Hugh Grantham

Review article: Improving the hospital clinical handover between paramedics and emergency department staff in the deteriorating patient

Clinical communication and recognising and responding to a deteriorating patient are key current patient safety issues in healthcare. The aim of this literature review is to identify themes associated with aspects of the hospital clinical handover between paramedics and ED staff that can be improved, with a specific focus on the transfer of care of a deteriorating patient. Extensive searches of scholarly literature were conducted using the main medical and nursing electronic databases, including Cumulative Index to Nursing and Allied Health Literature, Medline and PubMed, during 2011 and again in July 2012. Seventeen peer‐reviewed English‐language original quantitative and qualitative studies from 2001 to 2012 were selected and critically appraised using an evaluation tool based on published instruments. Relevant themes identified were: professional relationships, respect and barriers to communication; multiple or repeated handovers; identification of staff in the ED; significance of vital signs; need for a structured handover tool; documentation and other communication methods and education and training to improve handovers. The issues raised in the literature included the need to: produce more complete and concise handovers, create respectful and effective communication, and identify staff in the ED. A structured handover tool such as ISBAR (a mnemonic covering Introduction, Situation, Background, Assessment and Recommendations) would appear to provide a solution to many of these issues. The recording of vital signs and transfer of these data might be improved with better observation systems incorporating early warning strategies. More effective teamwork could be achieved with further clinical communications training.

Neuronal response in Alzheimer’s and Parkinson’s disease: the effect of toxic proteins on intracellular pathways

Accumulation of protein aggregates is the leading cause of cellular dysfunction in neurodegenerative disorders. Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease, Prion disease and motor disorders such as amyotrophic lateral sclerosis, present with a similar pattern of progressive neuronal death, nervous system deterioration and cognitive impairment. The common characteristic is an unusual misfolding of proteins which is believed to cause protein deposition and trigger degenerative signals in the neurons. A similar clinical presentation seen in many neurodegenerative disorders suggests the possibility of shared neuronal responses in different disorders. Despite the difference in core elements of deposits in each neurodegenerative disorder, the cascade of neuronal reactions such as activation of glycogen synthase kinase-3 beta, mitogen-activated protein kinases, cell cycle re-entry and oxidative stress leading to a progressive neurodegeneration are surprisingly similar. This review focuses on protein toxicity in two neurodegenerative diseases, AD and PD. We reviewed the activated mechanisms of neurotoxicity in response to misfolded beta-amyloid and α-synuclein, two major toxic proteins in AD and PD, leading to neuronal apoptosis. The interaction between the proteins in producing an overlapping pathological pattern will be also discussed.

Design of the RINSE Trial: The Rapid Infusion of cold Normal Saline by paramedics during CPR

BackgroundThe International Liaison Committee on Resuscitation (ILCOR) now recommends therapeutic hypothermia (TH) (33°C for 12-24 hours) as soon as possible for patients who remain comatose after resuscitation from shockable rhythm in out-of-hospital cardiac arrest and that it be considered for non shockable rhythms. The optimal timing of TH is still uncertain. Laboratory data have suggested that there is significantly decreased neurological injury if cooling is initiated during CPR. In addition, peri-arrest cooling may increase the rate of successful defibrillation. This study aims to determine whether paramedic cooling during CPR improves outcome compared standard treatment in patients who are being resuscitated from out-of-hospital cardiac arrest.Methods/DesignThis paper describes the methodology for a definitive multi-centre, randomised, controlled trial of paramedic cooling during CPR compared with standard treatment. Paramedic cooling during CPR will be achieved using a rapid infusion of large volume (20-40 mL/kg to a maximum of 2 litres) ice-cold (4°C) normal saline.The primary outcome measure is survival at hospital discharge. Secondary outcome measures are rates of return of spontaneous circulation, rate of survival to hospital admission, temperature on arrival at hospital, and 12 month quality of life of survivors.DiscussionThis trial will test the effect of the administration of ice cold saline during CPR on survival outcomes. If this simple treatment is found to improve outcomes, it will have generalisability to prehospital services globally.Trial RegistrationClinicalTrials.gov: NCT01172678

Comparison of high- and low-fidelity mannequins for clinical performance assessment

Objective:  A pilot study exploring the differences between high‐ and low‐fidelity mannequins in the assessment of clinical performance.

Induction of therapeutic hypothermia during out-of-hospital cardiac arrest using a rapid infusion of cold saline: The RINSE Trial (Rapid Infusion of Cold Normal Saline)

Background: Patients successfully resuscitated by paramedics from out-of-hospital cardiac arrest often have severe neurologic injury. Laboratory and observational clinical reports have suggested that induction of therapeutic hypothermia during cardiopulmonary resuscitation (CPR) may improve neurologic outcomes. One technique for induction of mild therapeutic hypothermia during CPR is a rapid infusion of large-volume cold crystalloid fluid. Methods: In this multicenter, randomized, controlled trial we assigned adults with out-of-hospital cardiac arrest undergoing CPR to either a rapid intravenous infusion of up to 2 L of cold saline or standard care. The primary outcome measure was survival at hospital discharge; secondary end points included return of a spontaneous circulation. The trial was closed early (at 48% recruitment target) due to changes in temperature management at major receiving hospitals. Results: A total of 1198 patients were assigned to either therapeutic hypothermia during CPR (618 patients) or standard prehospital care (580 patients). Patients allocated to therapeutic hypothermia received a mean (SD) of 1193 (647) mL cold saline. For patients with an initial shockable cardiac rhythm, there was a decrease in the rate of return of a spontaneous circulation in patients who received cold saline compared with standard care (41.2% compared with 50.6%, P=0.03). Overall 10.2% of patients allocated to therapeutic hypothermia during CPR were alive at hospital discharge compared with 11.4% who received standard care (P=0.71). Conclusions: In adults with out-of-hospital cardiac arrest, induction of mild therapeutic hypothermia using a rapid infusion of large-volume, intravenous cold saline during CPR may decrease the rate of return of a spontaneous circulation in patients with an initial shockable rhythm and produced no trend toward improved outcomes at hospital discharge. Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01173393.

Musculoskeletal disorder prevalence and risk factors in ambulance officers.

This review explores the prevalence and determinants of musculoskeletal disorders in ambulance officers, and the limitations of the current epidemiological evidence to inform the development of interventions. Relevant studies were selected using defined word search terms and inclusion criteria. Existing research shows a high annual prevalence of back, neck and shoulder musculoskeletal disorders in ambulance officers and emergency medical technicians, whilst limited research has demonstrated significant associations between individual, physical and psychosocial demands, and musculoskeletal disorders of the low-back and neck-shoulder area. However, methodological issues will need to be addressed in future epidemiological research in order to inform the development of industry specific risk assessment tools that will assist in identifying the complex array of interactive risk factors involved in ambulance work. The accurate identification of risk factors will in turn, better inform the establishment of multifaceted interventions to reduce the prevalence of musculoskeletal disorders in ambulance officers.

Establishing the Aus-ROC Australian and New Zealand out-of-hospital cardiac arrest Epistry.

Introduction Out-of-hospital cardiac arrest (OHCA) is a global health problem with low survival. Regional variation in survival has heightened interest in combining cardiac arrest registries to understand and improve OHCA outcomes. While individual OHCA registries exist in Australian and New Zealand ambulance services, until recently these registries have not been combined. The aim of this protocol paper is to describe the rationale and methods of the Australian Resuscitation Outcomes Consortium (Aus-ROC) OHCA epidemiological registry (Epistry). Methods and analysis The Aus-ROC Epistry is designed as a population-based cohort study. Data collection started in 2014. Six ambulance services in Australia (Ambulance Victoria, SA Ambulance Service, St John Ambulance Western Australia and Queensland Ambulance Service) and New Zealand (St John New Zealand and Wellington Free Ambulance) currently contribute data. All OHCA attended by ambulance, regardless of aetiology or patient age, are included in the Epistry. The catchment population is approximately 19.3 million persons, representing 63% of the Australian population and 100% of the New Zealand population. Data are collected using Utstein-style definitions. Information incorporated into the Epistry includes demographics, arrest features, ambulance response times, treatment and patient outcomes. The primary outcome is ‘survival to hospital discharge’, with ‘return of spontaneous circulation’ as a key secondary outcome. Ethics and dissemination Ethics approval was independently sought by each of the contributing registries. Overarching ethics for the Epistry was provided by Monash University HREC (Approval No. CF12/3938—2012001888). A population-based OHCA registry capturing the majority of Australia and New Zealand will allow risk-adjusted outcomes to be determined, to enable benchmarking across ambulance providers, facilitate the identification of system-wide strategies associated with survival from OHCA, and allow monitoring of temporal trends in process and outcomes to improve patient care. Findings will be shared with participating ambulance services and the academic community.

Global review of delay time in seeking medical care for chest pain: An integrative literature review

OBJECTIVES The aim of this review is to summarise research from a range of countries describing the differences in time taken to seek medical care for chest pain and factors which contribute to delay times. METHODS An integrative literature review was undertaken using the Medline, CINAHL and Scopus databases for publications between 1994 and 2014. Articles dealing with delay time, and the factors associated with delay time, were extracted from the literature. RESULTS The search yielded 395 articles of which 205 full-text articles were assessed for eligibility. Finally, twenty-three articles met the inclusion criteria for the review. It was found that time to seeking treatment (delay times) varied between countries, ranging from 1.6 to 12.9h, with a mean of 3.4h. The mean delay times reported in all the selected studies were greater than the recommended time-frame for seeking treatment. As well, time to decision to seek treatment (decision time) was reported as a major component of delay time. Meanwhile, the utilisation rates of ambulance services ranged from 3.1% in Brazil to 61.0% in Australia. A majority of the reviewed studies reported on the factors associated with longer delay times, including old age, female gender, ethnicity, low education level, history of chronic disease, lack of knowledge of the symptoms, and underutilisation of ambulance services. Only three studies included a sub-analysis by ethnicity, reporting that ethnic groups had longer delay times than Caucasians. CONCLUSION Variability in delay times occurred across countries and within continents. The mean time taken to seek care for chest pain in the countries reviewed did not meet the recommended times according to international guidelines. Demographic and social factors, as well as cognitive and emotional factors, influenced delay times. Further research on these influencing factors is recommended, including the impact of ethnicity on patients care-seeking behaviours for chest pain.

Randomized Comparison of High-Sensitivity Troponin Reporting in Undifferentiated Chest Pain Assessment

Background—High-sensitivity troponin T (hs-TnT) assays promise greater discrimination of evolving myocardial infarction, but the impact of unguided implementation on the effectiveness of care is uncertain. Methods and Results—We evaluated the impact of hs-TnT reporting on care and outcome among chest pain patients presenting to 5 emergency departments within a multicenter randomized trial. Patients were allocated to hs-TnT reporting (hs-report) or standard reporting (std-report; Roche Elecys). The primary end point was death and new or recurrent acute coronary syndrome by 12 months. A total of 1937 patients without ST-segment elevation were enrolled between July 2011 and March 2013. The median age was 61 (interquartile range, 48–74) years, and 46.3% were women. During the index hospitalization, 1466 patients (75.7%) had maximal troponin <30 ng/L within 24 hours. Randomization to hs-report format did not alter the admission rate (hs-report: 57.7% versus std-report: 58.0%; P=0.069). There was no difference in angiography (hs-report: 11.9% versus std-report: 10.9%; P=0.479). The hs-reporting did not reduce 12-month death or new/recurrent acute coronary syndrome in the overall population (hs-report: 9.7% versus std-report: 7.2% [hazard ratio, 0.83 (0.57–1.22); P=0.362]). However, among those with troponin levels <30 ng/L, a modest reduction in the primary end point was observed (hs-report: 2.6% versus std-report: 4.4%, [hazard ratio, 0.58; 95% confidence interval, 0.34–0.1.00; P=0.050). Conclusions—High-sensitivity troponin reporting alone is associated with only modest changes in practice. Clinical effectiveness in the adoption of high-sensitivity troponin may require close coupling with protocols that guide interpretation and care. Clinical Trial Registration—URL: http://www.ANZCTR.org.au. Unique identifier: ACTRN12611000879965.

Early Glycogen Synthase Kinase‐3β (GSK‐3β) and Protein Phosphatase 2A (PP2A) independent tau dephosphorylation during global brain ischemia and reperfusion following cardiac arrest and the role of the Adenosine Monophosphate Kinase (AMPK) pathway

Abnormal tau phosphorylation (p‐tau) has been shown after hypoxic damage to the brain associated with traumatic brain injury and stroke. As the level of p‐tau is controlled by Glycogen Synthase Kinase (GSK)‐3β, Protein Phosphatase 2A (PP2A) and Adenosine Monophosphate Kinase (AMPK), different activity levels of these enzymes could be involved in tau phosphorylation following ischaemia. This study assessed the effects of global brain ischaemia/reperfusion on the immediate status of p‐tau in a rat model of cardiac arrest (CA) followed by cardiopulmonary resuscitation (CPR). We reported an early dephosphorylation of tau at its AMPK sensitive residues, Ser396 and Ser262after 2 min of ischaemia, which did not recover during the first two hours of reperfusion, while the tau phosphorylation at GSK‐3β sensitive but AMPK insensitive residues, Ser202/Thr205 (AT8), as well as the total amount of tau remained unchanged. Our data showed no alteration in the activities of GSK‐3β and PP2A during similar episodes of ischaemia of up to 8 min and reperfusion of up to 2 h, and 4 weeks recovery. Dephosphorylation of AMPK followed the same pattern as tau dephosphorylation during ischaemia/reperfusion. Catalase, another AMPK downstream substrate also showed a similar pattern of decline to p‐AMPK, in ischaemic/reperfusion groups. This suggests the involvement of AMPK in changing the p‐tau levels, indicating that tau dephosphorylation following ischaemia is not dependent on GSK‐3β or PP2A activity, but is associated with AMPK dephosphorylation. We propose that a reduction in AMPK activity is a possible early mechanism responsible for tau dephosphorylation.