Adverse drug events (ADEs) are more likely to affect geriatric patients due to physiological changes occurring with aging. Even though this is an internationally recognized problem, similar research data in Finland is still lacking. The aim of this study was to determine the number of geriatric medication-related hospitalizations in the Finnish patient population and to discover the potential means of recognizing patients particularly at risk of ADEs. The study was conducted retrospectively from the 2014 emergency department patient records in Oulu University Hospital. A total number of 290 admissions were screened for ADEs, adverse drug reactions (ADRs) and drug-drug interactions (DDIs) by a multi-disciplinary research team. Customized Naranjo scale was used as a control method. All admissions were categorized into “probable,” “possible,” or “doubtful” by both assessment methods. In total, 23.1% of admissions were categorized as “probably” or “possibly” medication-related. Vertigo, falling, and fractures formed the largest group of ADEs. The most common ADEs were related to medicines from N class of the ATC-code system. Age, sex, residence, or specialty did not increase the risk for medication-related admission significantly (min p = 0.077). Polypharmacy was, however, found to increase the risk (OR 3.3; 95% CI, 1.5–6.9; p = 0.01). In conclusion, screening patients for specific demographics or symptoms would not significantly improve the recognition of ADEs. In addition, as ADE detection today is largely based on voluntary reporting systems and retrospective manual tracking of errors, it is evident that more effective methods for ADE detection are needed in the future.

No abstract

The aim of this study was to investigate the effects of beta-stimulation in deep (25 degrees C) hypothermia. Cardiac catheterization was performed on seven anesthetized beagle dogs. They were cooled between ice bags down to 25 degrees C and received isoproterenol administered intravenously three times: at the normal body temperature (37 degrees C) before cooling, after cooling at 25 degrees C, and after rewarming at 37 degrees C. Circulatory function was measured for every 1 degree C of temperature change. Isoproterenol infusion at 37 degrees C induced cardiac acceleration, including the increases of heart rate, cardiac output, and peak first derivative of the left ventricular pressure curve. Systemic vascular and mean outflow resistances and mean aortic pressure decreased. During cooling, shivering thermogenesis continued, even down to 25 degrees C. At 25 degrees C, cardiac acceleration after isoproterenol infusion did not exist but relaxation rate increased slightly. Systemic vascular and mean outflow resistances decreased, but left ventricular end-diastolic and filling pressures increased. beta-Stimulation at normal body temperature increases shivering thermogenesis during cooling. The venous return to the left ventricle at 25 degrees C increased after isoproterenol infusion while systemic vascular resistance decreased, indicating systemic vasodilatation. This increase in preload is probably due to vasoconstriction in pulmonary vessels, which may be mediated by prejunctional beta-adrenoceptors. For cardiac inotrophy, the isoproterenol had no physiologically significant effects at 25 degrees C. After rewarming at 37 degrees C, the effects of isoproterenol were physiologically similar to the effects at the same temperature before cooling.

Hypothermia is commonly found in accidents on land and at sea, yet its pulmonary circulatory effects have not been studied before. To study the effects of hypothermia on the right heart function and pulmonary circulation, cardiac catheterization was carried out on nine anaesthetized beagle dogs. The dogs were cooled between ice bags until the temperature in the pulmonary artery was 25 degrees C and then rewarmed using a heating box especially constructed for this purpose. Heart rate decreased significantly (P < 0.01) during cooling. Cardiac output also diminished mainly because of decreased heart rate. Total pulmonary resistance increased in the cold (P < 0.05) and returned to the initial level during rewarming. The peak rate of increase in pressure (dP/dtmax) of the right ventricular pressure curve did not show any significant change. Retardation in relaxation in hypothermia was indicated by an increase (P < 0.01) in the peak negative dP/dt of the right ventricular pressure curve. According to our results, the contraction rate did not change, but the relaxation rate decreased significantly during cooling. No signs of heart failure were observed and all parameters returned to normal during rewarming. In conclusion, right ventricular function was not compromised even during deep hypothermia.

Intravenous administration of warm fluids is used clinically as first aid either alone or as a contributing method, to rewarm hypothermic patients back to normal body temperature. The aim of this study was to determine the effects of an acute volume load in hypothermic conditions on the canine circulatory system. Cardiac catheterization was performed on 18 anaesthetized beagle dogs. Eleven of them were cooled and at a body temperature of 25 degrees C they received 40 ml.kg-1 dextran administered intravenously. The control group received dextran at normal body temperature. During cooling the body from 37 degrees C down to 25 degrees C most of the volume load escaped from the circulation due to extravazation. During rewarming, the opposite effect could be seen and the volume load persisted up to 29 degrees C and signs of cardiac decompensation were observed. According to these results, the intravenous administration of warm fluids to rewarm hypothermic patients should not be used routinely when hypovolaemia is the only result of hypothermia.