Evaluation of an established oncology triage hotline in a model of emergency department avoidance: assessing the UKONS triage tool and call outcomes.

PURPOSE: In response to a demonstrable need for 24/7, specialist oncology advice for patients undergoing systemic anti-cancer therapy, many healthcare institutions have adopted a telephone triage (TT) service. This is true of the Clatterbridge Cancer Centre which uses the UKONS framework to guide its decisions. This study aims to investigate the utilisation and outcomes of this TT service, with a focus on the most unwell call outcomes and factors leading to referrals to accident and emergency departments that could be mitigated with service development and modifications. METHODS: A retrospective evaluation study was conducted of calls occurring between 1st September 2021 and 31st August 2022. A descriptive analysis of call UKONS grading, triage outcome and primary complaint was performed. RESULTS: The TT hotline received 23,766 calls of which only 9066 were for clinical advice. Of the clinical calls, 45.2% were UKONS red. The majority of red calls 53.3% were directed to AED. The proportion of red calls going to AED changed drastically depending on the timing of call and the corresponding services available at those times, with 38.3% of reds being sent to AED in hours but 72.3% out of hours. The profile of complaints also showed significant differences in hours versus out of hours. CONCLUSION: Significant use of the hotline supports a genuine demand for oncology TT services. In order to reduce referrals to AED, this study supports the creation of alternative destinations of emergency care, especially out of hours.

Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches.

Cardiac sympathetic overactivity is a well-established contributor to the progression of neurogenic hypertension and heart failure, yet the underlying pathophysiology remains unclear. Recent studies have highlighted the importance of acutely regulated cyclic nucleotides and their effectors in the control of intracellular calcium and exocytosis. Emerging evidence now suggests that a significant component of sympathetic overactivity and enhanced transmission may arise from impaired cyclic nucleotide signalling, resulting from compromised phosphodiesterase activity, as well as alterations in receptor-coupled G-protein activation. In this review, we address some of the key cellular and molecular pathways that contribute to sympathetic overactivity in hypertension and discuss their potential for therapeutic targeting.