Interpreting hospital mortality data. The role of clinical risk adjustment

This study uses national Medicare data as well as data that were abstracted to calibrate the Medicare Mortality Predictor System to assess the usefulness of a risk adjustment system in interpreting hospital mortality rates. The majority of variation in annual hospital death rates for the four conditions studied (stroke, pneumonia, myocardial infarction, and congestive heart failure) is chance variability that results from the relatively small numbers of patients treated in most hospitals in a year. For hospitals in the highest and lowest quartiles of observed death rates, the difference between observed rates and those predicted by the Medicare Mortality Predictor System is not quite on third smaller than the difference between observed rates and unadjusted national rates. Risk adjustment methods do not show whether the unexplained difference in mortality rates results from differences in effectiveness of care or unmeasured differences in patient risk at the time of admission. Risk-adjusted mortality rates, therefore, should be supplemented by review of the actual care rendered before conclusions are drawn regarding effectiveness of care.     

Comparison of ultrasonic cleaning schemes: a pilot study.

OBJECTIVE: Ultrasonic cleaning is an effective method for cleaning dental instruments prior to sterilisation. However, there are few studies that directly compare precleaning and ultrasonic cleaning solutions. This study evaluated the efficacy of different ultrasonic cleaning schemes. METHOD AND MATERIALS: Twenty representative dental instruments, five of which were soiled with a mixture of blood and hydroxyapatite, were used in a series of cleaning runs. Cleaning employed a presoaking agent, ultrasonic cleaning, or a combination of both. Two presoaking agents (Non-ionic Ultrasonic Cleaning Solution and ProEZ Foaming Enzymatic Spray) plus five ultrasonic cleaners (UltraDose, General Purpose Cleaner, Co-enzyme Concentrate, Enzol Enzymatic Detergent, and Non-ionic Ultrasonic Cleaning Solution) were compared, with tap water serving as a control. There were two cleaning times: seven and 15 minutes. After rinsing, the working ends of the instruments underwent scrubbing for 20 seconds using a dental polishing brush held in a haemostat. After scrubbing, the brush and instrument were placed in a tube containing sterile saline. Vortexing of the tube lasted 30 seconds. Testing for the post-cleaning presence of blood involved Hemastix dipsticks. These sticks measure minute amounts of blood in urine and can detect as few as 35 red blood cells per ml. Comparisons of colour change were made to a standard scale followed by assignment of numeric values. RESULTS: Tap water was the poorest cleaning solution, while UltraDose was the most effective. Blood removal improved when cleaning time was increased from seven to 15 minutes. The combined effect of a presoak immersion followed by ultrasonic cleaning was the most effective cleaning scheme overall. Cleaning by either ultrasound or presoaking only was less effective. Some instruments were more difficult to clean than others. CONCLUSION: Within the constraints of the small number of test runs performed, it was concluded that application of a presoak agent before ultrasonic cleaning produced the most effective instrument-cleaning regimen.     

Effects of 1,3-di-o-tolylguanidine (DTG), a sigma ligand, on local cerebral glucose utilization in rat brain.

The 2-deoxy-D-[1-14C]glucose ([14C]DG) method was used to examine the effects of the relatively selective sigma ligand 1,3-di-o-tolylguanidine (DTG) on cerebral metabolism in freely moving rats. Each animal received an i.p. injection of DTG (0.2, 1, or 5 mg/kg) or normal saline 20 min prior to the infusion of [14C]DG. DTG induced dose-dependent changes in local cerebral glucose utilization (LCGU) in several motor and limbic structures. Most structures showed increases in LCGU, with a maximum effect at 1 mg/kg. The most profound increases in LCGU were observed in brain regions that are rich in sigma receptors. These included cerebellar and related nuclei (interpositus, lateral and medial cerebellar n., vestibular n., olivary n.), ambiguus n., superior colliculus (superior layers), hippocampus (CA2, CA3, DG), n. basalis of Meynert interpeduncular n., and the substantia nigra pars compacta and pars reticulata. No significant decreases in glucose utilization were observed at any dose. Although the areas affected by DTG are similar to those previously reported for other sigma ligands, future studies employing a range of doses for additional selective sigma ligands must be carried out in order to confirm whether these changes in LCGU were sigma-mediated.     

Dose-escalation study of intravenous nicardipine in patients with aneurysmal subarachnoid hemorrhage

A dose-escalation study of the calcium ion entry blocking drug nicardipine was performed using large dose infusions in 67 patients with recent aneurysmal subarachnoid hemorrhage (SAH). A safe, potentially therapeutic dose of the drug was determined. Patients admitted within 7 days of SAH from a documented cerebral aneurysm were entered into the study if no spasm was present on the initial angiogram. Nicardipine was administered as a continuous intravenous infusion throughout the 14-day period after SAH, regardless of the timing of surgery. To determine the safest possible dose, nicardipine was administered at seven dose levels from 0.01 to 0.15 mg/kg/hr. The total daily doses ranged from 27.7 mg to 375.0 mg. A follow-up angiogram was carried out on all 67 patients 7 to 10 days after SAH. Computerized tomography and neurological examinations were used to determine the presence of cerebral infarction. No major adverse effects, unexpected reactions, or permanent sequelae could be attributed to nicardipine. A decline in blood pressure was noted following administration of the drug. This occurred more frequently among patients given the largest dose but did not produce clinical problems or require discontinuation of the drug. Favorable outcomes were noted in 52 patients (78%). Vasospasm was found by arteriography in 31 patients (46%). A dose-related trend was noted: only eight (24%) of 33 patients treated at the highest dose level (approximately 10 mg/hr) developed arteriographic evidence of vasospasm. Symptomatic vasospasm was diagnosed in only two (6%) of 33 patients treated with this dose. Of the 34 patients receiving the lower dose levels, angiographic spasm was observed in 68% and symptomatic vasospasm in 27%. No deaths due to vasospasm occurred. Nicardipine appears to prevent both vasospasm and cerebral ischemia after SAH. A multicenter randomized double-blind trial to test this hypothesis is planned.