Using clinical indicators in emergency medicine: documenting performance improvements to justify increased resource allocation.

OBJECTIVES: To demonstrate how emergency department triage scale and thrombolysis indicator data can be used to document the impact of a substantial increase in resource allocation. METHODS: Descriptive study in an emergency department of an adult tertiary hospital in Perth, Australia during similar periods of the year both before and after a substantial increase in emergency department staff, equipment, and system resources. The study group comprised a total of 11,048 emergency department attendances and all cases of emergency department initiated thrombolysis or acute angioplasty. Outcome was measured using numbers seen and percentage seen within indicator threshold time together with admission rates in each of the five triage categories as well as by using time from presentation to initiation of reperfusion treatment in acute myocardial infarction. RESULTS: The proportion of patients seen within the prescribed indicator time increased by 16.4% (95% confidence interval 14.4% to 18.2%). The increase was most pronounced in triage category 2 (32.7%). Median time to thrombolysis fell by 30 minutes to 37 minutes (p = 0.0002). CONCLUSIONS: Use of the Australasian national triage scale and time to thrombolysis clinical indicator data allows a quantitative assessment of the impact of increased emergency department resource allocation.

Differential responses to fasting and subsequent feeding by microsomal systems of rat liver: 6- and 9-desaturation of fatty acids.

Hepatic microsomal preparations from nonfasted, fasted, and fasted-fed rats were employed, together with cofactors, in studies of 9-desaturation of stearate-1-(14)C and 6-desaturation of linolenate-1-(14)C. Prior fasting sharply reduced 9-desaturation but did not affect 6-desaturation; feeding restored 9-desaturation. Position of desaturation was determined by permanganate-periodate oxidation and separation of the dicarboxylic acids. Feeding after fasting stimulated both desaturase systems but either dl-ethionine or actinomycin D prevented this. Dietary carbohydrate or saturated fat increased 9-desaturation and dietary protein increased 6-desaturation. Insulin treatment of nonfasted rats increased 9-desaturation but not 6-desaturation. High dietary unsaturated fat (20% safflower oil) stimulated 6-desaturation but inhibited the 9-desaturation response to feeding. The results indicate that the two desaturases are distinct and are inducible in response to different substances.