Before 2015, the standard of care for emergency ischaemic stroke treatment was intravenous thrombolysis with tissue plasminogen activator (IV-tPA). This stemmed from the National Institute of Neurological Disorders and Stroke trial in 1995, which showed that compared with placebo, patients who were given IV-tPA within 3 hours from symptom onset were 30% more likely to have minimal or no disability at 3 months.1 The therapeutic window was further extended to 4.5 hours from symptom onset by the European Cooperative Acute Stroke Study III, which demonstrated similar benefits when IV-tPA was administered between 3 and 4.5 hours to selected patients.2

Nonetheless, in patients with ischaemia due to occlusion of a major cerebral artery, such as the intracranial internal carotid artery or the first and second segment of middle cerebral artery (M1, M2), the efficacy of intravenous thrombolysis was limited, with a recanalisation rate of only 4% to 30%.3 This group of patients frequently had a grave neurological prognosis and high mortality owing to the large infarct territory, and could develop malignant cerebral oedema that required decompressive craniectomy.4

To improve the recanalisation rate, endovascular mechanical thrombectomy to remove the occluding clot was proposed. Early studies of this technique showed conflicting results and were attributed to poor patient selection and suboptimal endovascular devices that resulted in a low recanalisation rate, thus failing to show the expected benefits of endovascular thrombectomy.5 6 7

With modern improved thrombectomy devices, the publication of five positive randomised trials of acute mechanical thrombectomy for ischaemic stroke resulting from anterior circulation large-vessel occlusion in the New England Journal of Medicine in 2015 marked a paradigm shift in stroke treatment.8 9 10 11 12 Since then, emergency endovascular thrombectomy has been internationally regarded as the new standard of care for acute ischaemic stroke caused by major vessel occlusion, and is recommended by all major stroke guidelines.

The five independent randomised controlled trials that provided strong evidence to support endovascular thrombectomy were MR CLEAN,8 REVASCAT,9 ESCAPE,10 EXTEND-IA,11 and SWIFT PRIME,12 conducted in the US, Europe, and Australia from 2010 to 2015. Although there were differences in terms of inclusion and exclusion criteria, all five studies recruited only acute stroke patients with angiogram-proven major vessel occlusion in the anterior circulation, and used newer-generation thrombectomy devices (mostly stent retrievers) that achieved higher recanalisation rates than earlier devices used in previous trials.

All patients in the five trials were given IV-tPA as standard treatment when eligible, and were then randomised to receive endovascular thrombectomy or standard care alone. All these trials unanimously showed significant benefit in the thrombectomy group in terms of improved functional outcome at 3 months, as measured by the modified Rankin scale (mRS) [Table 18 9 10 11 12 13].

A meta-analysis of the above five trials with a total of 1287 eligible patients showed that 46% of patients treated by endovascular thrombectomy achieved functional independence (mRS score, 0-2) at 90 days, compared with 26.5% of patients in the control group13 (Table 1). The number needed-to-treat was 2.6 for one patient to improve functionally by at least 1 point on mRS. In terms of safety, there was no significant difference between the intervention group and the control group in symptomatic intracranial haemorrhage (4.4% vs 4.3%; P=0.81) or mortality rate at 90 days (15.3% vs 18.9%; P=0.15).13

Moreover, the clinical benefit was maintained whether the patient was eligible to receive IV-tPA in the first place, and across all age-groups including the patients older than 80 years. Patients improved after thrombectomy regardless of the initial severity of stroke, as documented by the National Institutes of Health Stroke Scale (NIHSS) and the initial Alberta Stroke Program Early CT Score.

Regarding the treatment time frame, thrombectomy within 6 hours from symptom onset was consistently beneficial across all five thrombectomy trials. In the REVASCAT trial that included patients within 8 hours of symptom onset, the median onset-to-reperfusion time was still within 6 hours in the thrombectomy group, although no separate data were provided for those who presented between 6 and 8 hours.9 Similarly, in the ESCAPE trial, which included patients up to 12 hours from stroke onset, the median time to reperfusion was 4 hours from symptom onset and very few patients beyond 6 hours were recruited.10 At present, two clinical trials are underway to investigate the benefits of endovascular thrombectomy for anterior circulation stroke beyond 6 hours, and both require computed tomography (CT) perfusion or magnetic resonance imaging (MRI) to assess infarct core and perfusion mismatch to determine eligibility (NCT02586415, NCT02142283). Therefore, the efficacy and risk of anterior circulation thrombectomy beyond 6 hours without advanced imaging selection criteria are uncertain, and should be performed with discretion or in a clinical research setting.

At present, there is no evidence from randomised trials regarding thrombectomy for posterior circulation large-vessel occlusion or paediatric patients.

One major improvement of these five trials8 9 10 11 12 compared with previous negative thrombectomy trials5 6 7 was the exclusive use of newer stent retriever devices and a consequent higher recanalisation rate. Near-complete/complete (TICI 2b/3) recanalisation was achieved in 59% to 88% of patients, compared with only 25% to 41% in early studies that used intra-arterial tPA and first-generation devices.14

Another contemporary thrombectomy device was the direct aspiration catheter (ADAPT technique),15 which applied suction to remove the clot via a large-bore endovascular catheter (Fig 1). This technique was supported by multiple single-centre series that showed comparable and sometimes superior results over stent retrievers, although none of these were head-to-head comparative trials.16 17 18 The 2016 THERAPY trial was the only randomised study to compare aspiration thrombectomy versus IV-tPA alone.19 It was terminated prematurely with a limited sample size after publication of the positive stent retriever trials, and as such failed to demonstrate a statistically significant benefit for aspiration thrombectomy over intravenous thrombolysis alone.

Cost-utility analyses have been performed in several health care systems around the world and all have shown the cost-effectiveness of endovascular thrombectomy. The cost per quality-adjusted life year (QALY) gained for thrombectomy over standard thrombolysis treatment varies between US$7988 (Sweden), US$9386 (US), US$11 651 (UK), and US$11 990 (Canada).18 20 21 22 Using internationally accepted willingness-to-pay per QALY threshold of the gross domestic product per capita, all of the above health care systems found endovascular thrombectomy to be cost-effective.

The overwhelming clinical evidence to support application of thrombectomy in anterior circulation stroke prompted the European Stroke Organisation (ESO) and subsequently the American Heart Association/American Stroke Association (AHA/ASA) to release a focused update of early stroke treatment guidelines in 2015, recommending endovascular thrombectomy with stent retriever device if onset of symptoms was within 6 hours and was due to a major vessel occlusion of the anterior circulation, and when suitable criteria were met (Class I, Level of Evidence A).23 24 The Box lists the latest AHA/ASA and ESO recommendations regarding endovascular thrombectomy.23 24

Endovascular thrombectomy for ischaemic stroke is a relatively new procedure in Hong Kong and is not routinely available. Although it was practised in certain centres prior to 2015 for selected cases,25 there was no consensus on treatment indications, patient selection criteria, or operative techniques. With acute mechanical thrombectomy now becoming the international standard of care for acute anterior circulation ischaemic stroke, we undertook a survey to identify the availability, clinical practice, and potential obstacles of an acute stroke thrombectomy service in Hong Kong.

We designed a survey which addressed the availability of expertise, the indications, patient selection for stroke treatment, interventional techniques, and perceived obstacles to timely stroke treatment. This was a web-based survey consisting of 43 questions and was administered from May to August 2016. Respondents were drawn from the Hong Kong Stroke Society, Hong Kong Neurosurgical Society, and Hong Kong Society of Interventional and Therapeutic Neuroradiology. Invitations to participate were sent by email. Participants did not receive any incentive to complete this survey. We received 44 responses from the three societies. Background characteristics of the respondents are shown in Figure 2.

Overall, 24 (54.5%) respondents from six public hospitals and five private practices were regularly involved in the decision and provision of mechanical thrombectomy for patients with acute ischaemic stroke. Most were neurosurgeons (75.0%), and the remainder were neurologists and interventional radiologists. In most centres, the interventionist capable of performing thrombectomy was a neurosurgeon or interventional radiologist, whereas in half of the responding centres there were also neurologists who were able to perform this procedure. For the majority of interventionists (62.5%), mechanical thrombectomy was offered only on an ‘ad hoc’ basis with no official service hours. The mean number of interventionists currently available was 4.3 per centre. The questions and responses of the survey are shown in Table 2.

Direct aspiration technique (ADAPT15) was the most popular first-line thrombectomy technique, adopted by 83.3% of respondents. A stent retriever was chosen as a second-line thrombectomy device by 91.7% of interventionists. The majority of local practitioners used 6 hours as the time limit for anterior circulation thrombectomy in accordance with current guidelines, but a significant number of respondents (37.5%) adopted a more liberal limit of 8 hours or beyond. Most practitioners would prescribe intravenous thrombolysis using the standard dosage in patients who fulfilled thrombolysis indications, regardless of thrombectomy decision, and in line with current guidelines.

For patient selection, most local interventionists used CT angiography as the predominant imaging modality. This finding is unsurprising considering CT perfusion and MRI scanners were not routinely available in an emergency setting in many public hospitals where most acute stroke patients were treated. Apart from angiographic evidence of major vessel occlusion (intracranial internal carotid artery, M1/M2 segment of middle cerebral artery and basilar artery), stroke symptom severity of NIHSS score of >5 and pre-stroke functional status (mRS score ≤2) were regarded as important selection criteria by over 70% of respondents.

Up to 87.5% of respondents performed thrombectomy without general anaesthesia. This practice has been recommended after a recent meta-analysis that confirmed better outcome in patients treated under conscious sedation than in those under general anaesthesia.26 A more recent randomised trial, however, showed no difference in outcome whether general anaesthesia or conscious sedation was used.27

Locally, an acute ischaemic stroke service is heavily dependent on a public health system that handles over 80% of emergency hospital admissions in Hong Kong.28 Our neurologists and stroke physicians in public hospitals have made major contributions over the past two decades in implementing intravenous thrombolysis and spearheading 24-hour acute stroke care. As a result of much effort, currently seven of 17 emergency hospitals in the public hospital system provide 24-hour IV-tPA thrombolysis service.29 Future enhancement of an acute stroke service should aim to provide timely and universal access for patients with acute ischaemic stroke, and divert potentially eligible thrombectomy patients to centres that can provide such service (Fig 3).

Our survey identified the most common reported obstacles in implementing prompt stroke interventions as poor inter- and in-hospital logistics of patient transfer and triage, delayed presentation, and insufficient interventionists, as well as difficulty in obtaining emergency CT angiogram in an urgent setting.

The two-tier primary and comprehensive stroke centre model that aims to give priority access to patients with suspected acute stroke may be seen as a framework for acute stroke service.30 31 32 The first-tier stroke centre should be capable of providing 24-hour urgent CT and CT angiogram with round-the-clock IV-tPA service. All patients with suspicious stroke symptoms, such as acute hemiplegia or dysphasia, should be directly transferred to one of these first-tier stroke centres, bypassing other non-stroke centres in emergency hospitals to avoid unnecessary delay in diagnosis. When major vessel occlusion is suspected, immediate CT angiography should be performed in the same setting to determine thrombectomy eligibility. Second-tier stroke centres should additionally be capable of 24-hour endovascular thrombectomy, and be equipped with full-time neurosurgery, neurocritical care, and advanced radiological imaging support.31 Among the local stroke specialists, a median number of four second-tier comprehensive stroke centres is believed to be appropriate in Hong Kong. Support from the health administration, structured training for endovascular techniques, and efficient use of existing resources are required to effectively incorporate emergency thrombectomy into routine clinical service locally.

There is a strong body of clinical evidence and international guidelines to support emergency endovascular thrombectomy for acute ischaemic stroke due to anterior circulation major vessel occlusion. As the local stroke community embraces this new treatment modality, efforts should be directed towards providing universal and timely access to emergency ischaemic stroke therapy for the Hong Kong population.

All authors have disclosed no conflicts of interest.

This paper is supported by the Hong Kong Stroke Society Research Scholarship 2015 and the Health and Medical Research Fund (01150027). We thank Dr GKK Leung for his valuable advice in the course of this study. We also thank the Hong Kong Stroke Society, Hong Kong Neurosurgical Society, and Hong Kong Society of Interventional and Therapeutic Neuroradiology for their support in the survey study.

1. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;333:1581-7. Crossref

2. Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med 2008;359:1317-29. Crossref

3. Bhatia R, Hill MD, Shobha N, et al. Low rates of acute recanalization with intravenous recombinant tissue plasminogen activator in ischemic stroke: real-world experience and a call for action. Stroke 2010;41:2254-8. Crossref

4. Jüttler E, Schwab S, Schmiedek P, et al. Decompressive surgery for the treatment of malignant infarction of the middle cerebral artery (DESTINY): a randomized, controlled trial. Stroke 2007;38:2518-25. Crossref

5. Broderick JP, Palesch YY, Demchuk AM, et al. Endovascular therapy after intravenous t-PA versus t-PA alone for stroke. N Engl J Med 2013;368:893-903. Crossref

6. Ciccone A, Valvassori L, Nichelatti M, et al. Endovascular treatment for acute ischemic stroke. N Engl J Med 2013;368:904-13. Crossref

7. Kidwell CS, Jahan R, Gornbein J, et al. A trial of imaging selection and endovascular treatment for ischemic stroke. N Engl J Med 2013;368:914-23. Crossref

8. Berkhemer OA, Fransen PS, Beumer D, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med 2015;372:11-20. Crossref

9. Jovin TG, Chamorro A, Cobo E, et al. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med 2015;372:2296-306. Crossref

10. Goyal M, Demchuk AM, Menon BK, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med 2015;372:1019-30. Crossref

11. Campbell BC, Mitchell PJ, Kleinig TJ, et al. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med 2015;372:1009-18. Crossref

12. Saver JL, Goyal M, Bonafe A, et al. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med 2015;372:2285-95. Crossref

13. Goyal M, Menon BK, van Zwam WH, et al. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet 2016;387:1723-31. Crossref

14. Higashida RT, Furlan AJ, Roberts H, et al. Trial design and reporting standards for intra-arterial cerebral thrombolysis for acute ischemic stroke. Stroke 2003;34:e109-37. Crossref

15. Turk AS, Frei D, Fiorella D, et al. ADAPT FAST study: a direct aspiration first pass technique for acute stroke thrombectomy. J Neurointerv Surg 2014;6:260-4. Crossref

16. Hentschel KA, Daou B, Chalouhi N, et al. Comparison of non-stent retriever and stent retriever mechanical thrombectomy devices for the endovascular treatment of acute ischemic stroke. J Neurosurg 2017;126:1123-30. Crossref

17. Lapergue B, Blanc R, Guedin P, et al. A direct aspiration, first pass technique (ADAPT) versus stent retrievers for acute stroke therapy: an observational comparative study. AJNR Am J Neuroradiol 2016;37:1860-5. Crossref

18. Turk AS, Turner R, Spiotta A, et al. Comparison of endovascular treatment approaches for acute ischemic stroke: cost effectiveness, technical success, and clinical outcomes. J Neurointerv Surg 2015;7:666-70. Crossref

19. Mocco J, Zaidat OO, von Kummer R, et al. Aspiration thrombectomy after intravenous alteplase versus intravenous alteplase alone. Stroke 2016;47:2331-8. Crossref

20. Aronsson M, Persson J, Blomstrand C, Wester P, Levin LÅ. Cost-effectiveness of endovascular thrombectomy in patients with acute ischemic stroke. Neurology 2016;86:1053-9. Crossref

21. Nguyen-Huynh MN, Johnston SC. Is mechanical clot removal or disruption a cost-effective treatment for acute stroke? AJNR Am J Neuroradiol 2011;32:244-9. Crossref

22. Ganesalingam J, Pizzo E, Morris S, Sunderland T, Ames D, Lobotesis K. Cost-utility analysis of mechanical thrombectomy using stent retrievers in acute ischemic stroke. Stroke 2015;46:2591-8. Crossref

23. Wahlgren N, Moreira T, Michel P, et al. Mechanical thrombectomy in acute ischemic stroke: Consensus statement by ESO-Karolinska Stroke Update 2014/2015, supported by ESO, ESMINT, ESNR and EAN. Int J Stroke 2016;11:134-47. Crossref

24. Powers WJ, Derdeyn CP, Biller J, et al. 2015 American Heart Association/American Stroke Association focused update of the 2013 guidelines for the early management of patients with acute ischemic stroke regarding endovascular treatment: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2015;46:3020-35. Crossref

25. Wong EH, Yu SC, Lau AY, et al. Intra-arterial revascularisation therapy for acute ischaemic stroke: initial experience in a Hong Kong hospital. Hong Kong Med J 2013;19:135-41.

26. Brinjikji W, Murad MH, Rabinstein AA, Cloft HJ, Lanzino G, Kallmes DF. Conscious sedation versus general anesthesia during endovascular acute ischemic stroke treatment: a systematic review and meta-analysis. AJNR Am J Neuroradiol 2015;36:525-9. Crossref

27. Schönenberger S, Uhlmann L, Hacke W, et al. Effect of conscious sedation vs general anesthesia on early neurological improvement among patients with ischemic stroke undergoing endovascular thrombectomy: a randomized clinical trial. JAMA 2016;316:1986-96. Crossref

28. Public health. Hong Kong: the facts. Information Services Department, Hong Kong SAR Government. February 2016.

29. Hospital Authority Annual plan 2015-2016. Hong Kong: The Hospital Authority; 2015.

30. Alberts MJ, Latchaw RE, Jagoda A, et al. Revised and updated recommendations for the establishment of primary stroke centers: a summary statement from the brain attack coalition. Stroke 2011;42:2651-65. Crossref

31. Alberts MJ, Latchaw RE, Selman WR, et al. Recommendations for comprehensive stroke centers: a consensus statement from the Brain Attack Coalition. Stroke 2005;36:1597-616. Crossref

32. Gorelick PB. Primary and comprehensive stroke centers: history, value and certification criteria. J Stroke 2013;15:78-89. Crossref

The prognosis of out-of-hospital cardiac arrest (OHCA) in Hong Kong is poor. Fewer than one in 44 persons with OHCA survive to hospital discharge. The number of survivors with good neurological outcome is even smaller (one in 67 persons with OHCA).1 Public access defibrillation (PAD) has been proposed as a strategy to improve survival. The concept was first put forward by the American Heart Association Task Force on Automatic External Defibrillation in 1995.2 There is no strict definition of PAD but it is considered to include defibrillation by persons not medically trained. There were initially four levels of responders, ie persons performing the defibrillation before the arrival of the emergency medical services (EMS). Level 1 referred to the traditional first responders, eg police and firefighters. Level 2 were persons who had a duty of care, eg life guards and security personnel. Laypersons who had been trained in cardiopulmonary resuscitation (CPR) or use of an automated external defibrillator (AED) constituted the third level. Level 4 referred to minimally trained or untrained laypersons who may respond to an emergency.

Advances in technology have ensured the current AED is compact in size and easy to operate. Visual and auditory instructions allow a person without prior training to perform defibrillation.3 Fourteen years ago, a group of emergency physicians questioned whether PAD was needed in Hong Kong.4 In response to the culminating scientific evidence to support the use of PAD in OHCA, and the change in the environment and population demographics of Hong Kong over the past 14 years, this paper aimed to answer the same question again. A literature search was conducted using the electronic database of MEDLINE, Embase, and Scopus for primary clinical studies, as well as Cochrane Reviews and Health Technology Assessment and Database for secondary reviews, published from 1995 to the present. Keywords of cardiac arrest, survival, defibrillator, defibrillation, effectiveness, and AED were used singly or in combination. Additionally a manual search was performed of bibliographies listed in articles used for review. An article was included for review if all investigators agreed that it could provide data to answer the research question. It is hoped that the findings of this review will inform the health authorities and the government about community-based PAD programmes.

Ventricular fibrillation (VF) is one of the causes of sudden OHCA. Defibrillation is the most effective treatment for patients with VF. The probability of successful defibrillation is time-dependent, dropping by 7% to 10% with each passing minute.5 Defibrillation by a bystander with an AED prior to the arrival of EMS may shorten the time between arrest and defibrillation and thus increase the chance of survival. Early studies that compared CPR versus CPR plus AED by level 1 responders, ie police and firefighters, did not reveal any survival advantage of using an AED.6 7 In 2004, the PAD trial investigators published their report on PAD and survival after OHCA and presented the most convincing evidence of the clinical effectiveness of an AED.8 They randomised over 19 000 volunteer responders from nearly 1000 communities in North America to an intervention group that used CPR and AED or a control group that used CPR alone. The intervention resulted in a 2-fold increase in the chance of survival to hospital discharge.8 The failure to demonstrate any benefits of AED in the early studies may be related to the exclusion of the lay public in using AED. A meta-analysis that studied nearly 1600 cases of OHCA also demonstrated an increased probability of survival to hospital discharge if an AED was used for OHCA before EMS arrival (relative risk of 1.39 of surviving to hospital discharge for people treated with CPR + AED compared with CPR-only).9 In conclusion, there is concrete evidence that AED is clinically effective in OHCA.

Before a PAD programme is implemented, policymakers need to consider many factors. Clinical effectiveness alone is not sufficient to justify the implementation of a PAD programme when there are competing demands for resources. An important question is how cost-effective of an AED is. Clinical effectiveness cannot be directly translated into cost-effectiveness. In fact, opinions about the cost-effectiveness of public placement of AEDs are divided.10 11

In general, important factors that affect the cost-effectiveness of public placement of AEDs include the incidence of OHCA at the placement site, the existing survival rate of OHCA in the community, and the number of AEDs required to provide adequate coverage. Different recommendations exist regarding the incidence of OHCA. The American Heart Association (AHA) recommends an AED be placed in sites where an OHCA can be expected every 5 years while the European Resuscitation Council recommends placing an AED in sites where an OHCA is expected every 2 years.12 13 If cardiac arrest at the placement site is rare, the AED is unlikely to be cost-effective. The survival to hospital discharge rate of OHCA in most regions is lower than 10%.14 The higher the survival rate, the lower the incremental benefit of adding an AED. It should also be noted that the survival rate is influenced by multiple factors and is not easily modifiable. A way to evaluate adequacy of coverage by an AED is to check whether a layperson can get an AED to the patient in 1 to 1.5 minutes.15 Based on the average speed of brisk walking, this can be translated into an AED being placed within 100 metres of a cardiac arrest. Nonetheless it is difficult to estimate the number of AEDs required even with perfect matching with the sites of possible arrest. This is because historical data used for matching cannot predict the future risk of an arrest at the same site. Therefore, the incidence of cardiac arrest at the placement site is probably a more significant factor to consider when the cost-effectiveness of an AED is analysed. A number of studies have been conducted in the last decade on the cost-effectiveness of AED in public sites in terms of cost per quality-adjusted life year (QALY). Depending on the analytic model, maintenance and system support cost and the chance that the AED was used, in turn related to the incidence of cardiac arrests, the QALY ranged from US$31 000 to $198 000.16 17 18 Overall these studies concluded that sites where the incidence of cardiac arrests is more than once every 5 to 7 years will assume a more sustainable cost-benefit for AED placement. Examples include casinos, airports, and fitness centres.19

Presence of an AED does not mean that it will or can be used. The modern AED is easy to operate and skill retention by a lay rescuer is good. Data from the PAD trial indicate that it took 7 minutes only for re-training in AED operation more than a year after the initial training.20 Nonetheless completion of AED training does not guarantee that lay responders will use it when it is needed. In a Finnish study, the AED was available but not used in 65% of OHCAs.21 A similar figure was found in the PAD trial.8 There are likely multiple reasons for this high underutilisation rate. It may be that the responder is simply unaware of the presence of an AED or does not know its location. In addition, the public’s willingness to use the AED may play a part. Fear of legal liability because a lack of Good Samaritan legislation is sometimes quoted as a reason for not providing help to the needy.22 Factors related to the AED itself may also be a concern. A survey on the functional status of public AEDs by Haskell et al23 identified problems such as battery expiry, inaccessibility, and invisibility of the AED. In other words, mere installation of AEDs is not enough to ensure success in a PAD programme. Proper organisation and maintenance of the AEDs must accompany any PAD programme.

Another important factor is the characteristics of the population at risk, eg age of patients with sudden cardiac death. The incidence of VF is lower in those older than 70 years than those below.24 The overall incidence of VF in OHCA has also fallen over the last two decades.25 This is believed to be a result of improved primary and secondary prevention of coronary heart disease as evidenced by the drop in the associated mortality in many parts of the world.26 Since defibrillation is only effective for OHCA with an initial rhythm of VF or pulseless ventricular tachycardia (VT), the need to implement PAD in regions, where the risk of VF is low, is less compelling.

On the basis of the previous discussion, this question is to be addressed from two perspectives: the likelihood of PAD to improve survival of OHCA in Hong Kong, and factors that will affect the likelihood of successful implementation of a PAD programme.

The chain of survival is a widely accepted framework to improve OHCA survival. The chain is composed of early recognition with a call for EMS, early CPR, early defibrillation, effective advanced life support, and integrated post-arrest care. Almost all early local studies of OHCA highlighted the need to strengthen particularly the first three links in the chain.27 28 29 30 Of note, OHCA patients with VF in Hong Kong have a better prognosis than those with a non-shockable rhythm.31 32 33 The rate of survival to hospital discharge of patients with VF initially is 6 times that of patients with a non-VF rhythm.33 It is therefore not surprising to find that the time to first defibrillation is an independent predictor of OHCA survival in Hong Kong.1

Over the past 20 years, there has been a remarkable improvement in the time from arrest recognition to first defibrillation. The time interval was shortened by nearly 11 minutes from 23 minutes to 12 minutes.1 34 A possible important contribution to this improvement is the reduced recognition-to-activation interval from over 7 minutes to almost instantly. The reason for this reduction is unknown although wider use of mobile phones is a possibility. Whatever the reason, a time gap of at least 12 minutes between collapse and defibrillation is still far from desirable. The chance of successful defibrillation remains low. It is vital that means to reduce this time gap be found in order to increase the chance of successful defibrillation. Fourteen years ago, public education about OHCA, graded dispatch by ambulances, and a first responder (AED) programme by police or firefighters were discussed.4 No local studies have specifically addressed the issue of public education. On the contrary, there is evidence that the percentage of the public who have received CPR training has increased over the last 10 years.35 36 Whether this increase in number of CPR-trained citizens can be translated to an increase in OHCA awareness is questionable. This is because even in the survey published in 2014, only 21% of the 1013 respondents had been trained; and overall, their CPR knowledge was poor.35 A graded dispatch system refers to one that prioritising the EMS response time is based on the urgency of calls. Similar to 14 years ago, there remains concern about affecting the overall service commitment by the Fire Services Department. It is unlikely that this practice will be adopted in the foreseeable future. With regard to the last suggestion to recruit police or firefighters as first responders, overseas experience has already shown that it is unlikely to improve OHCA survival.6 7 Based on the calculation of the investigators 14 years ago, employing this means could reduce the collapse to defibrillation interval by 4 minutes. Even with this optimistic assumption, the interval of 8 minutes remains long when applying the latest data. As a result, PAD by level 2 to 4 responders is probably needed to shorten the time to first defibrillation to 5 minutes or shorter, and hopefully improve the probability of OHCA survival.

Public access defibrillation primarily involves public placement of AEDs to be used by non–medically trained members of the public in OHCA patients who present with a shockable rhythm. Factors that may affect the success of a PAD programme are multiple and those specific to Hong Kong are discussed below.

Public placement of AEDs has to be pre-planned. Evidence suggests that unguided AED placement is not effective in improving survival in OHCA.37 In general, appropriate sites include locations where one can expect an OHCA every 5 years (AHA recommendation), EMS response time beyond 5 minutes, or facilities serving high-risk people.38 How the sites of AED placement are related to the cost-effectiveness of a PAD programme has also been discussed. In Hong Kong, because there is no compulsory AED registry, the location of all AEDs is unknown to the public. To make the best use of these AEDs, first of all, their location should be known by the public. The Government is in the best position to lead the development of an AED registry. Efforts to facilitate public knowledge of AED locations are also underway. For instance, a mobile phone application with an AED locating function is now available.39 Besides, the AED should be accessible by the public. A study of the accessibility and availability of 207 AEDs in 670 facilities in New Territories (NT) West published in 2014 provided some insight into this issue.40 The investigators found that many of the AEDs (37.7%) were placed in schools in NT West. Whether these AEDs were truly accessible by the public was questionable as schools have limited opening hours. Nonetheless in Hong Kong, most OHCAs occur with the patient at home. Only 13.5% of cases occurred in public places or streets.1 Detailed planning of AED placement is thus essential to ensure that they are accessible and can be used by the public in an emergency. Regarding accessibility, Hong Kong may take reference from Japan and Singapore. In Japan, AEDs can be found in many vending machines on the streets and internet-based maps for AED location have been created in several cities.41 In 2015, Singapore launched a pilot programme that installed an AED in taxis with taxi drivers trained to use it.42

Since it is expected that an AED will be used by a layperson, public knowledge of and attitude to AED will influence the success of a PAD programme. According to a recently published survey, only 18% of respondents would use an AED in an OHCA and approximately 77% had no knowledge of the location of an AED near their home or workplace.22 These findings probably explain the very low rate of bystander defibrillation (1.4%) in OHCA in Hong Kong.1 Simply increasing the number of AEDs installed without more extensive engagement of the public is bound to fail. Education, including recurrent training in AED use, by government or non-governmental organisations is indispensable in this aspect.

As defibrillation is only indicated for VF or pulseless VT, the incidence of these shockable rhythms in OHCA is an important consideration in a PAD programme. In Hong Kong, a fall in the incidence of VF in OHCA has been observed alongside a similar downward trend elsewhere.1 28 The latest study revealed an incidence rate of 8.7%.1 Whether the advanced age of the local OHCA patients is a contributing factor is unknown. It seems reasonable to postulate that like elsewhere, improved medical care of patients with coronary artery disease may be contributory. Nonetheless caution is needed in interpreting this incidence rate when PAD is considered. It is well known that patients with VF will soon become asystolic in the absence of any intervention. With a call to patient’s side with an interval of 9 minutes by the EMS, it is possible that a proportion of VF cases will have already degenerated into asystole when the EMS connect them to the cardiac monitor. It has been estimated that about 53% of patients may be in VT or VF within 4 minutes of collapse from OHCA.43 If an effective PAD programme is in place, more VF cases will be identified by the AED machine.

Automated external defibrillator is clinically effective in improving the survival outcome of OHCA. Cost-effectiveness is nonetheless dependent on multiple factors. In Hong Kong, there is a need to implement a PAD programme in order to shorten the time to first defibrillation, with itself being a predictor of survival. Based on the best available evidence for Hong Kong, strategic planning, eg matching the incidence of OHCA with AED placement, ensuring accessibility, and establishing an AED registry with an infrastructure of AED maintenance are recommended. Unguided placement of AEDs is discouraged because it is likely a waste of resources. In parallel, public engagement is essential. Both knowledge and attitude should be enhanced through education. Early defibrillation is just one of the links in the chain of survival. From the community perspective, basic life support by a bystander, eg CPR, deserves continued encouragement despite the increased bystander CPR rate to nearly 30% over the past 14 years. This is because high-quality bystander CPR may help prevent degeneration to asystole.

All authors have disclosed no conflicts of interest.

1. Fan KL, Leung LP, Siu YC. Out-of-hospital cardiac arrest in Hong Kong: a territory-wide study. Hong Kong Med J 2017;23:48-53.

2. Weisfeldt ML, Kerber RE, McGoldrick RP, et al. Public access defibrillation. A statement for healthcare professionals from the American Heart Association Task Force on Automatic External Defibrillation. Circulation 1995;92:2763. Crossref

3. Eames P, Larsen PD, Galletly DC. Comparison of ease of use of three automated external defibrillators by untrained lay people. Resuscitation 2003;58:25-30. Crossref

4. Lo CB, Wong TW, Lai KK. Is public access defibrillation needed in Hong Kong? Hong Kong Med J 2003;9:113-8.

5. Valenzuela TD, Roe DJ, Cretin S, Spaite DW, Larsen MP. Estimating effectiveness of cardiac arrest interventions: a logistic regression survival model. Circulation 1997;96:3308-13. Crossref

6. van Alem AP, Vrenken RH, de Vos R, Tijssen JG, Koster RW. Use of automated external defibrillator by first responders in out of hospital cardiac arrest: prospective controlled trial. BMJ 2003;327:1312. Crossref

7. Sayre MR, Evans J, White LJ, Brennan TD. Providing automated external defibrillators to urban police officers in addition to a fire department rapid defibrillation program is not effective. Resuscitation 2005;66:189-96. Crossref

8. Hallstrom AP, Ornato JP, Weisfeldt M, et al. Public-access defibrillation and survival after out-of-hospital cardiac arrest. N Engl J Med 2004;351:637-46. Crossref

9. Sanna T, La Torre G, de Waure C, et al. Cardiopulmonary resuscitation alone vs. cardiopulmonary resuscitation plus automated external defibrillator use by nonhealthcare professionals: a meta-analysis on 1583 cases of out-of-hospital cardiac arrest. Resuscitation 2008;76:226-32. Crossref

10. Gold LS, Eisenberg M. Cost-effectiveness of automated external defibrillators in public places: pro. Curr Opin Cardiol 2007;22:1-4. Crossref

11. Pell J, Walker A, Cobbe SM. Cost-effectiveness of automated external defibrillators in public places: con. Curr Opin Cardiol 2007;22:5-10. Crossref

12. Hazinski MF, Idris AH, Kerber RE, et al. Lay rescuer automated external defibrillator (“public access defibrillation”) programs: lessons learned from an international multicenter trial: advisory statement from the American Heart Association Emergency Cardiovascular Committee; the Council on Cardiopulmonary, Perioperative, and Critical Care; and the Council on Clinical Cardiology. Circulation 2005;111:3336-40. Crossref

13. Handley AJ, Koster R, Monsieurs K, et al. European Resuscitation Council guidelines for resuscitation 2005. Section 2. Adult basic life support and use of automated external defibrillators. Resuscitation 2005;67 Suppl 1:S7-23. Crossref

14. Berdowski J, Berg RA, Tijssen JG, Koster RW. Global incidences of out-of-hospital cardiac arrest and survival rates: Systematic review of 67 prospective studies. Resuscitation 2010;81:1479-87. Crossref

15. Aufderheide T, Hazinski MF, Nichol G, et al. Community lay rescuer automated external defibrillation programs: key state legislative components and implementation strategies: a summary of a decade of experience for healthcare providers, policymakers, legislators, employers, and community leaders from the American Heart Association Emergency Cardiovascular Care Committee, Council on Clinical Cardiology, and Office of State Advocacy. Circulation 2006;113:1260-70. Crossref

16. Cram P, Vijan S, Fendrick AM. Cost-effectiveness of automated external defibrillator deployment in selected public locations. J Gen Intern Med 2003;18:745-54. Crossref

17. Nichol G, Huszti E, Birnbaum A, et al. Cost-effectiveness of lay responder defibrillation for out-of-hospital cardiac arrest. Ann Emerg Med 2009;54:226-35.e1-2.

18. Groeneveld PW, Owens DK. Cost-effectiveness of training unselected laypersons in cardiopulmonary resuscitation and defibrillation. Am J Med 2005;118:58-67. Crossref

19. Reed DB, Birnbaum A, Brown LH, et al. Location of cardiac arrests in the public access defibrillation trial. Prehosp Emerg Care 2006;10:61-76. Crossref

20. Riegel B, Birnbaum A, Aufderheide TP, et al. Predictors of cardiopulmonary resuscitation and automated external defibrillator skill retention. Am Heart J 2005;150:927-32. Crossref

21. Kuisma M, Castren M, Nurminen K. Public access defibrillation in Helsinki—costs and potential benefits from a community-based pilot study. Resuscitation 2003;56:149-52. Crossref

22. Fan KL, Leung LP, Poon HT, Chiu HY, Liu HL, Tang WY. Public knowledge of how to use an automatic external defibrillator in out-of-hospital cardiac arrest in Hong Kong. Hong Kong Med J 2016;22:582-8.

23. Haskell SE, Post M, Cram P, Atkins DL. Community public access sites: compliance with American Heart Association recommendations. Resuscitation 2009;80:854-8. Crossref

24. Tresch DD, Thakur R, Hoffmann RG, Brooks HL. Comparison of outcome of resuscitation of out-of-hospital cardiac arrest in persons younger and older than 70 years of age. Am J Cardiol 1988;61:1120-2. Crossref

25. Bunch TJ, White RD. Trends in treated ventricular fibrillation in out-of-hospital cardiac arrest: ischemic compared to non-ischemic heart disease. Resuscitation 2005;67:51-4. CrossRef

26. World Health Organization (WHO). Health for all database. Available from: http://www.euro.who.int/en/data-and-evidence/databases. Accessed 1 Mar 2017.

27. Wong TW, Yeung KC. Out-of-hospital cardiac arrest: two and a half years experience of an accident and emergency department in Hong Kong. J Accid Emerg Med 1995;12:34-9. Crossref

28. Leung LP, Wong TW, Tong HK, Lo CB, Kan PG. Out-of-hospital cardiac arrest in Hong Kong. Prehosp Emerg Care 2001;5:308-11. Crossref

29. Wai AK, Cameron P, Cheung CK, Mak P, Rainer TH. Out-of-hospital cardiac arrest in a teaching hospital in Hong Kong: descriptive study using the Utstein style. Hong Kong J Emerg Med 2005;12:148-55.

30. Lau CL, Lai JC, Hung CY, Kam CW. Outcome of out-of-hospital cardiac arrest in a regional hospital in Hong Kong. Hong Kong J Emerg Med 2005;12:224-7.

31. Leung KL, Lui CT, Cheung KH, Tsui KL, Tang YH. Outcome and prognostic factors of patients in out-of-hospital cardiac arrests presenting with non-shockable rhythm in Hong Kong. Hong Kong J Emerg Med 2012;19:6-12.

32. Chan TH, Lui CT, Cheung KH, Tang YH, Tsui KL. Outcome predictors of patients in out-of-hospital cardiac arrests with pre-hospital defibrillation in Hong Kong. Hong Kong J Emerg Med 2013;20:131-7.

33. Fan KL, Leung LP. Prognosis of patients with ventricular fibrillation in out-of-hospital cardiac arrest in Hong Kong: prospective study. Hong Kong Med J 2002;8:318-21.

34. Lui JC. Evaluation of the use of automatic external defibrillation in out-of-hospital cardiac arrest in Hong Kong. Resuscitation 1999;41:113-9. Crossref

35. Chair SY, Hung MS, Lui JC, Lee DT, Shiu IY, Choi KC. Public knowledge and attitudes towards cardiopulmonary resuscitation in Hong Kong: telephone survey. Hong Kong Med J 2014;20:126-33.

36. Cheung BM, Ho C, Kou KO, et al. Knowledge of cardiopulmonary resuscitation among the public in Hong Kong: telephone questionnaire survey. Hong Kong Med J 2003;9:323-8.

37. Ringh M, Herlitz J, Hollenberg J, Rosenqvist M, Svensson L. Out of hospital cardiac arrest outside home in Sweden, change in characteristics, outcome and availability for public access defibrillation. Scand J Trauma Resusc Emerg Med 2009;17:18. Crossref

38. Atkins DL. Public access defibrillation: where does it work? Circulation 2009;120:461-3. Crossref

39. The University of Hong Kong. Technology Enhanced Learning Initiatives (TELI). Available from: http://teli.hku.hk/portfolio/aed-locator-app/. Accessed 1 Mar 2017.

40. Ho CL, Lui CT, Tsui KL, Kam CW. Investigation of availability and accessibility of community automated external defibrillators in a territory in Hong Kong. Hong Kong Med J 2014;20:371-8.

41. Mitamura H. Public access defibrillation: advances from Japan. Nat Clin Pract Cardiovasc Med 2008;5:690-2. Crossref

42. Singapore Civil Service College. SCDF’s myResponder App helps saves lives. Available from: https://www.cscollege.gov.sg/Knowledge/Pages/SCDF-myResponder-App-Helps-Saves-Lives.aspx. Accessed 5 Jul 2017.

43. Herlitz J, Ekström L, Wennerblom B, Axelsson A, Bång A, Holmberg S. Type of arrhythmia at EMS arrival on scene in out-of-hospital cardiac arrest in relation to interval from collapse and whether a bystander initiated CPR. Am J Emerg Med 1996;14:119-23. Crossref

The prevalence of diabetes increases with age such that among the older population (age ≥65 years), it was 6 times that of the younger population (age 18-64 years), reaching 21.4% in Hong Kong in 2004 to 2005.1 Although the prevalence among older people is quite constant over time, with an ageing population the number of older people with diabetes is expected to continuously increase in the future.

In addition to the increasing population of older diabetic people, heterogeneity among older people with varying levels of cognitive and functional ability, life expectancy, and social support present a challenge in clinical practice because there is no single treatment goal or management plan that can address all of the issues in this patient group. Recently, individualised and tailored care approaches to cater for the individual characteristics of older people have been promoted.2 3 4 5 6 7 Increasing attention to avoid treatment-related hypoglycaemia has also been emphasised.2 3 4 5 6 7 However, there is a gap in knowledge of the optimal management due to the paucity of clinical trials among older diabetic people, in particular those with frailty. This has led to a lack of consensus and variation of management in clinical practice.

A special interest group on diabetes mellitus, under the auspices of The Hong Kong Geriatrics Society (HKGS), has been established to raise the awareness of diabetes among older people; to address the special issues of older people associated with their varied physical, cognitive, and social needs; and to enhance their care. A survey on the opinions of local geriatricians about diabetes management in older people and data analysis of hypoglycaemia among diabetic patients in the local public sector were performed. A round-table discussion with geriatricians from the HKGS and endocrinologists from the Hong Kong Society of Endocrinology, Metabolism and Reproduction was then held on 24 January 2015. Discussion was based on evidence-based review of the current literature, scientific presentations by experts in the field, opinions from both geriatricians and endocrinologists, and the analysis of local data on hypoglycaemia of the diabetic patients. After the meeting, statements were drafted and circulated among the council members of HKGS and the Hong Kong Society of Endocrinology, Metabolism and Reproduction for comments. The final version was approved by all participants. The purpose of the round-table discussion was to arrive at a consensus on the management approach for older people with diabetes. This position statement was developed to serve as a reference for local clinicians.

An online survey was conducted to collect the opinions of geriatricians about the management of type 2 diabetes in older people between December 2014 and January 2015 (Appendix 1). The questionnaires were distributed to all 113 members of the HKGS. Approximately half (46.3%) of the HKGS members returned the questionnaires. The following summarises the results of the questionnaire; details are shown in Appendix 2.

Most (60%) of the respondents ranked risk of hypoglycaemia as the most important domain in setting an individualised diabetes management plan. Physical and mental functions, and co-morbidities and associated vascular diseases were also considered to be important.

Almost all of the respondents agreed that physical frailty (98%) and cognitive impairment (96%) should be assessed when managing older people with diabetes. More than 80% of respondents agreed that polypharmacy and nutritional problems should also be assessed.

Respondents agreed that an individual’s co-morbidities, cognitive and functional status, and life expectancy must be considered when determining a glycaemic goal, such that more stringent control (target glycated haemoglobin [HbA1c] 6.5%-7%) should be considered for robust elderly people (59% of respondents), less stringent control (target HbA1c 7%-9%) for those who are physically frail or cognitively impaired (52%-57% of respondents), and relaxed control (target HbA1c ≥9%) for those receiving end-of-life care (50% of respondents). Blood pressure targets set for older diabetic people were quite varied among the respondents; these ranged from ≤130/80 mm Hg to ≤150/90 mm Hg for robust elderly people, and ≤160/100 mm Hg and avoidance of diastolic blood pressure of <60 mm Hg for those at the end of life.

The risk of hypoglycaemia was the most important concern for almost all the respondents (98%) when prescribing glucose-lowering therapy. Dosing frequency was also a major concern (76% of respondents). A vast majority (93% of respondents) would prescribe metformin as the first-line glucose-lowering therapy for robust elderly people, while a dipeptidyl peptidase-IV (DPP-IV) inhibitor (45%) or sulphonylurea (45%) was considered suitable for older people with organ failure or estimated glomerular filtration rate of <30 mL/min, and metformin (52%) and a DPP-IV inhibitor (34%) was considered suitable for those at high risk of hypoglycaemia.

A majority (>80%) of respondents considered that a restrictive diabetic diet should only be allocated for robust elderly people, but not for octogenarians, physically frail or cognitively impaired patients, and nursing home residents.

Preventing hypoglycaemia was the goal of almost all the respondents (98%). This was followed by preventing hospitalisation and avoiding acute metabolic complications (approximately 80% of respondents).

A study of hypoglycaemia in the older diabetic population was performed. The study involved collection of data from the Clinical Data Analysis and Reporting System. Clinical data on diabetic people attending the accident and emergency department (AED) with the diagnosis of hypoglycaemia were collected. The study involved two parts: (1) analysis of all the AED attendance data on diabetic patients diagnosed with hypoglycaemia during the period between 1 July 2013 and 30 June 2014; and (2) subanalysis of data of diabetic patients attending the AED for hypoglycaemia from five hospitals (Alice Ho Miu Ling Nethersole Hospital, Caritas Medical Centre, Pok Oi Hospital, Queen Elizabeth Hospital, and Tuen Mun Hospital) during the period between 1 January 2014 and 31 January 2014.

A total of 2416 diabetic patients had attended all AEDs under the Hospital Authority in Hong Kong for hypoglycaemia between 1 July 2013 and 30 June 2014. The majority (78.2%) of them were aged 65 years or older; 14.4% were from old-age homes, and the hospital admission rate was 81.1% (Table 1). Older patients (≥65 years) had a significantly higher rate of hospital admission and 12-month mortality than patients younger than 65 years.

Of the 133 diabetic patients included in the subanalysis, 105 (78.9%) were older patients (≥65 years) [Table 2]. Tight glycaemic control with HbA1c of ≤7% was associated with a significantly higher 12-month mortality in older diabetic patients than those with less stringent control (27.8% vs 11.8%; P=0.04). In addition, older patients with very tight glycaemic control (HbA1c ≤6%) had a longer duration of stay in hospital than those with less stringent control (6.8 days vs 3.8 days; P=0.001). On the other hand, loose glycaemic control with HbA1c of ≤8% and patients aged younger than 65 years were not associated with increased short-term (28-day readmission) and long-term (12-month mortality) adverse outcomes. Multivariate analysis showed that male sex, higher Charlson Comorbidity Index score, dementia, and lower HbA1c level were independent predictors for 12-month mortality among the older diabetic patients (Table 3).

Advanced age is an independent risk factor for hypoglycaemia.8 Older people are intrinsically prone to hypoglycaemia. With increasing age, hypoglycaemic warning symptoms become less intense and hypoglycaemic unawareness becomes more common even with intact physiological glucose counter-regulatory response (ie decreased insulin secretion, and increased glucagon and epinephrine secretion).9 10 11 12 Furthermore, the physiologically higher blood glucose level for the initiation of neurogenic warning symptoms (eg palpitation, tremor, and sweating—the result of automonic activation) than that for onset of neuroglycopenic symptoms (eg confusion, seizure, and loss of consciousness—the result of brain glucose deprivation), which allows time to take measures to avoid neuroglycopenia and severe hypoglycaemia, tends to be lost in the older people.12 The impaired perception of the warning symptoms of hypoglycaemia and the narrower or even absence of a glycaemic threshold gap between the development of neurogenic and neuroglycopenic symptoms put elderly people at a high risk for severe hypoglycaemia.

Furthermore, with a longer duration of type 2 diabetes and subsequent progression to endogenous insulin deficiency, counter-regulatory responses to hypoglycaemia are compromised. Additionally, the neurogenic warning symptoms become attenuated and lead to hypoglycaemic unawareness. Compromised glucose counter-regulation and hypoglycaemia unawareness increase the risk of severe iatrogenic hypoglycaemia by 25-fold and 6-fold, respectively.13 14 Multiple co-morbidities, polypharmacy, and cognitive dysfunction associated with advancing age are also risk factors for hypoglycaemia (see below).

Diabetes predisposes older people to the development of geriatric syndromes as it is associated with risk for dementia, depression, polypharmacy, fall and fracture, urinary incontinence, visual impairment, and chronic pain. The presence of geriatric syndromes is linked with functional decline and increasing frailty that would limit a patient’s functional independence and complicate medical management. Early recognition and including geriatric syndromes in the management plan are recommended.

Patients with diabetes are at increased risk for dementia. They have been shown to have a 1.2- to 1.5-fold higher rate of decline in cognitive function than those without diabetes,15 and were at a higher risk for developing Alzheimer’s disease and vascular dementia by approximately 1.5-fold and 2.5-fold, respectively.16 Additionally, adverse effect of treatment-related hypoglycaemia, especially if it is severe, has been shown to be associated with subsequent dementia in older diabetic patients.17 18 19 There was also a graded increase in dementia risk with the number of severe hypoglycaemic episodes experienced, such that the risk was almost double for three or more episodes when compared with only one episode.17 Furthermore, there is a bidirectional association of hypoglycaemia with dementia in which hypoglycaemia damages the brain and that, in turn, decreases one’s ability to manage diabetes or recognise hypoglycaemic symptoms leading to the subsequent risk of hypoglycaemia, that further impairs cognitive function in a vicious cycle.20

A systematic review and meta-analysis found people with type 2 diabetes had a 24% increased risk of developing depression.21 On the other hand, depression was associated with a 60% increased risk of type 2 diabetes in another systematic review.22 Despite the fact that depression in diabetic patients is common, it is often undiagnosed and untreated.23 Like cognitive dysfunction, depression may impede functionality and diabetic self-management causing erratic timing of medication intake, irregular eating, inability to self-monitor blood glucose, and failure to recognise hypoglycaemic symptoms to enable prompt management. These may worsen glycaemic control and increase the risk of diabetic and treatment-related complications. Early detection of depression, especially in those with unexplained decline in clinical status, is warranted.24

Medications prescribed for co-morbidities predispose patients to the impact of polypharmacy. Because of the age-related changes in pharmacokinetics and pharmacodynamics, the adverse effects of drugs and drug-drug interactions are further exacerbated in older patients. Older diabetic patients using four or more concomitant medications have been found to be at increased risk for developing serious hypoglycaemia.8 25 Polypharmacy can also precipitate geriatric syndromes such as fall, cognitive impairment, urinary incontinence, and malnutrition.26 27

Diabetic complications (such as autonomic dysfunction with orthostatic hypotension, peripheral neuropathy with gait disorder, and diabetic retinopathy with poor vision)28 and treatment complications (such as metformin-associated vitamin B₁₂ deficiency with resultant neuropathy)29 increase the susceptibility of diabetic patients to fall. Besides, diabetes has been shown to be an independent risk factor for fracture.30 Patients who have longer diabetes duration, suboptimal glucose control, diabetic retinopathy, insulin use or thiazolidinedione use in women, and increased risk for fall are particularly at high risk for fracture.30 31 32

Neuropathic pain affects up to one third of patients with diabetes and is more prevalent in women.33 Its occurrence may not relate to the severity of neuropathy and may even occur in patients without clinical neuropathy. Besides, pain from other sources such as bone, joint, and back is common in older people. Urinary incontinence is also common in diabetic patients, especially women. Up to one third of female patients with diabetes had reported incontinence at least weekly in a survey in which urge incontinence was associated with advancing age.34 Managing treatable causes such as urinary tract infection, faecal impaction, use of offensive medications, and poor glycaemic control with polyuria may alleviate incontinence.24 Both pain and urinary incontinence are often neglected in clinical practice and may lead to adverse outcomes such as anxiety, depression, decreased socialisation, fall and fracture if left untreated.35 36 37

As many as 40% of older people with diabetes have four or more chronic conditions.38 Multiple co-morbidities may have profound effects on patients’ ability to self-care. Additionally, the level of co-morbidities affects treatment outcomes. Diabetic patients with low-to-moderate co-morbidity have been found to have a lower incidence of cardiovascular events than those with high co-morbidity, even with comparable HbA1c levels.39 Furthermore, co-morbidity, especially renal impairment, hepatic disease and cognitive dysfunction increase the risk of severe hypoglycaemia,25 which is associated with twice the risk of cardiovascular disease (myocardial infarction, congestive heart failure, stroke, and cardiovascular death) in diabetic patients.40 Diabetic patients with concomitant coronary artery disease who experience hypoglycaemia are particularly prone to ischaemic heart attack.41 These have clinical implications—in patients with multiple co-morbidities, intensive glucose treatment may not be beneficial, but might make patients prone to treatment-related hypoglycaemia which, in turn, may exacerbate the cardiovascular event, especially in those at risk for cardiovascular disease.

Management of other cardiovascular factors to lower the cardiovascular risk is also important. Systolic blood pressure (SBP) of ≥140 mm Hg increases the risk of cardiovascular events, whereas lowering blood pressure from a high level reduces both cardiovascular and microvascular complications in older diabetic patients.42 43 44 There is no further benefit to lowering SBP to <130 mm Hg however, as compared to SBP of 130-140 mm Hg, but may increase mortality.45 46 Furthermore, a low diastolic blood pressure of <70 mm Hg that may result from SBP reduction is associated with higher cardiovascular disease risk.42 Thus, the recommended target blood pressure for older diabetic patients is <140/90 mm Hg, if tolerated.2

Lipid lowering by statins has been shown to reduce the incidents of major vascular events by approximately 20% per mmol/L low-density lipoprotein cholesterol reduction in diabetic patients and in patients age ≥65 years.47 This benefit emerges quite rapidly, within 1 to 2 years of treatment, suggesting that most older people could benefit from statins except for those with very limited life expectancy. There is limited evidence with drugs other than statins for reduction of cardiovascular risk.

The UKPDS (UK Prospective Diabetes Study) that recruited patients with newly diagnosed type 2 diabetes (mean age, 53 years) showed a 25% risk reduction in microvascular complications in the intensive-therapy group (HbA1c achieved, 7%) after a median follow-up of 11 years.48 Macrovascular benefit, in terms of a 15% risk reduction for myocardial infarction, emerged only during 10 years of extended post-trial follow-up.49 In three more recent large-scale trials—ACCORD (Action to Control Cardiovascular Risk in Diabetes), ADVANCE (Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation), and VADT (Veterans Affairs Diabetes Trial)—which recruited older people (mean age, 60-66 years) with type 2 diabetes duration of 8 to 11.5 years and of whom 32% to 40% had a history of cardiovascular events, the intensive-therapy group (HbA1c achieved, 6.4%-6.9%) showed no benefit in the reduction of overall major cardiovascular events and death over 5 years of follow-up but only a lower rate of non-fatal myocardial infarction in the ACCORD trial.50 51 52 53 Instead, there was higher mortality in the intensive-therapy group of the ACCORD trial that led to premature discontinuation of intensive therapy after 3.5 years of follow-up. For the microvascular outcomes, the intensive-therapy group had lowered macroalbuminuria by 30%, decreased progression of retinopathy by 33%, and a modest risk reduction in the development of peripheral neuropathy.51 54 55 All of these trials revealed that intensive therapy was associated with a higher rate of hypoglycaemic episodes, with up to 2- to 3-fold increase in severe hypoglycaemia. The findings imply that good glycaemic control is most beneficial if it commences earlier, before the establishment of long-term complications. Furthermore, it takes time for intensive glycaemic control to reap microvascular benefit (over 5 years) and even longer for macrovascular benefit (over 10-20 years).48 49 51 52 54 55 For patients with limited life expectancy and multiple co-morbidities, the adverse effects are likely to outweigh the benefits.

The primary aim of diabetes management is to optimise glycaemic control to avoid acute hyperglycaemia complications and prevent long-term diabetic complications, both microvascular and macrovascular, and to minimise the adverse effect of treatment-related hypoglycaemia. Given the heterogeneous health status of older people, diabetes intervention strategies designed for long-term benefits may not be appropriate for all older people. A patient-centred approach for diabetes management that takes account of the potential benefits and risks of treatment, health and functional state, and social background for an individual patient has been increasingly emphasised. Accordingly, various frameworks or guidelines have been developed to assist in determining glycaemic treatment goals in older diabetic patients.2 3 4 5 6 In general, for older people who are relatively young, healthy and active, the same glycaemic target as for young people may be worthwhile to prevent long-term complications. For frail older people with multiple co-morbidities and limited life expectancy, the aim of glycaemic control is to prevent acute hyperglycaemic complications (polyuria, dehydration, hyperglycaemic hyperosmolar syndrome, infection, and poor wound healing) while avoiding treatment adverse effects, rather than to gain long-term benefit. The suggested target HbA1c varies from 7.0% to 7.5% for healthy older people to 8% to 9% for those who are in very poor health.2 3 4 5 6 The choice of anti-glycaemic agents should focus on safety, with low risk for hypoglycaemia, and metformin is generally considered to be the first-line therapy for older people.2 3 4 5 6 Avoidance of drugs with potential adverse effects that may exacerbate underlying conditions such as heart failure, osteoporosis with risk of fracture, and renal dysfunction is also advised.

Because of altered taste and smell, anorexia of ageing, difficulty in swallowing, and decreased functional state, food intake tends to decline with advancing age. A restrictive diet for glycaemic control that is designed for young and middle-aged diabetic patients may not be suitable for all older diabetic patients.56 Instead, a restrictive diet may limit the variety and flavour of food offered, which may exacerbate poor food intake leading to unintentional weight loss and undernutrition. Those who are frail, institutionalised, or underweight are particularly at risk, with increased morbidity and mortality.57 Thus, a less restrictive diet or even a liberal diet with modification of medications to control blood glucose may be advisable for susceptible patients.58 Nutritional assessment taking account of a patient’s circumstances to guide individual nutritional intervention is advocated.

After the round-table discussion, consensus was reached on the following six domains to address the management of older diabetic people:
(1) When setting an individualised glycaemic goal, the important considerations should include:
   (a) risk of hypoglycaemia;
   (b) physical and mental function;
   (c) co-morbidities and associated vascular disease; and
   (d) family support and community resources.
(2) In view of the high risk of the associated co-morbidities with functional and cognitive impairment, use of an extended diabetic complication screening tool to include the geriatric syndromes is recommended. Other important reasons for screening include the close association of geriatric syndromes with diabetes, implications for choosing therapeutic interventions, and the considerable impact on quality of life. Common syndromes that could be included are:
   (a) frailty;
   (b) cognitive dysfunction;
   (c) polypharmacy;
   (d) nutrition;
   (e) falls;
   (f) hearing, visual impairment;
   (g) depression;
   (h) pain; and
   (i) urinary incontinence.
(3) Because of the heterogeneous health status of older people, glucose and blood pressure targets should be individualised. An important consideration would be whether the time frame of potential benefits from treatment in long-term clinical trials is within the life expectancy of an individual patient:
   (a) glycaemic target:
      (i) HbA1c goal similar to that of general adults, but without excessive hypoglycaemia, should be considered for robust elderly people;
      (ii) higher HbA1c up to 8.5% can be considered for those who are physically and cognitively frail or in nursing homes; and
      (iii) liberal HbA1c without setting a target, aiming at symptomatic control, for those at the end of life.
      (NB: HbA1c level would be potentially influenced by co-morbidities such as anaemia, which is more prevalent in older adults.)
   (b) blood pressure target:
      (i) similar to general adults (≤140/90 mm Hg) for robust elderly people;
      (ii) ≤150/90 mm Hg for physically or cognitively frail elderly people, with avoidance of hypotension; and
      (iii) liberal without setting a target for those at the end of life.
(4) In view of the risk of polypharmacy and the age-related changes in pharmacokinetics and pharmacodynamics, the following points need to be noted:
   (a) when prescribing glucose-lowering agent(s), the major considerations should include:
      (i) risk of hypoglycaemia;
      (ii) dosing frequency and complexity of drug regimen;
      (iii) tolerability and adverse effects such as gastrointestinal intolerance, change in fluid status, heart failure, fracture risk, weight change, and risk of urogenital infection;
      (iv) glucose-lowering effect; and
      (v) overall health status and quality of life of the patient.
   (b) Choice of drugs:
      (i) Metformin is generally chosen as a first-line agent because of robust clinical efficacy and low risk of hypoglycaemia. Its use is mainly limited by gastrointestinal tolerability, renal insufficiency, risk of lactic acidosis, and subclinical vitamin B₁₂ deficiency.
      (ii) Sulphonylureas are of low cost with high anti-glycaemic efficacy. However, they are associated with higher risk of hypoglycaemia and should be used with caution in older people. A long-acting sulphonylurea such as glibenclamide should be avoided because of the high incidence of prolonged hypoglycaemia and possibly increased mortality.
      (iii) DPP-IV inhibitors have a low hypoglycaemia risk, modest clinical efficacy, good tolerability, and convenient dosing. The disadvantage is their higher cost.
      (iv) Thiazolidinediones have low hypoglycaemia risk, and good efficacy and durability. The adverse effects include fluid retention, weight gain, and increased fractures. Lower doses are generally better tolerated.
      (v) Sodium-glucose cotransporter 2 inhibitors have low hypoglycaemia risk, with decreased body weight, and modest clinical efficacy with some favourable cardiovascular safety data. Adverse effects include urogenital infection, urinary frequency, and dehydration. There may also be reduction of blood pressure so dose adjustment of any anti-hypertensive agent may be needed. They are of a higher cost with limited efficacy in patients with impaired renal function.
      (vi) Alpha-glucosidase inhibitors have modest anti-glycaemic efficacy and low hypoglycaemic risk. Adverse effects include bloating, flatulence, and diarrhoea.
      (vii) Glucagon-like peptide 1 agonists have low hypoglycaemia risk and good antiglycaemic efficacy with associated weight loss. The disadvantages are the high cost; the need for injections; and adverse effects of nausea, vomiting, and anorexia.
      (viii) Insulins are highly effective in lowering glucose with various regimens. They are associated with significant hypoglycaemic risk and weight gain. The requirement for a high level of self-management education may be difficult for older people with physical or mental disabilities.
(5) A restrictive (therapeutic) diabetic diet may not be beneficial for some elderly diabetic people and may lead to decreased intake, unintentional weight loss, and undernutrition. Individualised nutritional approaches addressing personal food preferences and goals with a wider variety of food choices should be adopted. This is particularly applicable to those who are:
   (a) >80 years old;
   (b) physically frail;
   (c) cognitively frail;
   (d) underweight; and
   (e) nursing home residents.
(6) Nursing home residents are distinct from community-dwelling older people because they are generally more frail with co-morbidities requiring high levels of care. The staff at long-term care facilities should be offered appropriate education and training in diabetes. The management of elderly nursing home residents with diabetes should aim to:
   (a) prevent hypoglycaemia;
   (b) prevent hospitalisation;
   (c) avoid acute metabolic complications; and
   (d) provide timely end-of-life care and advance care planning.

With the increasing population of older people with diabetes and the complexity and heterogeneity of older people, it is time to change our clinical practice in managing diabetes in older people—management should not be solely based on the clinical guidance for younger people with diabetes. We need to consider the course of the disease in the context of individual characteristics (co-morbidities, frailty, cognitive impairment, life expectancy, risk of treatment-induced hypoglycaemia, patients’ attitudes, social support, etc) to tailor a treatment goal and management plan. This approach has recently been advocated by several international organisations such as the American Diabetes Association and the American Geriatrics Society. Our consensus statement takes the initiative in promoting better diabetes care for older people in our locality. The guidance takes into consideration of local experience to address issues specifically related to older diabetic people, such as the inclusion of a comprehensive geriatric assessment to screen for geriatric syndromes and psychosocial needs, which is often missed in a busy clinic, and the glycaemic targets for broadly classified groups of patients, which could guide clinicians in daily practice. Nonetheless, the consensus statement is far from complete in addressing all the issues—the details on how to implement the geriatric assessment for optimal therapy, the appropriate treatment goals for all the multifaceted scenarios of older people, the optimal level of blood pressure control, and the allocation of social support for care in the community and much more, remain to be determined.

Additional material related to this article can be found on the HKMJ website. Please go to http://www.hkmj.org, and search for the article.

All authors have disclosed no conflicts of interest.

1. McGhee SM, Cheung WL, Woo J, et al. Trends of disease burden consequent to diabetes in older persons in Hong Kong: implications of population ageing. Hong Kong SAR: Hong Kong Jockey Club; 2009.

2. American Geriatrics Society Expert Panel on Care of Older Adults with Diabetes Mellitus, Moreno G, Mangione CM, Kimbro L, Vaisberg E. Guidelines abstracted from the American Geriatrics Society Guidelines for Improving the Care of Older Adults with Diabetes Mellitus: 2013 update. J Am Geriatr Soc 2013;61:2020-6. Crossref

3. Ismail-Beigi F, Moghissi E, Tiktin M, Hirsch IB, Inzucchi SE, Genuth S. Individualizing glycemic targets in type 2 diabetes mellitus: implications of recent clinical trials. Ann Intern Med 2011;154:554-9. Crossref

4. Sinclair A, Morley JE, Rodriguez-Mañas L, et al. Diabetes mellitus in older people: position statement on behalf of the International Association of Gerontology and Geriatrics (IAGG), the European Diabetes Working Party for Older People (EDWPOP), and the International Task Force of Experts in Diabetes. J Am Med Dir Assoc 2012;13:497-502. Crossref

5. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient-centered approach: position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care 2012;35:1364-79. Crossref

6. Kirkman MS, Briscoe VJ, Clark N, et al. Diabetes in older adults: a consensus report. J Am Geriatr Soc 2012;60:2342-56. Crossref

7. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes, 2015: A patient-centered approach: update to a position statement of American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 2015;38:140-9. Crossref

8. Shorr RI, Ray WA, Daugherty JR, Griffin MR. Incidence and risk factors for serious hypoglycemia in older persons using insulin or sulfonylureas. Arch Intern Med 1997;157:1681-6. Crossref

9. Bremer JP, Jauch-Chara K, Hallschmid M, Schmid S, Schultes B. Hypoglycemia unawareness in older compared with middle-aged patients with type 2 diabetes. Diabetes Care 2009;32:1513-7. Crossref

10. Brierley EJ, Broughton DL, James OF, Alberti KG. Reduced awareness of hypoglycaemia in the elderly despite an intact counter-regulatory response. QJM 1995;88:439-45.

11. Meneilly GS, Cheung E, Tuokko H. Altered responses to hypoglycemia of healthy elderly people. J Clin Endocrinol Metab 1994;78:1341-8. Crossref

12. Matyka K, Evans M, Lomas J, Cranston I, Macdonald I, Amiel SA. Altered hierarchy of protective responses against severe hypoglycemia in normal aging in healthy men. Diabetes Care 1997;20:135-41. Crossref

13. White NH, Skor DA, Cryer PE, Levandoski LA, Bier DM, Santiago JV. Identification of type I diabetic patients at increased risk for hypoglycemia during intensive therapy. N Engl J Med 1983;308:485-91. Crossref

14. Gold AE, Macleod KM, Frier BM, Frequency of severe hypoglycemia in patients with type I diabetes with impaired awareness of hypoglycemia. Diabetes Care 1994;17:697-703. Crossref

15. Cukierman T, Gerstein HC, Williamson JD. Cognitive decline and dementia in diabetes—systematic overview of prospective observational studies. Diabetologia 2005;48:2460-9. Crossref

16. Lu FP, Lin KP, Kuo HK. Diabetes and the risk of multi-system aging phenotypes: a systematic review and meta-analysis. PLoS One 2009;4:e4144. Crossref

17. Whitmer RA, Karter AJ, Yaffe K, Quesenberry CP Jr, Selby JV. Hypoglycemic episodes and risk of dementia in older patients with type 2 diabetes mellitus. JAMA 2009;301:1565-72. Crossref

18. Lin CH, Sheu WH. Hypoglycaemic episodes and risk of dementia in diabetes mellitus: 7-year follow-up study. J Intern Med 2013;273:102-10. Crossref

19. Aung PP, Strachan MW, Frier BM, et al. Severe hypoglycaemia and late-life cognitive ability in older people with type 2 diabetes: the Edinburgh Type 2 Diabetes Study. Diabet Med 2012;29:328-36. Crossref

20. Yaffe K, Falvey CM, Hamilton N, et al. Association between hypoglycemia and dementia in a biracial cohort of older adults with diabetes mellitus. JAMA Intern Med 2013;173:1300-6. Crossref

21. Nouwen A, Winkley K, Twisk J, et al. Type 2 diabetes mellitus as a risk factor for the onset of depression: a systematic review and meta-analysis. Diabetologia 2010;53:2480-6. Crossref

22. Mezuk B, Eaton WW, Albrecht S, Golden SH. Depression and type 2 diabetes over the lifespan: a meta-analysis. Diabetes Care 2008;31:2383-90. Crossref

23. Li C, Ford ES, Zhao G, Ahluwalia IB, Pearson WS, Mokdad AH. Prevalence and correlates of undiagnosed depression among U.S. adults with diabetes: the Behavioral Risk Factor Surveillance System, 2006. Diabetes Res Clin Pract 2009;83:268-79. Crossref

24. Brown AF, Mangione CM, Saliba D, Sarkisian CA; California Healthcare Foundation/American Geriatrics Society Panel on Improving Care for Elders with Diabetes. Guidelines for improving the care of the older person with diabetes mellitus. J Am Geriatr Soc 2003;51(5 Suppl Guidelines):S265-80.

25. Holstein A, Plaschke A, Egberts EH. Clinical characterisation of severe hypoglycaemia—a prospective population-based study. Exp Clin Endocrinol Diabetes 2003;111:364-9. Crossref

26. Huang ES, Karter AJ, Danielson KK, Warton EM, Ahmed AT. The association between the number of prescription medications and incident falls in a multi-ethnic population of adult type-2 diabetes patients: the diabetes and aging study. J Gen Intern Med 2010;25:141-6. Crossref

27. Maher RL, Hanlon J, Hajjar ER. Clinical consequences of polypharmacy in elderly. Expert Opin Drug Saf 2014;13:57-65. Crossref

28. Mayne D, Stout NR, Aspray TJ. Diabetes, falls and fractures. Age Ageing 2010;39:522-5. Crossref

29. Bauman WA, Shaw S, Jayatilleke E, Spungen AM, Herbert V. Increase intake of calcium reverses vitamin B12 malabsorption induced by metformin. Diabetes Care 2000;23:1227-31. Crossref

30. Schneider AL, Williams EK, Brancati FL, Blecker S, Coresh J, Selvin E. Diabetes and risk of fracture-related hospitalization: the Atherosclerosis Risk in Communities Study. Diabetes Care 2013;36:1153-8. Crossref

31. Loke YK, Singh S, Furberg CD. Long-term use of thiazolidinediones and fractures in type 2 diabetes: a meta-analysis. CMAJ 2009;180:32-9. Crossref

32. Ivers RQ, Cumming RG, Mitchell P, Peduto AJ; Blue Mountains Eye Study. Diabetes and risk of fracture: The Blue Mountains Eye Study. Diabetes Care 2001;24:1198-203. Crossref

33. Abbott CA, Malik RA, van Ross ER, Kulkarni J, Boulton AJ. Prevalence and characteristics of painful diabetic neuropathy in a large community-based diabetic population in the U.K. Daibetes Care 2011;34:2220-4. Crossref

34. Brown JS, Vittinghoff E, Lin F, Nyberg LM, Kusek JW, Kanaya AM. Prevalence and risk factors for urinary incontinence in women with type 2 diabetes and impaired fasting glucose: findings from the National Health and Nutrition Examination Survey (NHANES) 2001-2002. Diabetes Care 2006;29:1307-12. Crossref

35. AGS Panel on Persistent Pain in Older Persons. The management of persistent pain in older persons. J Am Geriatr Soc 2002;50(6 Suppl):S205-24.

36. Brown JS, Vittinghoff E, Wyman JF, et al. Urinary incontinence: does it increase risk for falls and fracture? J Am Geriatr Soc 2000;48:721-5. Crossref

37. Dugan E, Cohen SJ, Bland DR, et al. The association of depressive symptoms and urinary incontinence among older adults. J Am Geriatr Soc 2000:48:413-6. Crossref

38. Wolff JL, Starfield B, Anderson G. Prevalence, expenditures, and complications of multiple chronic conditions in the elderly. Arch Intern Med 2002;162:2269-76. Crossref

39. Greenfield S, Billmek J, Pellegrini F, et al. Comorbidity affects the relationship between glycemic control and cardiovascular outcomes in diabetes: a cohort study. Ann Intern Med 2009;151:854-60. Crossref

40. Goto A, Arah OA, Goto M, Terauchi Y, Noda M. Severe hypoglycaemia and cardiovascular disease: systematic review and meta-analysis with bias analysis. BMJ 2013;347:f4533. Crossref

41. Desouza C, Salazar H, Cheong B, Murgo J, Fonseca V. Association of hypoglycemia and cardiac ischemia: a study based on continuous monitoring. Diabetes Care 2003;26:1485-9. Crossref

42. Anderson RJ, Bahn GD, Moritz TE, et al. Blood pressure and cardiovascular disease risk in the Veterans Affairs Diabetes Trial. Diabetes Care 2011;34:34-8. Crossref

43. Curb JD, Pressel SL, Cutler JA, et al. Effect of diuretic-based antihypertensive treatment on cardiovascular disease risk in older diabetic patients with isolated systolic hypertension. Systolic Hypertension in the Elderly Program Cooperative Research Group. JAMA 1996;276:1886-92. Crossref

44. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. UK Prospective Diabetes Study Group. BMJ 1998:317:703-13. Crossref

45. Cooper-DeHoff RM, Gong Y, Handberg EM, et al. Tight blood pressure control and cardiovascular outcomes among hypertensive patients with diabetes and coronary artery disease. JAMA 2010;304:61-8. Crossref

46. Sleight P, Redon J, Verdecchia P, et al. Prognostic value of blood pressure in patients with high vascular risk in the Ongoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial study. J Hypertens 2009;27:1360-9. Crossref

47. Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: prospective metaanalysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005;366:1267-78. Crossref

48. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:837-53. Crossref

49. Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med 2008;359:1577-89. Crossref

50. Action to Control Cardiovascular Risk in Diabetes Study Group, Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med 2008;358:2545-59. Crossref

51. ADVANCE Collaborative Group, Patel A, MacMahon S, Chalmers J, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med 2008;358:2560-72. Crossref

52. Duckworth W, Abraira C, Moritz T, et al. Glucose control and vascular complications in veterans with type 2 diabetes. N Engl J Med 2009;360:129-39. Crossref

53. ACCORD Study Group, Gerstein HC, Miller ME, Genuth S, et al. Long-term effects of intensive glucose lowering on cardiovascular outcomes. N Engl J Med 2011;364:818-28. Crossref

54. Ismail-Beigi F, Craven T, Banerji MA, et al. Effect of intensive treatment of hyperglycaemia on microvascular outcomes in type 2 diabetes: an analysis of the ACCORD randomised trial. Lancet 2010;376:419-30. Crossref

55. ACCORD Study Group; ACCORD Eye Study Group, Chew EY, Ambrosius WT, Davis MD, et al. Effects of medical therapies on retinopathy progression in type 2 diabetes. N Engl J Med 2010;363:233-44. Crossref

56. Dorner B, Friedrich EK, Posthauer ME; American Dietetic Association. Position of the American Dietetic Association: individualized nutrition approaches for older adults in health care communities. J Am Diet Assoc 2010;110:1549-53. Crossref

57. Schafer RG, Bohannon B, Franz MJ, et al. Diabetes nutrition recommendations for health care institutions. Diabetes Care 2004;27 Suppl 1:S55-7. Crossref

58. American Diabetes Association, Bantle JP, Wylie-Rosett J, Albright AL, et al. Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care 2008;31 Suppl 1:S61-78.

Hong Kong is facing an unparalleled challenge of rapid population ageing.1 This demographic change results in an impending need for end-of-life care among older people with advanced dementia.2 One of the natural stages of the dementia disease process is eating problems with poor appetite and swallowing difficulty, leading to malnutrition, weight loss, and aspiration pneumonia (AP).3 4 Unless there is a valid advance directive (AD) refusing enteral feeding, family members and the health care team often feel compelled to initiate tube feeding. This leads to a very high prevalence of tube feeding in elderly with advanced dementia, especially those living in residential care homes for the elderly (RCHEs).5 6

There are many reasons for placing a feeding tube in patients with advanced dementia. Medical, social, cultural, economic, ethical, psychological, and medicolegal factors all play a part in the decision.7 Many older patients are commenced on tube feeding when they are dysphagic or are feeding inadequately. Probably due to inadequate information about the pitfalls of tube feeding, risk of AP and survival are the most frequently cited reasons by health care teams to insert a feeding tube.8 To date, however, evidence has proven that tube feeding does not prevent AP.9 On the contrary, AP might be increased by the use of enteral feeding.10 Placement of a nasogastric tube weakens the lower oesophageal sphincter and reduces the efficiency of the valve that prevents gastric reflux into the upper digestive tract.11 The use of tube feeding without oral feeding also leads to neglect of oral hygiene, resulting in bacterial colonisation and an increased risk of AP. Enteral feeding is unable to improve serum albumin, body weight, or lean muscle mass.12 The use of a feeding tube causes patient discomfort, increased use of restraints, and consequent greater likelihood of pressure sore development.13 14 Studies showed that RCHE residents with feeding tubes are frequently transferred to an emergency department for tube complications such as blockage and dislodgement.15 To date, studies have not shown survival benefits in older people with tube feeding.16 In a local study of 312 advanced cognitively impaired RCHE residents, 164 (53%) were being tube fed.6 The 1-year mortality rate was 34% and enteral feeding was cited as an important risk factor for 1-year mortality (odds ratio=2.0; 95% confidence interval, 2.0-3.4; P=0.008).6

Careful hand feeding (CHF) has been advocated as an alternative for older people with advanced dementia and eating problems.17 In CHF, the carer makes use of feeding techniques such as frequent reminders to swallow, multiple swallows, encouraging gentle coughs after each swallow, limiting bolus size to less than one teaspoon, and judicious use of thickeners. The carer observes the patient for choking and pocketing of food in the mouth. The carer focuses on the older person during the entire feeding process and avoids distraction. The older person is placed in an upright position during the meal. Moistening foods with water or sauces, or alternating food with appropriate liquid consistency may help swallowing, for example, in patients with a dry mouth.

In the 2014 position statement on feeding tubes in advanced dementia published by the American Geriatrics Society, feeding tubes are not recommended.18 It emphasises that CHF should be offered as it is at least as good as tube feeding for the outcomes of death, AP, functional status, and comfort.19 20 Older patients with dementia can still form a relationship with their carer. Actions by the carer can influence food intake of an older person with dementia and include touching, kissing, hugging, and responding to non-verbal cues.21 Caregivers can provide patients frequent reminders to swallow, perform multiple swallows, make gentle small coughs between feeds, and assume an appropriate posture to reduce the risk of AP. A pleasant quiet environment with less distraction is desirable during the whole feeding process.

Tube feeding is prevalent in Hong Kong among older patients with advanced dementia for multiple reasons. Family members may think that they cannot allow the demented relative to starve. This may be affected by the Chinese culture that emphasises eating and avoidance of hunger at all costs. To achieve this, there seems to be little other choice. Physicians may be too optimistic and inform family members that the tube can be removed if the patient regains the ability to eat normally.22 The chance of stopping tube feeding, however, is lower than 20% in all indications for tube feeding.23 Family members may insist on aggressive measures at all costs, despite the futility.

The current medical culture in Hong Kong is predominantly biomedical, with life preservation the overwhelming principle.24 Physicians may recommend tube feeding in older patients with advanced dementia because they believe clinical outcomes can be thereby improved.25 Many physicians are under pressure from family members when discussing tube feeding.26 The health care team may be unfamiliar with the current literature about the pitfalls of tube feeding and may not realise that there is also an option of CHF. The health care team may also fear legal consequences if patients with advanced dementia are not fed with a feeding tube.

Advance care planning (ACP) is a process of communication among patients, their family, and important others about the care they wish to receive if they are unable to make decisions.27 Often one of the discussions relates to the decision to start tube feeding in the presence of severe eating problems. One outcome of ACP is an expressed wish that is not legally binding. Another option is for the patient to sign an AD, a formal tool that respects the autonomy of patients and in which any decision must be adhered to by the health care team.28 In Hong Kong, life-sustaining treatment, including tube feeding, can be withheld if there is a valid AD when the patient is in an irreversible coma, persistent vegetative state, terminal illnesses, or other end-stage irreversible life-limiting condition.29 Nonetheless until recently ACP and AD have been seldomly discussed in Hong Kong.30 When a patient without an AD is unconscious due to an advanced irreversible illness, the decision to withhold or withdraw tube feeding is made by consensus of the health care team and family members according to the best interests of the patient, taking into account any prior wish or treatment preference. Without knowing the exact wishes of the patient, many health care teams and family members are compelled to start tube feeding.

In Hong Kong, there are practical issues associated with not using a feeding tube. Hand feeding is time-consuming. In the hospital environment, because of staff shortages, it is difficult to provide quality CHF to all patients with advanced dementia having eating problems. If an older patient is feeding poorly, it is difficult to discharge them from hospital, especially if they are returning to a RCHE. The environment can also affect feeding.31 Medical wards in Hong Kong public hospitals are often elderly unfriendly, crowded, noisy, and without privacy. In addition, nurses may be reluctant to hand feed the advanced dementia patient with dysphagia after assessment by a speech therapist. Without strong hospital policy support, nurses understandably are concerned about medicolegal consequences should the dysphagic elderly patient aspirate following CHF. Hence, not uncommonly, they will ask relatives who have ‘refused’ tube feeding of an elderly dysphagic older to feed them. Family members who are unable to come to the hospital 2 or 3 times a day will have little choice but to alter their decision and agree to tube feeding. In RCHEs, manpower issues and the crowded environment are barriers to quality feeding of those with dementia. Older RCHE residents who are offered CHF but are feeding poorly will soon become dehydrated, especially in summer. Staff in RCHEs will soon bring their older residents back to the emergency ward/department if they cannot eat or are eating poorly, leading to a ‘revolving door’ phenomenon. Alternative ways of hydration, including hypodermoclysis (subcutaneous fluid infusion), are not practised in RCHEs in Hong Kong.32 Not many family doctors are equipped with the knowledge or have the time to take care of advanced dementia cases with feeding problems in RCHEs. Many medications need to be taken orally and administration via an enteral tube may appear to be the only alternative in dysphagic patients.

Artificial nutrition and hydration (ANH) refers specifically to those techniques for providing nutrition or hydration which are used to bypass the swallowing process. They include the use of nasogastric tubes, percutaneous endoscopic gastrostomy, intravenous or subcutaneous fluid, and parenteral nutrition. In September 2015, the Hospital Authority guidelines on life-sustaining treatment in the terminally ill was updated. Among other key end-of-life care issues, the guidelines provide a clear picture of CHF and ANH from the ethical perspective.33 It states that when death is imminent (death is expected within a few hours or days) and inevitable in a mentally incompetent patient without a valid AD, it is acceptable to withhold or withdraw ANH. This follows the same principles that apply to other life-sustaining treatments. Notwithstanding, if a patient is in or near the end stage of a disease or condition and is mentally incompetent, and death is not imminent, the balance of benefits and burdens of ANH may become unclear. The guideline states that if the patient does not have a valid AD refusing ANH, the consideration of withholding or withdrawing ANH requires additional safeguards. There must be consensus within the health care team and with the family (if any) that a decision to withhold or withdraw ANH is in the best interests of the patient, taking into account their prior wishes and values. The health care team must include at least two doctors, one of whom must be a specialist in a relevant field, eg geriatrician or palliative care specialist. In addition, if the patient is unable to swallow, the health care team should seek advice from the ‘cluster clinical ethics committee’, before making a decision to withhold or withdraw ANH, unless before losing capacity, the patient has clearly expressed a wish to refuse ANH (as reported clearly by family members or documented in medical notes when the patient was still competent) or the patient actively and repeatedly resists ANH such as repeatedly pulling out a nasogastric tube. Based on the principles stipulated in the Hospital Authority guidelines,33 Figures 1 and 2 were drawn showing the flowcharts when death is imminent/inevitable and when death is not imminent, respectively.

There is no definitive solution for feeding problems in older patients with advanced dementia. In the absence of a valid AD, patient management should be individualised, and the decision for tube feeding or CHF should be shared between the health care team and family members, based on the patient’s previously expressed wishes and best interests. The health care team should accept and respect the family’s choice of CHF instead of tube feeding. Experienced nurses and doctors should be responsible for discussing the pros and cons of tube feeding with the family to achieve a consensus. Clear hospital guidelines and protocols should facilitate CHF and effect a cultural change.34 Staff sentiments and medicolegal concerns should be addressed. Clear Hospital Authority or hospital policy to support CHF will help alleviate the concerns of nursing staff. Training of doctors, nurses, and other members of the health care team is vital to the promulgation of CHF. There is an urgent need to enhance the environment of public hospital wards so that they are more elderly friendly. Training of RCHE staff and the staff ratio are important factors that will determine the success of CHF in the community of Hong Kong. Without a well-prepared staff, patients on CHF will soon be put on enteral feeding. The Social Welfare Department can ensure it is part of the licensing requirement to have end-of-life care that includes CHF in most, if not all, RCHEs. More palliative care training should be given to primary doctors who look after older people with advanced dementia.35 Recently, all medical students at the University of Hong Kong have been seconded to RCHEs to learn about community geriatrics as part of their undergraduate training. They have first-hand experience, under the guidance of geriatricians, of how the elderly with advanced dementia are cared for in RCHEs. More education about feeding issues in dementia should be offered to the public. Furthermore, ACP and AD should be promoted in Hong Kong so that patients can elect a particular mode of feeding while they are mentally capable.36 At the time of writing this article, the Hong Kong SAR Government is exploring the realisation of enduring power of attorney for health care decision, allowing mentally incapacitated older people to express their wishes through a chosen advocate.37 It is hoped that the decision to accept enteral feeding or not can be included in the scope of the power of attorney.

1. Hong Kong population projections 2012-2041. Census and Statistics Department, Hong Kong SAR Government; 2012.

2. Luk JK, Liu A, Ng WC, Lui B, Beh P, Chan FH. End-of-life care: towards a more dignified dying process in residential care homes for the elderly. Hong Kong Med J 2010;16:235-6.

3. Mitchell SL, Teno JM, Keily DK, et al. The clinical course of advanced dementia. N Engl J Med 2009;361:1529-38. Crossref

4. Hoffer LJ. Tube feeding in advanced dementia: the metabolic perspective. BMJ 2006;333:1214-5. Crossref

5. Luk JK, Chan FH, Pau MM, Yu C. Outreach geriatrics service to private old age homes in Hong Kong West Cluster. J Hong Kong Geriatr Soc 2002;11:5-11.

6. Luk JK, Chan WK, Ng WC, et al. Mortality and health services utilization among older people with advanced cognitive impairment living in residential care homes. Hong Kong Med J 2013;19:518-24.

7. Luk JK, Chan DK. Preventing aspiration pneumonia in older people: do we have the “know-how”? Hong Kong Med J 2014;20:421-7.

8. Li I. Feeding tubes in patients with severe dementia. Am Fam Physician 2002;65:1605-10, 1515.

9. Finucane TE, Christmas C, Travis K. Tube feeding in patients with advanced dementia: a review of the evidence. JAMA 1999;282:1365-70. Crossref

10. Vergis EN, Brennen C, Wagener M, Muder RR. Pneumonia in long-term care: a prospective case-control study of risk factors and impact on survival. Arch Intern Med 2001;161:2378-81. Crossref

11. Gomes GF, Pisani JC, Macedo ED, Campos AC. The nasogastric feeding tube as a risk factor for aspiration and aspiration pneumonia. Curr Opin Clin Nutr Metab Care 2003;6:327-33. Crossref

12. Ciocon JO, Silverstone FA, Graver LM, Foley CJ. Tube feedings in elderly patients. Indications, benefits, and complications. Arch Intern Med 1988;148:429-33. Crossref

13. Kuo S, Rhodes RL, Mitchell SL, Mor V, Teno JM. Natural history of feeding-tube use in nursing home residents with advanced dementia. J Am Dir Assoc 2009;10:264-70. Crossref

14. Teno JM, Mitchell SL, Kuo SK, et al. Decision-making and outcome of feeding tube insertion: a five-state study. J Am Geriatr Soc 2011;59:881-6. Crossref

15. Odom SR, Barone JE, Docimo S, Bull SM, Jorgensson D. Emergency departments visits by demented patients with malfunctioning feeding tubes. Surg Endosc 2003;17:651-3. Crossref

16. Mitchell SL, Tetroe JM. Survival after percutaneous endoscopic gastrostomy placement in older persons. J Gerontol A Biol Sci Med Sci 2000;55:M735-9. Crossref

17. DiBartolo MC. Careful hand feeding: a reasonable alternative to PEG tube placement in individuals with dementia. J Gerontol Nurs 2006;32:25-33.

18. American Geriatrics Society Ethics Committee and Clinical Practice and Models of Care Committee. American Geriatrics Society feeding tubes in advanced dementia position statement. J Am Geriatr Soc 2014;62:1590-3. Crossref

19. Hanson LC, Ersek M, Gilliam R, Carey TS. Oral feeding options for people with dementia: a systematic review. J Am Geriatr Soc 2011;59:463-72. Crossref

20. Hanson LC. Tube feeding versus assisted oral feeding for persons with dementia: using evidence to support decision-making. Ann Longterm Care 2013;21:36-9.

21. Lange-Alberts ME, Shott S. Nutritional intake. Use of touch and verbal cuing. J Gerontol Nurs 1994;20:36-40. Crossref

22. Carey TS, Hanson L, Garrett JM, et al. Expectations and outcomes of gastric feeding tubes. Am J Med 2006;119:527.e11-6.

23. Wolfsen HC, Kozarek RA, Ball TJ, Patterson DJ, Botoman VA, Ryan JA. Long-term survival in patients undergoing percutaneous endoscopic gastrostomy and jejunostomy. Am J Gastroenterol 1990;85:1120-2.

24. Pang MC, Volicer L, Chung PM, Chung YM, Leung WK, White P. Comparing the ethical challenges of forgoing tube feeding in American and Hong Kong patients with advanced dementia. J Nutr Health Aging 2007;11:495-501.

25. Shega JW, Hougham GW, Stocking CB, Cox-Hayley D, Sachs GA. Barriers to limiting the practice of feeding tube placement in advanced dementia. J Palliat Med 2003;6:885-93. Crossref

26. Solomon MZ, O’Donnell L, Jennings B, et al. Decisions near the end of life: professional views on life-sustaining treatments. Am J Public Health 1993;83:14-23. Crossref

27. Teno JM, Nelson HL, Lynn J. Advance care planning. Priorities for ethical and empirical research. Hasting Cent Rep 1994;24:S32-6. Crossref

28. Chu LW, Luk JK, Hui E, et al. Advance directive and end-of-life care preferences among Chinese nursing home residents in Hong Kong. J Am Med Dir Assoc 2011;12:143-52. Crossref

29. Guideline for HA clinicians on advance directives in adults (2014). Hong Kong: Hospital Authority; 2014.

30. Tse CY. Reflections on the development of advance directives in Hong Kong. Asian Bioethics Rev 2016;8:211-23. Crossref

31. Amella EJ. Factors influencing the proportion of food consumed by nursing home residents with dementia. J Am Geriatr Soc 1999;47:879-85. Crossref

32. Luk KH, Chan HW, Chu LW. Is hypodermoclysis suitable for frail Chinese elderly? Asian J Gerontol Geriatr 2008;3:49-50.

33. HA guidelines on life-sustaining treatment in the terminally ill 2015. Hong Kong: Hospital Authority; 2015.

34. Palecek EJ, Teno JM, Casarett DJ, Hanson LC, Rhodes RL, Mitchell SL. Comfort feeding only: a proposal to bring clarity to decision-making regarding difficulty with eating for persons with advanced dementia. J Am Geriatr Soc 2010;58:580-4. Crossref

35. Hong TC, Lam TP, Chao VK. Barriers for primary care physicians in providing palliative care service in Hong Kong—qualitative study. Hong Kong Pract 2010;32:3-9.

36. Luk JK, Liu A, Ng WC, Beh P, Chan FH. End of life care in Hong Kong. Asian J Gerontol Geriatr 2011;6:103-6.

37. The Law Reform Commission of Hong Kong Report. Enduring powers of attorney: personal care. July 2011. Available from: http://www.hkreform.gov.hk/en/docs/repa2_e.pdf. Accessed 29 Apr 2017.

Atherosclerotic cardiovascular disease (ASCVD), which includes coronary heart disease (CHD), peripheral vascular disease and stroke, is currently one of the most common causes of morbidity and mortality worldwide.1 Unfortunately the prevalence of ASCVD is expected to increase further over the next few decades due to a number of factors including an ageing population and increasing industrialisation. The latter is associated with increased exposure to known ASCVD risk factors such as smoking, low levels of physical activity, and poor dietary habits such as reduced consumption of fruit and vegetables and increased fat and salt intake.2

In Hong Kong, the prevalence of ASCVD risk factors has increased markedly over the past few decades. For example, the 2005-2008 Hong Kong Cardiovascular Risk Factor Prevalence Study-3 (CRISPS-3) reported an 8.6% increase in the prevalence of abdominal obesity (waist circumference ≥90 cm in men and ≥80 cm in women) and a 21.5% increase in the prevalence of hypertension among a cohort of 1803 subjects recruited from CRISPS-1, the first such survey conducted between 1995 and 1996.3 Of the 551 participants of the Hong Kong Cardiovascular Task Force Risk Management Programme, 65.4% had hypertension, 63.7% dyslipidaemia, and 33.3% diabetes at baseline (BMY Cheung, unpublished data).

Global efforts are underway to promote ASCVD prevention and reduce the risk of major ASCVD events. These efforts have yielded benefits—between 1990 and 2013, a substantial reduction in cardiovascular mortality was seen in central Europe (5.2%) and western Europe (12.8%), attributed primarily to birth cohorts’ decreased exposure to tobacco smoking, improvements in diet, improved treatment of cardiometabolic risk factors, and improved treatment of CVD.4

A multidisciplinary group of clinicians comprising the Hong Kong Cardiovascular Task Force—10 cardiologists, an endocrinologist, and a family physician—met in September 2014 and June 2015 in Hong Kong with the aim of updating the first Consensus Statement on Preventing Cardiovascular Disease in the Hong Kong Population published in 2008.5 Prior to the consensus meetings, group members reviewed the 2008 Consensus Statement and relevant guidelines from the American College of Cardiology/American Heart Association, the European Society of Hypertension/European Society of Cardiology, and the Eighth Joint National Committee for the Management of High Blood Pressure, among others.5 6 7 8 9 At the meetings, each topical recommendation of the 2008 Statement was assessed against the pooled recommendations on that topic from the international guidelines reviewed. A final recommendation on each topic was generated by consensus after discussion.

The recommendations included in this consensus statement constitute the consensus opinion of the members of the Hong Kong Cardiovascular Task Force regarding the most appropriate interventions for the Hong Kong population.

Total ASCVD risk is based on the complex interactions of a number of different risk factors that together have a multiplicative effect. That is, the risk of ASCVD is amplified to a greater extent by the interaction of multiple risk factors than would be expected due to the cumulative effect of each risk factor alone.7 9 The present standard of practice for the primary prevention of ASCVD is to determine a patient’s total ASCVD risk using a formal risk scoring algorithm.1 7 9

In Hong Kong, it is recommended that ASCVD prevention efforts should be focused on adults aged 40 years or older who have at least one ASCVD risk factor.1 9 The total ASCVD risk should be formally calculated for such individuals, and they should receive ASCVD prevention advice and/or treatment according to their determined level of risk (high, moderate, or low).1 9 High-risk patients will benefit most from treatment and include:

• patients with overt ASCVD (CHD, previous myocardial infarction, previous stroke, or peripheral vascular disease) or those who are symptomatic (eg have experience with angina)
• patients with diabetes mellitus
• patients with one major ASCVD risk factor (eg moderate-to-severe hypertension, severely elevated lipid levels)9

These patients automatically meet the threshold for intensive risk factor treatment and need not undergo formal risk scoring.1 9

It is important to note that the current recommendations do not espouse a preference for any particular method of risk projection, but recommend that formal ASCVD risk scoring should be performed for all potentially at-risk patients.

A patient’s 10-year (total) risk for ASCVD may be calculated using a variety of methods. The most recently published algorithm uses the American Pooled Cohort Risk Assessment Equations that are sex- and race-specific estimates for African-American and White men and women aged 40 to 79 years. They utilise age, total and high-density lipoprotein (HDL) cholesterol, systolic blood pressure (BP), diabetes, and current smoking status to calculate the total ASCVD risk.1 The European Systematic Coronary Risk Evaluation (SCORE) system is another well-validated system that uses sex, age, systolic BP, total cholesterol, and current smoking status to predict the risk of fatal cardiovascular events.7 Another risk assessment system, QRISK2, includes the risk factor of ‘self-assigned ethnicity’ (including Chinese) in the computation10 11; however, the model was validated for Chinese immigrants to the United Kingdom and, thus, its applicability to the local Chinese population is unknown.

The calculated risk score is used to stratify patients into low-, moderate-, and high-risk categories (Fig). When interpreting these scores, the clinician should bear in mind that they were developed and validated for western populations. In addition, it must be remembered that any calculated ASCVD score is simply an indicator of total cardiovascular risk.9 Although it can guide patient treatment, it cannot be a substitute for individualised patient evaluation and management. The clinician is advised to take all factors into account and to treat the patient individually rather than treat the risk score.

There is robust scientific evidence that the development of ASCVD in at-risk patients may be slowed and/or prevented by lifestyle modification, reduction of metabolic risk factors, and pharmacological treatment.7 9 10 11 12 13 14 15 16 17 18 19 Listed below are the major modifiable risk factors for ASCVD. The treatment goal is stated for each risk factor, along with general recommendations on how this goal may be achieved. Existing hypertension,7 8 dyslipidaemia,1 6 and diabetes20 21 22 treatment guidelines incorporate the latest evidence on how to treat these conditions and to what appropriate targets. The clinician is referred to these guidelines for further guidance.

All patients at increased risk of ASCVD should be given advice and specific recommendations for eating a healthy diet. Advice should include9:

• matching energy intake with energy needs;
• eating a variety of fruits, vegetables, grains, low- or non-fat dairy products, legumes, fish, poultry, and lean meats;
• reducing saturated and trans fats to <10% of total daily caloric intake, through replacement with polyunsaturated fats (vegetables, nuts, seeds, and seafood);
• reducing cholesterol intake;
• reducing salt intake; and
• limiting alcohol intake to no more than two drinks per day for men and one drink per day for women.

• Low-density lipoprotein cholesterol (LDL-C) reduction decreases cardiovascular events.9
• Recommended target LDL-C level for patients stratified by ASCVD risk is as follows:

• Very high ASCVD risk: LDL-C <1.8 mmol/L, or a ≥50% reduction if the baseline is between 1.8 and 3.5 mmol/L (Table 3)
• High ASCVD risk: LDL-C <2.6 mmol/L, or a ≥50% reduction if the baseline is between 2.6 and 5.1 mmol/L
• Low-to-moderate ASCVD risk: LDL-C <3.0 mmol/L9

• Patients at low and moderate risk should be given advice and specific recommendations on lowering LDL-C through dietary adjustments, increased physical activity, and weight reduction. If the target is not met after 6 months, they should be given a lipid-lowering agent (Tables 4 and 5).35
• Patients at high risk should immediately be started on lipid-lowering therapy with a high-intensity statin (Tables 4 and 5).35 Importantly, however, pharmacokinetic studies have shown that Chinese patients achieve a higher plasma concentration of statin compared with Caucasians, and this may be associated with an increased risk of adverse effects.36 Consequently, the maximum approved doses of the statins available in Asia are around half the maximum approved doses in the United States.37 The clinician should, therefore, exercise caution when prescribing high-intensity statin therapy.
• Inhibitors of proprotein convertase subtilisin/kexin type 9 have recently been approved for use in the United Kingdom and the United States as an adjunct to diet and maximally tolerated statin therapy for the treatment of individuals with primary hypercholesterolaemia or mixed dyslipidaemia, or those with clinical ASCVD who require additional lowering of LDL-C.38 39 Clinical trials have demonstrated decreases in LDL-C by up to 60% in subjects receiving these agents38; definitive evidence of reduced cardiovascular event rates associated with their use may be provided by ongoing trials.

Although clear, evidence-based guidelines and recommendations for ASCVD prevention have been available for a number of years and are regularly updated, there is evidence that they are not routinely implemented in clinical practice.9 41 42 For example, Yusuf et al43 reported worldwide poor use of medications for the secondary prevention of ASCVD. Their study included 153 996 adults aged 35 to 70 years from rural and urban communities in high-, upper-middle–, lower-middle–, and low-income countries, 5650 of whom had had a self-reported CHD event and 2292 a stroke. Few individuals with ASCVD took antiplatelet drugs (25.3%), β-blockers (17.4%), ACE inhibitors or ARBs (19.5%), or statins (14.6%). As expected, drug use was higher in high-income countries, with 11.2% of patients in these countries not receiving any drugs compared with 45.1% of patients in upper-middle–income countries, 69.3% in lower-middle–income countries, and 80.2% in low-income countries. Notably, despite the relative accessibility of drugs for secondary prevention of ASCVD in high- and upper-middle–income countries, many patients remained untreated.

Of the patients who do receive treatment for ASCVD risk factors, only a few attain their treatment goals. Findings from the Hong Kong Cardiovascular Task Force Risk Management Programme indicate that 84% of enrolled hypertensive patients were treated with one or two antihypertensive drugs, most commonly ARBs (63.5%) and calcium channel blockers (47.2%; BMY Cheung, unpublished data). Similarly 64% of the diabetic patients were treated with metformin (68.8%) and/or gliptins (36%), while 78.1% of patients with dyslipidaemia were treated with a statin. Notably, however, treatment goals for hypertension (<130/80 mm Hg for diabetic patients, <140/90 mm Hg for non-diabetics) and diabetes (glycated haemoglobin <7%) were met by just over 50% of hypertensive patients and approximately 60% of diabetics.

Ensuring physician compliance with evidence-based guidelines and improving clinician understanding of factors affecting patient compliance with treatment may be the key to decreasing ASCVD risk in the Hong Kong population.

The present update of the 2008 Consensus Statement introduces the use of the new American Pooled Cohort Risk Assessment Equations that have superseded the Framingham Risk Evaluation; ASCVD risk can be assessed using either these equations or the European SCORE system to stratify patients into low-, moderate-, or high-risk categories to aid targeting of therapies as well as the establishment of suitable treatment goals. The risk factor reduction goals for hypertension and dyslipidaemia have been updated to reflect the most current recommendations from the Eighth Joint National Committee, the European guidelines on the management of arterial hypertension, and the European guidelines on cardiovascular disease prevention in clinical practice. The HDL-C target included in the 2008 Consensus Statement has been omitted from the current update as increased HDL-C has not been proven to reduce ASCVD risk.

The development of ASCVD in at-risk patients may be slowed and/or prevented by lifestyle modification, reduction of metabolic risk factors, and pharmacological treatment. The clinician plays a central role in ASCVD prevention—identifying at-risk patients, calculating the total ASVCD risk score, encouraging lifestyle changes, and providing targeted interventions to achieve specific treatment goals. Nonetheless, it is vital that the clinician is not overly focused on the treatment of isolated ASCVD risk factors but should instead adopt a ‘whole-person’ approach to diagnosis and therapy. Many patients present with multiple risk factors and, therefore, individualised, nuanced patient evaluation and management is essential to achieve optimum outcomes. Finally, none of these interventions will result in ASVCD prevention without the cooperation of the patient. Clinicians are encouraged to build strong partnerships with their patients, with the aim of establishing individual ownership of their treatment plans and, thus, improved treatment compliance.

The authors would like to acknowledge Ms Lianne Cowie and Dr Jose Miguel (Awi) Curameng of MIMS (Hong Kong) Limited for providing editorial and writing support, which was funded by Pfizer Corporation Hong Kong Limited. The meetings during which these consensus points were formulated and discussed were supported by an unrestricted educational grant from Pfizer Corporation Hong Kong Limited.

Source of support: Editorial and writing services, and the meetings during which these consensus points were formulated and discussed, were supported by an unrestricted educational grant from Pfizer Corporation Hong Kong Limited.

1. Goff DC Jr, Lloyd-Jones DM, Bennett G, et al. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;129(25 Suppl 2):S49-73. Crossref

2. Yusuf S, Reddy S, Ounpuu S, Anand S. Global burden of cardiovascular diseases. Part I: general considerations, the epidemiologic transition, risk factors, and impact of urbanization. Circulation 2001;104:2746-53. Crossref

3. Cheung MY, Ong KL, Tso WK, Lam TH, Lam SL. Increasing prevalence of hypertension in Hong Kong Cardiovascular Risk Factor Prevalence Study: role of general and central obesity. Proceedings of the 16th Medical Research Conference; 2011 Jan 22; Department of Medicine, The University of Hong Kong, Hong Kong. Hong Kong Med J 2011;17(Suppl 1):16S.

4. Roth GA, Huffman MD, Moran AE, et al. Global and regional patterns in cardiovascular mortality from 1990 to 2013. Circulation 2015;132:1667-78. Crossref

5. Cheung MY, Chow CC, Chu DW, et al. The Hong Kong Cardiovascular Task Force. Towards cardiovascular disease protection. Consensus statement on preventing cardiovascular disease in the Hong Kong population. Med Prog 2008;35:473-9.

6. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63(25 Pt B):2889-934. Crossref

7. Mancia G, Fagard R, Narkiewicz K, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J 2013;34:2159-219. Crossref

8. James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA 2014;311:507-20. Crossref

9. Piepoli MF, Hoes AW, Agewall S, et al. 2016 European guidelines on cardiovascular disease prevention in clinical practice: The Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of 10 societies and by invited experts) developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR). Eur Heart J 2016;37:2315-81. Crossref

10. Collins GS, Altman DG. Predicting the 10 year risk of cardiovascular disease in the United Kingdom: independent and external validation of an updated version of QRISK2. BMJ 2012;344:e4181. Crossref

11. QRISK2. Available from: https://www.qrisk.org/2016/. Accessed 9 Jan 2017.

12. Scandinavian Simvastatin Survival Group. Randomized trial of cholesterol lowering in 4,444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994;344:1383-9.

13. Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med 1995;333:1301-7. Crossref

14. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:837-53. Crossref

15. Retinopathy and nephropathy in patients with type 1 diabetes four years after a trial of intensive therapy. The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. N Engl J Med 2000;342:381-9. Crossref

16. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71-86. Crossref

17. US Department of Health and Human Services. The health benefits of smoking cessation. Washington DC: US Department of Health and Human Services; 1990.

18. Taylor R, Brown A, Ebrahim S, et al. Exercise-based rehabilitation for patients with coronary heart disease: systematic review and meta-analysis of randomized controlled trials. Am J Med 2004;116:682-92. Crossref

19. Prevention of cardiovascular disease. Guidelines for assessment and management of cardiovascular risk. Geneva, World Health Organization; 2007.

20. American Diabetes Association. Standards of medical care in diabetes—2014. Diabetes Care 2014;37(Suppl 1):S14-80. Crossref

21. The Hong Kong reference framework for diabetes care for adults in primary care settings. Available from: http://www.pco.gov.hk/english/resource/files/RF_DM_full.pdf. Accessed 1 Dec 2014.

22. Rydén L, Grant PJ, Anker SD, et al. ESC guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD: the Task Force on diabetes, pre-diabetes, and cardiovascular diseases of the European Society of Cardiology (ESC) and developed in collaboration with the European Association for the Study of Diabetes (EASD). Eur Heart J 2013;34:3035-87. Crossref

23. Wang C, Collet JP, Lau J. The effect of Tai Chi on health outcomes in patients with chronic conditions: a systematic review. Arch Intern Med 2004;164:493-501. Crossref

24. WHO Expert Consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. Lancet 2004;363:157-63. Crossref

25. International Diabetes Federation. The IDF consensus worldwide definition of the metabolic syndrome. Available from: http://www.idf.org/webdata/docs/MetSyndrome_FINAL.pdf. Accessed 10 Jul 2015.

26. West R, McNeill A, Raw M. Smoking cessation guidelines for health professionals: an update. Health Education Authority. Thorax 2000;55:987-99. Crossref

27. National Institute for Health and Clinical Excellence. Hypertension in adults: diagnosis and management. NICE guideline (CG127). August 2011. Available from: https://www.nice.org.uk/guidance/cg127. Accessed 10 Jul 2015.

28. National Institute for Health and Clinical Excellence. Type 2 diabetes: The management of type 2 diabetes. NICE guideline (CG87). May 2009. Accessed 10 Jul 2015.

29. National Institute for Health and Care Excellence. Chronic kidney disease in adults: assessment and management. NICE guideline (CG182). July 2014. Accessed 10 Jul 2015.

30. Shen L, Shah BR, Reyes EM, et al. Role of diuretics, β blockers, and statins in increasing the risk of diabetes in patients with impaired glucose tolerance: reanalysis of data from the NAVIGATOR study. BMJ 2013;347:f6745. Crossref

31. Bangalore S, Parkar S, Grossman E, Messerli FH. A meta-analysis of 94,492 patients with hypertension treated with beta blockers to determine the risk of new-onset diabetes mellitus. Am J Cardiol 2007;100:1254-62. Crossref

32. Messerli FH, Bangalore S. Half a century of hydrochlorothiazide: facts, fads, fiction, and follies. Am J Med 2011;124:896-9. Crossref

33. Williams B, MacDonald TM, Morant S, et al. Spironolactone versus placebo, bisoprolol, and doxazosin to determine the optimal treatment for drug-resistant hypertension (PATHWAY-2): a randomised, double-blind, crossover trial. Lancet 2015;386:2059-68. Crossref

34. National Institute for Health and Care Excellence. Cardiovascular disease: risk assessment and reduction, including lipid modification. NICE guideline (CG181). July 2014. Accessed 10 Jul 2015.

35. Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90 056 participants in 14 randomised trials of statins. Lancet 2005;366:1267-78. Crossref

36. Tomlinson B, Hu M, Zhang Y, Liu ZM, Chan P. Response to the letter “No evidence to support high-intensity statin in Chinese patients with coronary heart disease”. Int J Cardiol 2016;209:192-3. Crossref

37. Liao JK. Safety and efficacy of statins in Asians. Am J Cardiol 2007;99:410-4. Crossref

38. Everett BM, Smith RJ, Hiatt WR. Reducing LDL with PCSK9 inhibitors—the clinical benefit of lipid drugs. N Engl J Med 2015;373:1588-91. Crossref

39. Mayor S. NICE recommends PCSK9 inhibitors for patients not responding to statins. BMJ 2016;353:i2609. Crossref

40. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes, 2015: a patient-centered approach: update to a position statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 2015;38:140-9. Crossref

41. Ma J, Sehgal NL, Ayanian JZ, Stafford RS. National trends in statin use by coronary heart disease risk category. PLoS Med 2005;2:e123. Crossref

42. Pearson TA. The prevention of cardiovascular disease: have we really made progress? Health Aff (Millwood) 2007;26:49-60. Crossref

43. Yusuf S, Islam S, Chow CK, et al. Use of secondary prevention drugs for cardiovascular disease in the community in high-income, middle-income, and low-income countries (the PURE Study): a prospective epidemiological survey. Lancet 2011;378:1231-43. Crossref