of five glucose meters with data management capabilities.

Technical performance and data management features are prominent criteria in the selection of an appropriate meter for a point-of-care glucose testing program. We evaluated the technical performance of 5 currently available glucose meters with data management capabilities. The performance of all 5 meters was technically equivalent. Linear regression slopes vs the reference method are in the range of 0.94 to 1.02 and indicate correlation more to plasma values than to whole blood values. The percentage of glucose meter results within +/- 15% of the laboratory value was at least 90%; however, the percentage within +/- 10% was 75% to 87% for most meters. Within-day and between-day precision ranged from 2% to 5% coefficient of variation. Evaluation of linearity with glucose-spiked venous specimens demonstrated that the linearity of each meter agreed with the manufacturer's stated range in most cases. Meter glucose values tended to bias negative as the hematocrit increased, an effect that may be more pronounced at higher glucose concentrations. No volume effects were noted between 5 microL and 40 microL. The results suggest that all meters tested will likely satisfy technical performance criteria in a hospital setting and that selection of a system for point-of-care glucose testing will be influenced by the institution's data management requirements.

Pulmonary hydraulic impedance responses to hypoxia and hypercapnia in newborn pigs.

The purpose of this study was to determine the cumulative effects of brief intervals of hypoxia and hypercapnia on the pulsatile characteristics of the pulmonary arterial circulation of 48-h-old compared with 2-wk-old open-chest Yorkshire pigs while using two different anesthetic regimens: 1) azaperone and ketamine (4 and 12 mg/kg im, respectively) and 2) thiopental sodium (25 mg/kg i.v.). Animals 48 h old were randomly allocated to undergo mild hypoxia (inspired O2 fraction = 0.15), severe hypoxia (inspired O2 fraction = 0.05), or hypercapnia (inspired CO2 fraction = 0.20), whereas animals 2 wk old underwent severe hypoxia or hypercapnia. With use of Fourier analysis, characteristic impedance (Zo), mean input impedance (Zm), impedance moduli, and phase angles were determined. In 48-h-old pigs anesthetized with azaperone-ketamine, neither mild nor severe hypoxia altered Zo, Zm, or pulmonary vascular resistance (PVR), whereas hypercapnia increased Zo by 22% (P < 0.001), which persisted despite a return to normocapnia. In 48-h-old animals anesthetized with thiopental, baseline control Zo and Zm were lower than those in same-age pigs anesthetized with azaperone-ketamine. In thiopental-anesthetized 48-h-old pigs, both severe hypoxia and hypercapnia increased Zm and PVR but Zo was unaltered. In 2-wk-old pigs anesthetized with thiopental, severe hypoxia but not hypercapnia elevated Zm and PVR, whereas Zo was not changed with either stress. Results indicate age- and anesthetic-dependent responses of Zo, Zm, and PVR to severe hypoxia and hypercapnia. The persistent elevation in Zo caused by hypercapnia indicates a prolonged decrease in arterial compliance or a reduction in effective proximal pulmonary arterial radius.