BIDA Journal May2017 A4x28pp FINAL...Dr S Kumar Dr P Sarkar Dr S Sarker Mr C Selvasekar Dr S Senapati Any photographs offered for publication become the property of BIDA Journal and

The Journal of theBritish International Doctors’ AssociationIssue No.2, Volume 23. May 2017 Edition www.bidaonline.co.uk

Chest PainGood history takingis vital to diagnosis

Necrotizing FasciitisStrategies for management

SepsisThe biggest, least well-known killer

Mental Capacity ActNew developments, overview and facts

Novel Oral AnticoagulentsCase Report

When you’ve passed, book a place at thefree Welcome to UK practiceworkshop

There are huge differences in practising medicine in my home countryand the UK, and this session helped me realise that.

One of the most interesting courses that I have ever attended

You are invited to a freehalf-day workshop calledWelcome to UK practice.

Are you takingPLAB part 2?

If you are a new doctor, or a doctor whois new to working in the UK, theworkshop will help you understand theethical issues that will affect you andyour patients on a day-to-day basis.

What does the workshop cover?■ Find out about the role of the General Medical Council, including the standards that all doctors working in the UK need to follow.

■ Learn from the real life experiences of other doctors through the video Things I wish I’d known.

■ Work through interactive scenarios on the issues regularly faced by doctors new to working in the UK, including consent, confidentiality, raising and acting on concerns, caring for patients aged 0–18 years, and prescribing.

■ Use your own learning log to capture tips and reflections to take away with you.

How does the workshop help you?Over 1,000 doctors have taken part in theworkshop across the UK and feedback hasbeen universally positive. From a sample ofdoctors attending the programme:

■ 98% of doctors said it helped them to reflect on their practice

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Book your place!We hold sessions every month across theUK. Events are very popular and places goquickly!

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Issue No.2, Volume 23 May 2017 BIDA Journal www.bidaonline.co.uk 3

Contents

BIDA National Chairman’s Report......................4

BIDA Fellowships 2017...............................................4

BIDA National Secretary’s Report......................5

BIDA 2017 AGM Anouncement.........................6

BIDA GP Forum Chairman’s Report.................6

Chest Pain. A good history takingis vital for diagnosis.........................................7 –9

Acute Coronary SyndromesA review........................................................... 10 – 13

A case of Atrial Fibrillation with focuson Novel Oral Anticoagulents............14 – 16

Medical Quiz –Questions......................................16

Mental Capacity Act:New developments, overviewand interesting facts.............................................17

Sepsis: The biggest,least well-known killer?............................18 –21

Necrotising Fasciitis:Strategies for management...............22 –24

BIDA Divisional News..............................................25

BIDA Achievements..................................................25

BIDA Sports Events....................................................25

Erratum.............................................................................25

Medical Quiz –Answers.........................................26

BIDA National Elections 2017Article and Application Form............26 –27

GMC’s PLAB Advertisement.............................28

BIDA JournalEditorial Committee:Co-EditorsMr A SinhaDr A DhawanMembers:Dr S AryaDr B DasDr C KannegantiDr S KumarDr P SarkarDr S SarkerMr C SelvasekarDr S Senapati

Any photographs offered for publication become the property ofBIDA Journal and unfortunately cannot be returned.

Editorial Address:6 Castle Rise, Hawarden,Deeside, Flintshire CH5 3QUE-mail: [email protected] [email protected]: www.bidaonline.co.uk

Produced on behalf of theBritish International Doctors’ Association by:

Graphic Design & Digital Artwork:Nick Sample D&AD8 Fairways, Appleton, Cheshire WA4 5HAPhone: 0795 033 2645 E-mail: [email protected]: www.nicksample.com

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Any views or opinions that may be expressed in articles or letters appearing in BIDA Journal are those of the contributor and are not to be construed as an expression of opinion in behalf of the Editorial Committee or BIDA.Members are asked to ensure that all enquiries and correspondence relating to membership or other matters are sent directly to ODA House, 316A Buxton Road, Great Moor, Stockport SK2 7DD. (T: 0161 456 7828 F: 0161 482 4535) and not to BIDA Journal.

who show signs of sepsis with the same urgencygiven to those who complain of chest pain that mightbe a heart attack. There are around 150,000 casesof sepsis in the UK every year and it kills around40,000 people a year. NICE published its firstguidance on recognising, assessing and diagnosingsepsis last year. As doctors there is heavy relianceon the systematic inflammatory response (SIRS)criteria. But some, such as those taking steroids andimmunosuppressants will not display the expectedsigns. Therefore, we must be aware of the Sepsis -3definition: quick sepsis related organ failureassessment (qSOFA).

Finally, we would like to thank all our readers forsending us messages congratulating on our firstedition. It is always a great feeling when the hardwork that you have put in is appreciated.

We promise to keep on this good work and aspireto come up with interesting, informative and thoughtprovoking editions.

Best wishes

Ashish Dhawan & Amit SinhaJoint-Editors, BIDA Journal

Over the next few weeks our country is going tovote again and will choose a new government. Thisnew government will decide the direction of travelas to whether we go for a soft or a hard Brexit. Thiswill have a significant impact on the structure andworkforce of our NHS.

The on-going recruitment crisis for frontline healthcare staff could get much worse. Over the last manydecades, IMGs have made huge contributiontowards the NHS and healthcare in the UK andcontinues to do so. It is high time that the newincoming government appreciates this contributionfrom the IMGs. BIDA as an organisation shouldcontinue to pressurise government to ensure thatIMGs are not at a loss as a result of Brexit.

This edition of BIDA has cardiology theme to it.Advancing medical technology has significantlyimproved patient care and improved patientoutcomes. Due to the easy availability of verysensitive and hi tech diagnostic tools, good historytaking and clinical examination has virtually becomea dying skill.

In this edition, our article on differential diagnosis ofchest pain serves as a reminder that medicaltechnology and clinical skills should go hand in hand.Under the current climate of limited resources, thiseven becomes more relevant by cutting down theneed for unnecessary investigations and henceforthsaving money for cash strapped NHS.

The article on “Sepsis” presents in detail guidancefor health professionals of the possibility of sepsis inall patients who may have infection and treat those

BIDA Journal

EditorialMr. Amit SinhaFRCS (Trauma & Ortho)

Co-Editor, BIDA Journal.Consultant Orthopaedic Surgeon,

Glan Clwyd Hospital(North Wales NHS Trust)

Dr. Ashish Dhawan MD, MRCP

Co-Editor, BIDA Journal.Consultant Cardiologist &

Cardiac Electro Physiologist,Wigan Royal Infirmary

Welcome to new BIDA membersName Membership No.. . . . . . . . . . . . . . DivisionDr Ajay Mahajan 10484. . . . Nottingham & North TrentMr B K Jha 10485. . . . . Merseyside and CheshireDr N Prasad 10486. . . . . Merseyside and CheshireMrs A Prasad 10487. . . . . Merseyside and CheshireDr Ravish Katira 184. . . . . . . . . . . . . . . . . . . Wigan (Life Member)Dr Ira Katira 185. . . . . . . . . . . . . . . . . . . Wigan (Life Member)Dr Ajay Mudugal 10488. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . WiganDr Saibal Ganguly 10492. . . . . . . . . . . . . . . . . . . . . . WolverhamptonDr Abir Doger 10493. . . . . . . . . . . . . . . . . . . . . . . . . . . . . BirminghamDr Sujeeth Mangarai 10494. . . . . Merseyside and CheshireDr Manisha Mangarai 10495. . . . . Merseyside and CheshireDr Srinivas Rao Mangarai 10496. . . . . . Merseyside and Cheshire

Name Membership No.. . . . . . . . . . . . . . DivisionDr Rahul Kumar 10497. . . . . . Merseyside and CheshireDr M Vaswani 10498. . . . . Merseyside and CheshireDr Chakrapani 10499. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . North EastMr Samuel Vara P Prasad 10500. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . EssexDr M Garg 10501. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . BlackburnMr N Attanayake 10502. . . . . . . . . . Stoke-on-Trent & StaffsDr J Shibu 10503. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . BlackburnMr R Shah 10504. . . . . . . . . . . . . . . . . Preston & ChorleyMr Suresh Kanga 10505. . . . . Merseyside and CheshireDr V Sharma 10506. . . . . Merseyside and CheshireDr M Qasim 10507. . . . . . . . . . . . . . . . . . . . . . WolverhamptonDr SAJ Bukhari 10508. . . . . . . . . . . . . . . . . . . . . Wolverhampton

British International Doctors’ Association Issue No.2, Volume 23 May 20174

Dr Chandra KannegantiNational Chairman, BIDA

Dear Colleagues,

NHS is going through a difficult time with huge deficits in both primaryand secondary care services together with recruitment issues. The currentGP crisis is worsening with a number of GP practices closing every monthacross the U.K. GP Forward View package is considered by the NHSEas rescue package for the current crisis, but it is proving to be hard todeliver across the nation. BIDA is actively involved in a number of GPForward View schemes particularly around the planned recruitment of500 international doctors. We have offered mentorship and support forthe international doctors, who are planning to come to the U.K.

I am looking forward to the ARM 2017 in October, which will be hostedby the Rochadale and Bury Division. Preparations are going on well andwe are awaiting confirmation of the full program. We have invitedesteemed guest speakers, who have given their confirmation for theARM. Please look out for the forms for the ARM 2017, which will be sentin the next few weeks.

BIDA’s International Congress in Argentina and Brazil is now completelyfilled and the program for the congress is being finalized. We hope to havean outstanding international congress in October 2017.

There is lot of activity among BIDA Divisions and I would like to commendthe divisions of the enthusiasm and participation. We are encouraging

some new divisions to form and any proposal for new divisions will get fullsupport from National Executive.

BIDA continued to work with all key stakeholders including GMC, CQC,NHSE, and RCGP. We have been invited by the RCP to meet them abouttheir work on college examinations and a meeting date is being finalised.We are working with BMA on a number of national issues.

BIDA’s National elections are due now and nomination forms have beensent to all registered members. I hope a good number of members willput forward their nominations to represent the members.

It is with great sadness I would like to pay my homage to our beloved officemanager Pauline Gahan, who has died after a brave fight with cancer.BIDA officers attended her funeral on the 19th of May. This is a big loss toour organisation and BIDA will always remember the services of Paulineto our organisation.

Please continue support to our organisation, your local divisions and wecan continue to work for the equality and justice for all doctors in NHS.

Dr Chandra Kanneganti National Chairman, BIDA

National Chairman’sR E P O R T

BIDA

Dear Colleagues,

As you know BIDA awards ‘Fellowships’ to some members who have made anoutstanding contribution to the Association. These awards are made at theARM/AGM in the Autumn and if you would like to nominate a member from yourdivision, please do so, but kindly note that nominations are to be received no laterthan Friday 30th June 2017.

It would be of assistance if the nomination could be supported by a brief CV of thenominee.

I look forward to receiving your nominations.

Yours sincerely

Dr Sabyasachi SarkerNational President – BIDA

President: Dr Sabyasachi Sarker Chairman: Dr Chandra Kanneganti General Secretary: Mr P K Sarkar Treasurer: Dr Birendra K Sinha“ODA House” 316A Buxton Road Great Moor Stockport SK2 7DD Telephone: 0161 456 7828 Fax: 0161 482 4535 Email: [email protected] Website: www.bidaonline.co.uk

BIDA FELLOWSHIP AWARDS 2017


Mr Pranab K SarkarNational General Secretary, BIDA

Dear members,

This October, I will be completing 3 years of myterm as the National General Secretary. I wouldlike to take this opportunity to thank all NECmembers and in particular Dr S Sarker, ourPresident, Dr C Kanneganti, National Chairmanand Dr B K Sinha, National Treasurer for theiradvice and support. I would also thank themembers of the NEC for their hard work and thecontributions to our association over the past year.

It has been a very busy year since my last annualreport. Our Chairman has remained committedto working in collaboration with various nationalorganisations e.g. RCGP, DH, GMC, and BMAetc. and in the process he has been able tosuccessfully raise our profile nationally.

You will be pleased to know that last year a recordnumber of new members have joined BIDA. Thissurge in membership has been mainly due to anumber of high profile Leadership workshops andthe Annual Cancer Conference organised onbehalf of BIDA. I would be failing in my duties if Ido not acknowledge the contributions made by DrVinod Gadiyar, Dr Umesh Prabhu, Mr SibaSenapati, Mr C R Selvasekar, Dr Raghuraman andtheir teams for hosting these events. BIDA shouldcontinue to support high profile activities thatwould encourage new BME doctors to BIDA.

During the year, some of our members wereaffected by a technical hitch in the IT system at thecentral office. We tried our very best to resolve thematter as soon as this was detected. However, onbehalf of BIDA, I would like to give my sincereapologies to our members for the inconveniencecaused. I have serious concerns about some of ourdivisions which are struggling to remain active andto keep the members engaged. BIDA needs acollective approach in order to remain connectedwith these divisions. Otherwise, we will run the risklosing them.

Our last ARM/AGM in October 2016 hosted bythe Stoke & Staffordshire division was a hugesuccess. I would like to thank Dr Vellaturi, theconvenor and the entire organising team for theirhard work. This year’s ARM/AGM, on 13-15October 2017, will be hosted by the Rochdale &Bury division. Our convenor, Dr Vinod Gadiyarand his team in collaboration of the central officestaff are working very hard to make thisARM/AGM a successful one. I would urge alldivisions to participate in this important annualevent of BIDA and take the opportunity to havetheir voices heard.

BIDA 12th International congress in 2016 inSouth Africa was highly entertaining and success-ful. This year in October, BIDA is organising aspecial International Congress in South America.Our President, Dr S Sarker, has volunteered toconvene of the forthcoming congress, which hasbeen oversubscribed long before the closingdate.

This is our election year when our members willget an opportunity to elect National EC officebearers for the year 2017-2020. I wouldencourage you all to get involved and influencethe decision making of BIDA.

We all remain concerned about a number ofNHS issues that are relevant to all BME doctors.Although, we would welcome the publication ofNext steps on the NHS five year forward viewand in particular its support for a more integratedhealth and social care system, we remainconcerned that this ambitious plan will bechallenging to deliver unless the chronic under-funding issue is resolved first. BIDA should remindthe DH that professionals cannot be expected todeliver more high quality service for less fundingand demand that the NHS England must urgentlyaddress these problems.

Last year BIDA fellowship was awarded to fivemembers for their contributions to the organisa-tion. As a nationally recognised nominating body,BIDA was also pleased to nominate five membersfor the prestigious NHS ACCEA award.

Dr Sanjay Arya, who recently stepped down fromthe post of the editor of BIDA Journal after 6 yearsof service, deserves our sincere thanks for raisingthe standard of the Journal over the past 6 years.The new co-editors of the Journal, Mr Amit Sinhaand Dr Ashish Dhawan have promised to raise thestandard further to a new height. In their pursuit, Iwould request you to support them by submittingarticles and divisional news for publication. I wouldalso request you to contribute to BIDA websitewhich is a readily available source of informationon BIDA matters.

Dr Raghu Hegde, our national sports coordinator,has been doing a marvellous job in coordinatingBIDA President Cup Cricket Tournament andBIDA Annual Badminton & Table TennisChampionship. I would like to thank him for all hishard work.

It is with great sadness, I report the passing awayof Pauline Gahan, our central office Manager whomade a very positive contribution to the runningof the central office over the past five years. We allwill miss her very badly. I send my heartfeltcondolences to her bereaved family.

Finally, I would like to take this opportunity to thankAlison and Julie our central office staff as withouttheir support it would not have been possible torun this responsible office.

Mr Pranab K SarkarNational General Secretary, BIDA

National General Secretary’sA N N U A L R E P O R T

BIDA

Notice is hereby given that the42nd Annual General Meeting of theBritish International Doctors’ Associationwill be held onSunday 15th October 2017at theThe Last Drop Village Hotel, Bromley Cross, Bolton, BL7Hosted by BIDA’s Rochdale and Bury Division. Convenor: Dr Vinod Gadiyar.

(All fully paid members are cordially invited to attend, but please note that prior notification to Central Office is required).

BIDA A.G.M. 2017


Dr Surendra KumarG.P. Forum Chair, BIDA

In this issue, I would like to highlight the contractual changes that have been addedto the GP’s contract for 2017/18 and to the hospitals contract 2017-2019.GP’s Contract Changes 2017/18

l Avoiding Unplanned Admissions (AUA) directed enhanced services:NHS England has agreed that AUA DES will be discontinued on the 31st March 2017 and the money £1.567 million will be added to the global sum automatically. GP’s would not need to claim them by any claim forms.

l CQC Fees:For the very first time GPC has been able to negotiate and secure full reimbursement of CQC fees for 2017/18.

l Indemnity fee rises: Once again, for the very first time GPC has secured £30 million to cover the rises in indemnity costs for the year 2017. The rises will be paid to practices on per patient basis. The rises have been based in the information received from medical defence organisations. As the money is going to be paid directly to the practices, the practices will have to ensure that this money does not only go to the partners, but it is also divided to reach the salaried GP as well as locum GP’s.

l Expenses and pay uplift: I am also pleased to report that NHSE has agreed to fund the expenses that should deliver a pay uplift of 1%, which will be added to the global sum. I accept that many GP’s would have wanted to see a higher uplift but I’m afraid that this was the best that could be achieved during this year’s negotiations, particularly keeping in mind the Government’s stand on public services pay.

l Sickness reimbursement: This would really come as very welcome news to the majority of GPs. NHSE has agreed to significantly improve GP’s sickness cover reimbursement. Payments will be made after two weeks of a GP being absent from the practice due to sickness. Additional benefit is that NHSE will have no objection if the existing GP’s in the practice provide this cover. The amount for sickness cover has also been increased to £1734.18 per week.

l Maternity payments: From this year onwards these will not be calculated on a pro-rata basis. To claim this the practices will need to submit the invoice.

l Learning Disability DES: NHSE has agreed that this DES payment will increase from £116.00 to £140.00 for every health check that will be performed by the GPs.

l Extended Hours DES: It has been a matter of concern to NHSE that there are some practices which regularly close the surgeries for half days and yet are being paid under the extended hours DES to offer additional appointments. GPC has agreed that from this year onwards this should not normally be allowed. However, there are going to be some exceptions e.g. some branch surgeries. In any case, no changes will be made to this until October 2017.

l Access to Healthcare: Under this initiative the Government would be able to identify patients who have used the NHS with a non-UK issued EHIC so that NHS can reclaim the fees for hospital treatment from the country of origin with which the UK has reciprocal arrangements. For this extra workload, NHSE will add £5 million to the global sum of the practice.

l GP Retainers Scheme: From 2017 onwards a new GP retainer’s scheme has been agreed with significant improvements and greater funding than the previous one.

All these changes with further details can be viewed on BMA website.

I’m sure you would all like me to congratulate GPC for negotiating these substantialimprovements to the GP contract.

Hospital Contract 2017/18

For a long time, GPC has been concerned that the hospitals regularly transfer theirworkload to the General Practitioners without any additional resources. Keeping

New contracts for GPs and Hospitals

this in mind, and also looking at the pressures and sustainability in General Practice,the NHSE has agreed with GPC to introduce new changes to the 2017-2019hospital contracts.

The important changes are as follows:

l Hospitals to issue sick notes, covering the full period until the date by which it is expected that the patient will have recovered and not only for the period that the patient was in hospital

l Hospital trusts to respond to patient queries for matters relating to their care for which that patient is already under them. They will not be able to ask the patients to contact their GP and instead be contractually obliged to respond to these queries themselves.

This will require a change in the culture and attitude. We know that it is often when hospitals pass on the queries regarding hospital test results, treatments and investigations and issues regarding follow up or delays in appointments etc to the GP. Under the new contract the hospital trusts will have to respond to the patients themselves and not ask the patient to speak to their referrer.

l Hospitals must not transfer management under shared care unless with prior agreement from the GP.

It will be no more acceptable for the consultants to write to GPs asking to prescribe medications unless a proper shared care agreement has been agreed by the GP.

l Hospital clinic letters to be received by the GP within ten days from 1st April 2017 and within 7 days from April 2016.

l Issuing medication following outpatient’s attendance – it will be the hospitals responsibility to issue enough medication to meet the patient’s immediate clinical needs until their GP has received the clinic letter.

Please remember that these are not recommendations from NHSE but contractualrequirements and if the hospitals do not abide by these standards, they are inbreach of their contract.

As I’ve said earlier, this is part of the hospital culture that has been followed for along time and it will take some time for them to realise that they can’t do thisanymore. It is a responsibility of every GP, every LMC and every CCG to remindthe hospitals of their contractual obligation and in the event of this not happening,CCG’s will be entitled to give the hospitals the notices of remedial action ifnecessary which may include financial sanction.

Finally

As I’m sure you are all aware that on Friday 12th May 2017, a ransomwarecampaign relating to version two of the ‘WannaCry’ malware affected a wide rangeof organisations globally. In the UK, it had a major impact on NHS and we knowthat at least 341 surgeries were affected by this virus. We understand that the virusattacked systems which were vulnerable and where updates were not applied onwindows operating systems. The reason could be that these were obsoleteoperating systems or that these were not supported in the security setting byCCGs/PCTs. It has been a matter of major concern not only to the doctors butalso to the patients and it could potentially compromise patients care and security.

To take this matter forward GPC will soon be meeting NHSE. I would hope toreport the progress of this to you in future issue of the BIDA journal.

I have no doubt that many GPs will experience some difficulties due to these newchanges but I’m sure, that once the teething problems have been resolved, boththese contracts will bring substantial benefits to the GP.

Dr Surendra KumarGP Forum Chairman, BIDA

GP Forum Chairman’s R E P O R T

BIDA


What is pain?The International Association for the Study of Pain's widely useddefinition states: "Pain is an unpleasant sensory and emotionalexperience associated with actual or potential tissue damage, ordescribed in terms of such damage” (1). Pain involves a number ofcomplex pathways including peripheral nerves, spinal cord tracts andthe central nervous system. Sometimes pain arises in the absence ofany detectable stimulus,

Chest painChest pain is a common complaint but it is often difficult to reach a firmdiagnosis as it can be a symptom due to numerous differentpathologies. Chest pain can originate from several sites: the heart andrelated structures, major blood vessels, pleura, gastro-esophagealtract, muscles and bones. Furthermore anxious patients can complainof chest pain as manifestation of underlying anxiety.

Chest pain is seen commonly in all aspects of health care. It accountsfor approximately six million annual visits to emergency departmentsin the United States, making chest pain the second most commoncomplaint (2) after abdominal pains.

A study looking at primary care presentations found that 1.5% ofprimary care consultations are for chest pain, but only 17% of these areassociated with possible angina (3).

A thorough history is therefore essential to understand the etiology ofchest pain. This should help avoid unnecessary and invasiveinvestigations.

Previous history – such as previous coronary artery disease

Risk factors – e.g. smoking, diabetes, hypercholesterolemia, familyhistory, hypertension, obesity

Common causes of chest painu Cardiac

Acute coronary syndrome: this includesunstable angina (UA), non ST segmentelevation (NSTEMI) myocardial infarction andST segment elevation myocardial infarction(STEMI).

Myocardial infarction occurs when bloodflow to the heart is limited by an athero-sclerotic plaque and this causes damage

to the heart muscle. Pain is usually inthe center or left side of the chest

and it can travel into left shoulder, arm, neck or jaw. It is often describedas tightness or a heaviness which occurs at rest in the majority of cases.It lasts more than 15 minutes (after this time risk of myocardial necrosisincreases). The associated symptoms include sweating, shortness ofbreath, nausea, dizziness and palpitations (4). Levine’s sign has beendescribed as a clenched fist held over the chest whilst describingcardiac chest pain.

Hospital attendance is required and assessment with history, ECG(electrocardiogram) and cardiac enzymes (Troponin) for diagnosis.

The National Institute of Clinical Assessment guidelines (5) from 2016define typical anginal chest pain as: -

u Constricting discomfort in the front of the chest, or in the neck,shoulders, jaw or arms.

u Precipitated by physical exertion.u Relieved by rest or GTN within about 5 minutes.

Presence of three of the features aboveis defined as typical angina, two of thethree as atypical angina and if nofeatures are present as non-anginalchest pain.

Angina is a progressive conditionwhich requires treatment of the riskfactors such as high cholesterol,smoking and high blood pressure.Medical therapy is required in the firstinstance. Invasive angiography may berequired in some cases.

Dr Oliver McConnellCardiology St4 – North West Deanery

Dr Mellissa Bouchard Cardiology St4 – North West Deanery

Dr Ashish Dhawan Cardiology & Electrophysiology

Consultant – Wigan, Wrightingtonand Leigh NHS Foundation Trust

CHESTPain

A good history taking is vital for diagnosis

History of chest pain must include:u Location u Onset u Character u Radiationu Associated symptoms

u Change over the timeu Exacerbating & relieving factorsu Severityu Duration

ECG showing Anterior STEMI (Image courtesy Dr Smith’s ECG Blog)

NSTEMI ECG (Image courtesy LIFTL medical Blog)

(Source: Pinterest.com)


u Pericarditis

Inflammation of the pericardium - the most common cause is viralillness (following upper respiratory infection mainly) and idiopathicmaking up 90% of cases (6). The pain tends to be sharp, retrosternaland can radiate to the trapezium ridge. Lying flat or deep inspirationcan make the pain worse, and it tends to be relieved by sitting up andbending forward. Other symptoms of pericarditis may include drycough, fever and fatigue. On auscultation it sometimes possible to elicita pericardial rub. Specific ECG changes include ST elevation in allleads but often excluding aVR and V1.

u Vascular

Aortic dissection

Aortic dissection is relatively uncommon, but it often presents acutelyas a catastrophic illness with severe chest pain and acute hemodynamiccompromise. Early and accurate diagnosis and treatment are crucialfor survival. Acute aortic dissection can result in fatal complications,the mortality rate increases at the rate of 1% to 2% per hour withoutany treatment (7).

Dissection occurs when a tear in the inside of the aorta causes bloodto flow between the layers of the wall of the aorta, forcing the layersapart.

Most common presenting symptoms of acute aortic dissection areacute severe pain in the chest or back. Pain may be present alone, or itcan be present with syncope, signs of congestive heart failure, and signsof cerebrovascular accident or even mesenteric ischemia with abdom-inal discomfort. It is often described as a tearing pain, occurringsuddenly and with no variation in severity with posture or breathing (8).

Associated symptoms are vomiting, sweating, and lightheadedness.The symptoms can change as the dissection progresses.

Aortic dissection can occur after certain medical procedures such asangiograms, but the most common risk factors include uncontrolledhypertension, smoking and Marfan’s syndrome (9).

There are two major classification sytems for aortic dissection. TheStanford system is more widely used. It classifies dissections that involvethe ascending aorta as type A, regardless of the site of the primaryintimal tear, and all other dissections as type B.

Pulmonary Embolus

A clot found in one or more of the pulmonary arteries. The chest painis often pleuritic in nature, i.e. worse on deep inspiration and expiration.It is associated with shortness of breath and can have associatedhaemoptysis. It is often of sudden onset and in cases of large clots cancause cyanosis, collapse, and haemodynamic instability.

Diagnosis is based on history taking, risk factors, D dimers and CTpulmonary angiography.

Continued

(Source: Advanced critical care journal)

CHESTPain

Risk factors include: (10)

u Deep vein thrombosisu Immobilisation during hospitalisation or post-operativelyu Long haul flightu Pregnancyu Smokingu Obesityu Genetic factor: coagulopathu Intravenous drug useu Malignancyu Recent fracture of a long bone – predisposes to fat emboli.

(Source: Lifeinthefastlane.com)

9Issue No.2, Volume 23 May 2017 BIDA Journal www.bidaonline.co.uk

u Infection

Pneumonia

This is caused by infection and inflammation of the alveoli. The pain iscaused by the inflammation, and tends to be sharp or stabbing and getsworse during breathing or coughing i.e. pleuritic. It may be relieved bytaking shallow breaths. It is usually located over the area of infection. Ifthis occurs near diaphragm then the pain may be felt in other area suchas neck or shoulder as referred pain.

The most commonly associated symptoms are productive cough,shortness of breath, fever, loss of appetite and headache. There aremany causes of pneumonia and pneumonitis: bacteria, viruses, fungiand various chemicals.

u Musculoskeletal

Costochondritis

It is an acute and often temporary inflammation of the costal cartilage,which usually resolves spontaneously. It makes up 30% of all causesof musculoskeletal chest pain. Costochondritis causes chest pain feltat the front of the chest, typically sharp and stabbing in nature and worseon movement. Chest wall tenderness is present in 70% of cases. Thepain is usually confined to a small area but it can radiate to causewidespread pain. The management is with anti-inflammatory drugsboth non-steroidal and steroidal with some evidence sulphasalazinecan be helpful in recurrent cases (12).

u Gastric

Gastro-oesphageal reflex disease

This a chronic condition of mucosal damage caused by stomach acidregurgitating from the stomach into the esophagus. Heartburn is themain symptom of GORD. This is a burning sensation that radiates fromthe epigastrium or lower chest to the neck. Other common symptomsinclude nausea, acid taste in the mouth in the morning, bloating,belching and a burning pain when swallowing hot drinks. Thesymptoms tend to come and go, get worse after meals and are relievedby antacids or PPI. Chest pain from GORD is associated with obesity,hiatus hernia, caffeine, fatty and spicy food and alcohol. It is diagnosedmainly by history taking and examination. Invasive procedures such asOGDs are diagnostic.

References1. Bonica JJ. Derived from The need of a taxonomy. Pain. 1979;6(3):247–8.

2. Nawar EW et al. National Hospital Ambulatory Medical Care Survey:2005 Emergency Department Summary. Advance Data:2007, June 29(386):1-32

3. Nilsson S, Scheike M, Engblom D, et al. Chest pain and ischaemic disease in primary care.Br J Gen Pract. 2003;53:378–82..

4. National heart lung and blood institute. What Are the Signs and Symptoms of Coronary HeartDisease? September 29, 2014. Retrieved 25 May 2017.

5 National Institute for Clinical Excellence. “Chest pain of recent onset: assessment and diagnosis.November 2016. Clinical guideline 95.

6. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med. 2004; 351:2195.

7. Olsson C, Thelin S, Stahle E at al. Thoracicaortic aneurysm and dissection: increasing prevalenceand improved outcomes reported in a nationwide population-based study of more than 14,000cases from 1987 to 2002. Circulation. 2006;114:2611–2618.

8. Spittell PC, Spittell JA, Jr, Joyce JW, Tajik AJ, Edwards WD, Schaff HV, et al. Clinical features anddifferential diagnosis of aortic dissection: experience with 236 cases (1980 through 1990)Mayo Clin Proc. 1993;68:642–651.

9. Criado FJ . "Aortic dissection: a 250-year perspective". Tex Heart Inst J. 2011; 38 (6): 694–700.

10. Wells PS, Anderson DR, Rodger M et al. "Derivation of a simple clinical model to categorizepatients probability of pulmonary embolism: increasing the models utility with the SimpliREDD-dimer". Thromb Haemost. 2000 Mar;83(3):416-20.

11 Jordi A, Mateu, SP, Ignasi B. Risk factors for community-acquired pneumonia in adults:Recommendations for its prevention. Community Acquired infection. 2015 2(2): 32-37.

12. Wilson P, Watson P, Haythornwaite J et al. Clinical Pain Management Second Edition:Chronic Pain, Volume 2. 2008 Sept:554.

Common risk factors: (11)

u Smoking: destruction of cilia that sweep mucus out of the lungs.u Recent viral respiratory infections.u Swallowing difficulties: increased risk of aspiration.u Chronic lung diseases: increased risk of colonisation of bacteria and use of inhaled steroids and diabetes.

(Source: nethealthbook.com)

(Source: Myoclinic.org)


AbstractAcute coronary syndromes encompass a spectrum of conditions rangingfrom unstable angina through non ST elevation myocardial infarction andST elevation myocardial infarction.

This article provides an overview of the current concepts in the diagnosisand management of acute coronary syndromes in keeping with currentEuropean Society of Cardiology (ESC) recommendations and guidelines.

Key Wordsacute coronary syndrome, myocardial infarction, percutaneous coronaryintervention, cardiac troponins

IntroductionAcute coronary syndromes (ACS) encompass a spectrum of conditionsranging from unstable angina through non ST elevation myocardial infarc-tion and ST elevation myocardial infarction, although the common under-lying pathology is rupture of an atheromatous plaque with resultant partialor complete thrombosis of the infarct related artery. (Figure 1a and 1b)

Chest pain is the predominant symptom at presentation in patients withan ACS.

The electrocardiogram (ECG) at presentation differentiates the patientsinto two main groups:

1. Those with persistent (>20 minutes) ST-segment elevation (ST-elevation ACS). This reflects an acute total coronary occlusion, withmost patients ultimately developing an ST-elevation myocardialinfarction (STEMI). Immediate reperfusion by primary angioplasty orfibrinolytic therapy is the key treatment. (1)

2. Those with chest pain, but no persistent ST-segment elevation. TheECG changes at presentation may include transient ST-segmentelevation, transient or persistent ST-segment depression, T waveinversion, flat T waves or pseudo-normalisation of T waves. In somepatients the ECG may be normal.

The spectrum of clinical presentation varies from patients being symptomfree to patients with ongoing ischaemia, electrical and/or haemodynamicinstability or cardiac arrest.(2)

Universal Definition of Myocardial Infarction Acute myocardial infarction (MI) defines myocardial necrosis in a clinicalsetting consistent with acute myocardial ischaemia.

The detection of an increase and/or decrease of a cardiac biomarker, suchas high-sensitivity cardiac troponin, with at least one value above the 99thpercentile of the upper reference limit and at least one of the following arerequired to meet the diagnostic criteria of acute MI.

1. Symptoms of ischaemia2. New or presumed new significant ST-T wave changes or left bundle

branch block (LBBB) on 12-lead ECG3. Development of pathological Q waves on ECG4. Imaging evidence off new or presumed new loss of viable

myocardium or regional wall motion abnormality5. Intracoronary thrombus detected on angiography or autopsy.

Table 1 lists the types of MI.(3)

Diagnosis of ACSClinical Presentation

Angina in ACS may present at prolonged (>20 minutes) pain at rest, newonset angina class II or III of the Canadian Cardiovascular Society, CCSclassification), recent destabilisation of previously stable angina with at leastCCS III angina (crescendo angina) or post MI angina.(2)

Typical chest pain is characterised by retrosternal pressure or heavinessradiating to the left arm, neck or jaw and may be intermittent or persistent.This could be associated with sweating, nausea, abdominal pain, dyspnoeaand syncope.

Atypical presentations are observed in women, the elderly and in patientswith diabetes, chronic kidney disease or dementia.

Physical examination

Physical findings vary from frequently unremarkable findings to signs ofheart failure or haemodynamic/electrical instability, systolic murmur dueto ischaemic mitral regurgitation or aortic stenosis and rarely due to amechanical complication such as papillary muscle rupture or ventricularseptal defect.

Electrocardiogram

The resting 12-lead ECG is the first line diagnostic tool in assessing patientswith suspected ACS. The ESC guidelines recommend obtaining an ECG

AcuteCoronary Syndromes

Figure 1b:Pathology ofacute coronarysyndromes(courtesy ofAstra ZENECA)

Unstable Angina (UA)

Plaque rupture and thrombus formation

Non ST-elevation myocardialinfarction (NSTEMI)

ST-elevation myocardialinfarction (STEMI)

Figure 1a: Pathology of acute coronary syndromes (courtesy of Astra ZENECA)

Table 1: Types of acute MI

Type 1 MI Atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal coronary thrombus leading to decreased myocardial blood flow and/ or distal embolisation and myocardial necrosis

Type 2 MI An imbalance between myocardial oxygen supply and demand due to coronary artery spasm, coronary endothelial dysfunction, tachy/brady arrhythmias, anaemia, respiratory failure, hypotension and severe hypertension cause myocardial necrosis

Myocardial necrosis in critically ill patients and in those undergoing major non-cardiac surgery related to injurious effects of pharmacological agents and toxins

Type 3 MI MI resulting in death when biomarkers are not available

Type 4 MI MI related to percutaneous coronary intervention (PCI)

Type 5 MI MI related to coronary artery bypass grafting surgery (CABG)


within 10 minutes of the patient’s arrival in accident and emergency, or atfirst contact with emergency medical services pre-hospital and to interpretit by a qualified physician. The ECG may be normal in more than one thirdof patients.

Comparison with previous ECG tracings is useful in patients with pre-existing ECG abnormalities. Additional ECGs are recommended in caseof persistent or recurrent symptoms or diagnostic uncertainty.

ECG is of no help for the diagnosis of NSTEACS in patients with bundlebranch block or paced rhythm.

The finding of persistent ST elevation with suggestive symptoms and signsindicates STEMI and mandates immediate reperfusion.(1)

Biomarkers

Biomarkers, particularly high sensitivity cardiac troponins complementclinical assessment and 12-lead ECG in the diagnosis, risk stratificationand treatment of patients with suspected ACS. Measuring troponins ismandatory in all patients with suspected ACS.

In patients with MI, cardiac troponin levels rise rapidly, usually within 1 hourafter symptom onset and remain elevated for several days.

(Figure 2) illustrates the initial assessment of a patient based on acombination of likelihood features derived from clinical presentation,12-lead ECG and cardiac troponin. (2)

Table 2 illustrates the clinical implications of high-sensitivity cardiactroponins and table 3 illustrates conditions other than acute type I MIassociated with cardiac troponin elevation.

Rule in/ rule out algorithms

Higher sensitivity and diagnostic accuracy has enabled the shortening timeinterval to second cardiac troponin assessment for detecting acute MI atpresentation. The ESC recommends use of 0 hour and 3 hour algorithm(Figure 3).

Non-invasive imaging

Functional evaluation

Transthoracic echocardiography in an emergency setting is useful toidentify abnormalities suggestive of myocardial ischaemia or necrosis, suchas segmental hypokinesia or akinesia.

Echocardiography is useful to detect alternative pathologies associatedwith chest pain, including acute aortic dissection, pericardial effusion, aorticvalve stenosis, hypertrophic cardiomyopathy or right ventricular dilatationsuggestive of acute pulmonary embolism.

It is the diagnostic tool of choice for patients with haemodynamic instabilityof suspected cardiac origin. (4)

Cardiac magnetic resonance (CMR) can be used to assess both perfusionand wall motion abnormalities, as also to detect scar tissue (using lategadolinium enhancement) and differentiate this from recent infarction(using T2-weighted imaging to delineate myocardial oedema). CMR alsofacilitates the differential diagnosis between infarction, myocarditis or Tako-Tsubo cardiomyopathy.(5-7)

Anatomic evaluation

Multi-detector computed tomography (MDCT) is useful to assesscoronary arteries, with a normal scan ruling out coronary arterydisease.(8)

CT imaging can also exclude other causes of acute chest pain includingpulmonary embolism, aortic dissection and tension pneumothorax.(9)

Risk stratification

Quantitative assessment of ischaemic risk by scores has been shown tobe superior to clinical assessment alone. The GRACE risk score has beenproven to be the most accurate for risk stratification both on admissionand at discharge.(10, 11)

The GRACE 2.0 risk calculator (http://www.gracescore.org/WebSite/default. aspx?ReturnUrl=%2f) provides a direct estimation of mortality inhospital, at 6 months, 1 year and 3 years. The combined risk of death/MIat 1 year is also provided. (12)

Dr V J Karthikeyan MD MRCP (UK) FESC

Consultant CardiologistNorth Wales Cardiac Centre,

Rhyl, UK

Figure 2: Initial assessment of the patient (2)

Table 2: Clinical implications of high-sensitivity cardiac troponin assays

Figure 3: 0 / 3 hour rule-out algorithm of NSTEACS using high-sensitivity cardiac troponin assay (2)

u High negative predictive value for MIu Reduce the “troponin-blind” interval, allow earlier detection of acute MIu ~4% absolute & ~20% relative increase in detecting type I MI and decrease in the diagnosis of unstable anginau 2-fold increase in detecting type 2 MIu Levels are quantitative markers of cardiomyocyte damageu Elevations > 5-fold URL have high (>90%) PPV for acute type I MIu Elevations up to 3-fold URL limited (50-60%) PPVu Common to detect circulating levels in healthy individualsu Rising &/or falling levels differentiate acute from chronic cardiomyocyte damage

– a review


Treatment of ACSA rapid assessment of patients and risk stratification to identify those withongoing myocardial ischaemia and at risk of life-threatening arrhythmiasfor close surveillance and immediate corornary angiography is imperative.

Cardiac rhythm monitoring in coronary care unit or an intermediate careunit after an established diagnosis of NSTEACS is indicated in those withintermediate to high risk of cardiac arrhythmias.

Assessment of patients for bleeding using risk scores such as Can Rapidrisk stratification of Unstable angina patients Suppress ADverse outcomeswith Early implementation of the ACC/AHA guidelines (CRUSADE)(http://www.crusadebleedingscore.org) is recommended as major bleed-ing events are associated with increased mortality in NSTEACS.(13)

The Acute Catheterization and Urgent Intervention Triage strategY(ACUITY) bleeding risk score is another score that identified patients atincreased risk for non-CABG-related major bleeds at 30 days andsubsequent 1 year mortality. (14)

The ESC treatment algorithms for STEMI and NSTEMI are illustrated inFigure 4 and Figure 5 respectively. (2)

Treatment of ischaemia

Pharmacological treatment of ischaemia aims at reducing myocardialoxygen demand (related to a decrease in heart rate, blood pressure,preload or myocardial contractility) or increasing myocardial oxygen

supply (by administering oxygen or through coronary vasodilatation).

Oxygen administration is recommended when blood oxygen saturationis <90% or if the patient is in respiratory distress. Opiates for pain relief areindicated when ischaemic symptoms are not relieved with nitrates and betablockers.

Anti-platelet therapy

Aspirin and the P2Y12 class of drugs, including clopidogrel, prasugrel andticagrelor are the key agents used to achieve platelet inhibition in ACS.Cangrelor is an intravenous adenosine triphosphate (ATP) analogue thatbinds reversibly and with high affinity to the platelet P2Y12 receptor andhas a short plasma half life (<10 minutes). The anti-platelet agents aresummarised in table 4. (2)

Initiation of P2Y12 inhibitors is recommended as soon as a diagnosis ofNSTEMI is made, irrespective of the management strategy- whetherinvasive or conservative.

Dual anti-platelet therapy (DAPT) with aspirin and a P2Y12 inhibitor isusually given for a year following the index event. This is based on evidencefrom clinical trials with the latter agents. (15-17)

Glycoprotein IIb/IIIa inhibitors

Intravenous glycoprotein IIb/IIIa (GPIIb/IIIa) inhibitors block plateletaggregation by inhibiting fibrinogen binding to a conformationallyactivated form of the GPIIb/IIIa receptor on two adjacent platelets.(18)

GPIIb/IIIa inhibitors are limited to bailout situations or thromboticcomplications during percutaneous coronary intervention (PCI).

Anti-coagulation

During the acute phase, anti-coagulants inhibit thrombin generationand/or activity, hence reducing thrombus-related events, particularly inNSTEACS. They are more effective in combination with platelet inhibitorsthan either treatment alone. (19)

Unfractionated heparin (UFH) is used in the cardiac catheterisationlaboratory with monitoring of activated clotting time (ACT) and elsewherewith the activated partial thromboplastin time (aPTT).

Low molecular weight heparins (LMWH) are widely used in view of theirmore predictable dose-effect relationship than UFH and less frequentincidence of heparin induced thrombocytopaenia (HIT).

Oral anti-platelet agents in patients requiring long-term oral anticoagulants.

The ESC recommendations for patients admitted with an ACS and treatedwith oral anti-platelet agents, but who also require long term oral anti-coagulant therapy for non-valvular AF is summarised in Figure 6.

Invasive coronary angiography and revascularisation

Invasive coronary angiography followed by revascularisation if indicatedis the mainstay of treatment for patients presenting with an ACS. Thedecision to proceed with this strategy weighs the benefits of diagnosticaccuracy, risk stratification and risks related to revascularisation.

Coronary angiography allow clinicians to confirm the diagnosis of ACSrelated to obstructive epicardial coronary artery disease, and hence guideantithrombotic treatment; identify the culprit lesion(s), establish theindication for coronary revascularisation and assess suitability of thecoronary anatomy for PCI or CABG and finally, stratify the patient’s short-and long-term risk.

AcuteCoronarySyndromes– a review (continued)

Figure 4: ESC treatment algorithm for STEMI (2)

Figure 5: ESC treatment algorithm for NSTEMI (2)


The strategy and timing according to initial risk stratification is illustratedin Figure 7.

Long-term managementSecondary prevention

Optimal medical therapy as well as lifestyle changes including diet,exercise and smoking cessation are of particular importance following anACS event due to the persistent high risk for recurrent ischaemic events.

Optimal medical therapy typically includes high-intensity lipid loweringwith statins, anti-platelet and anticoagulation therapy, beta blockers(provided no contra-indications), aldosterone antagonists (such asEplerenone) in patients with left ventricular dysfunction (LV ejectionfraction +40%), anti-hypertensive therapy with an aim to achieve bloodpressures < 140/90 mm Hg, glucose lowering in diabetics.

A well structured cardiac rehabilitation / secondary preventionprogramme after an ACS enhances patient compliance with medicaltherapy and promotes lifestyle changes including regular physical exerciseand smoking cessation as well as dietary counselling.

ConclusionsThe diagnosis, risk stratification and management of acute coronarysyndromes involve a systematic time-bound approach. Prompt earlydiagnosis and management are extremely important to salvagemyocardium and minimise myocardial necrosis and damage, as also toprevent long term effects such as heart failure and death. Further, longterm management and secondary prevention measures are imperativefollowing discharge from hospital after the acute index event to achieveimproved clinical outcomes.

Conflict of interestThe author declares no conflict of interest relevant to this article.

Figure 6: Antithrombotic protocol in patients with NSTEACS and non-valvular AF (20)

Figure 7: Selection of NSTEACS treatment strategy & timing according to initial risk stratification (2)

More common conditionsu Tachyarrhythmias u Heart Failureu Critical illness (shock/ sepsis/ burns)u Myocarditisu Tako-Tsubo CMu Structural heart disease (AS)u Aortic dissectionu Pulmonary embolism, pulmonary hypertensionu Renal dysfunction and cardiac disease

Clopidogrel Prasugrel Ticagrelor CangrelorAdministration Oral Oral Oral IntravenousDose 300-600 mg 60mg 180mg 30μg/kg bolus & then 75 mg/day then 10 mg/day then 90 mg BD 4μg/kg/min infusionDosing in CKD None Not recommended in Stage 5 NoneBinding reversibility Irreversible Irreversible Reversible Reversible Activation Prodrug, with Prodrug, with Prodrug, with Active drug variable liver predictable liver additional active metabolism metabolism metabolism

Onset of loading dose effect 2-6 hours 30 minutes 30 minutes 2 minutesDuration of effect 3-10 days 7-10 days 3-5 days 1-2 hoursWithdrawal before surgery 5 days 7 days 5 days 1 hourPlasma half-life of active 30-60 minutes 30-60 minutes 6-12 hours 5-10 minutesP2Y12 inhibitorInhibition of adenosine No No Yes Yes (inactivereuptake metabolite only)

Less frequent conditionsu Coronary spasmu Acute neurological event (stroke or SAH)u Cardiac contusion or procedures (CABG, PCI, ablation, pacing, cardioversion, biopsy)u Thyroid disordersu Infiltrative disorders (amyloidosis, haemochromatosis, sarcoidosis, scleroderma)u Myocardial drug toxicity/ poisoning (doxorubicin, 5-FU, herceptin snake venoms)u Extreme endurance effortsu Rhabdomyolysis

References:1. Task Force on the management of STseamiotESoC, Steg PG, James SK, Atar D, Badano LP, Blomstrom-Lundqvist C, et al. ESC Guidelines for themanagement of acute myocardial infarction in patients presenting with ST-segment elevation. European heart journal. 2012 Oct;33(20):2569-619. PubMedPMID: 22922416.

2. Roffi M, Patrono C, Collet JP, Mueller C, Valgimigli M, Andreotti F, et al. 2015 ESC Guidelines for the management of acute coronary syndromes inpatients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting withoutPersistent ST-Segment Elevation of the European Society of Cardiology (ESC). European heart journal. 2016 Jan 14;37(3):267-315. PubMed PMID: 26320110.

3. Thygesen K, Alpert JS, White HD, Joint ESCAAHAWHFTFftRoMI. Universal definition of myocardial infarction. European heart journal. 2007Oct;28(20):2525-38. PubMed PMID: 17951287.

4. Lancellotti P, Price S, Edvardsen T, Cosyns B, Neskovic AN, Dulgheru R, et al. The use of echocardiography in acute cardiovascular care: recommen-dations of the European Association of Cardiovascular Imaging and the Acute Cardiovascular Care Association. European heart journal Acute cardiovascularcare. 2015 Feb;4(1):3-5. PubMed PMID: 25635106.

5. Kwong RY, Schussheim AE, Rekhraj S, Aletras AH, Geller N, Davis J, et al. Detecting acute coronary syndrome in the emergency department withcardiac magnetic resonance imaging. Circulation. 2003 Feb 04;107(4):531-7. PubMed PMID: 12566362.

6. Cury RC, Shash K, Nagurney JT, Rosito G, Shapiro MD, Nomura CH, et al. Cardiac magnetic resonance with T2-weighted imaging improves detectionof patients with acute coronary syndrome in the emergency department. Circulation. 2008 Aug 19;118(8):837-44. PubMed PMID: 18678772.

7. Lockie T, Nagel E, Redwood S, Plein S. Use of cardiovascular magnetic resonance imaging in acute coronary syndromes. Circulation. 2009 Mar31;119(12):1671-81. PubMed PMID: 19332480. Pubmed Central PMCID: 2730545.

8. Samad Z, Hakeem A, Mahmood SS, Pieper K, Patel MR, Simel DL, et al. A meta-analysis and systematic review of computed tomography angiographyas a diagnostic triage tool for patients with chest pain presenting to the emergency department. Journal of nuclear cardiology : official publication of theAmerican Society of Nuclear Cardiology. 2012 Apr;19(2):364-76. PubMed PMID: 22322526.

9. Ayaram D, Bellolio MF, Murad MH, Laack TA, Sadosty AT, Erwin PJ, et al. Triple rule-out computed tomographic angiography for chest pain: adiagnostic systematic review and meta-analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 2013Sep;20(9):861-71. PubMed PMID: 24050793.

10. Aragam KG, Tamhane UU, Kline-Rogers E, Li J, Fox KA, Goodman SG, et al. Does simplicity compromise accuracy in ACS risk prediction? A retro-spective analysis of the TIMI and GRACE risk scores. PloS one. 2009 Nov 23;4(11):e7947. PubMed PMID: 19956773. Pubmed Central PMCID: 2776353.

11. de Araujo Goncalves P, Ferreira J, Aguiar C, Seabra-Gomes R. TIMI, PURSUIT, and GRACE risk scores: sustained prognostic value and interactionwith revascularization in NSTE-ACS. European heart journal. 2005 May;26(9):865-72. PubMed PMID: 15764619.

12. Fox KA, Fitzgerald G, Puymirat E, Huang W, Carruthers K, Simon T, et al. Should patients with acute coronary disease be stratified for managementaccording to their risk? Derivation, external validation and outcomes using the updated GRACE risk score. BMJ open. 2014 Feb 21;4(2):e004425. PubMedPMID: 24561498. Pubmed Central PMCID: 3931985.

13. Subherwal S, Bach RG, Chen AY, Gage BF, Rao SV, Newby LK, et al. Baseline risk of major bleeding in non-ST-segment-elevation myocardial infarction:the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA Guidelines)Bleeding Score. Circulation. 2009 Apr 14;119(14):1873-82. PubMed PMID: 19332461. Pubmed Central PMCID: 3767035.

14. Mehran R, Pocock SJ, Nikolsky E, Clayton T, Dangas GD, Kirtane AJ, et al. A risk score to predict bleeding in patients with acute coronary syndromes.Journal of the American College of Cardiology. 2010 Jun 08;55(23):2556-66. PubMed PMID: 20513595.

15. Mehta SR, Yusuf S, Peters RJ, Bertrand ME, Lewis BS, Natarajan MK, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study. Lancet. 2001 Aug 18;358(9281):527-33. PubMed PMID:11520521. Epub 2001/08/25. eng.

16. Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, et al. Prasugrel versus clopidogrel in patients with acute coronary syn-dromes. The New England journal of medicine. 2007 Nov 15;357(20):2001-15. PubMed PMID: 17982182. Epub 2007/11/06. eng.

17. Wallentin L, Becker RC, Budaj A, Cannon CP, Emanuelsson H, Held C, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes.The New England journal of medicine. 2009 Sep 10;361(11):1045-57. PubMed PMID: 19717846. Epub 2009/09/01. eng.

18. Patrono C, Andreotti F, Arnesen H, Badimon L, Baigent C, Collet JP, et al. Antiplatelet agents for the treatment and prevention of atherothrombosis.European heart journal. 2011 Dec;32(23):2922-32. PubMed PMID: 22019823. Epub 2011/10/25. eng.

19. Eikelboom JW, Anand SS, Malmberg K, Weitz JI, Ginsberg JS, Yusuf S. Unfractionated heparin and low-molecular-weight heparin in acute coronarysyndrome without ST elevation: a meta-analysis. Lancet. 2000 Jun 03;355(9219):1936-42. PubMed PMID: 10859038. Epub 2000/06/20. eng.

20. Lip GY, Windecker S, Huber K, Kirchhof P, Marin F, Ten Berg JM, et al. Management of antithrombotic therapy in atrial fibrillation patients presentingwith acute coronary syndrome and/or undergoing percutaneous coronary or valve interventions: a joint consensus document of the European Society ofCardiology Working Group on Thrombosis, European Heart Rhythm Association (EHRA), European Association of Percutaneous Cardiovascular Interventions(EAPCI) and European Association of Acute Cardiac Care (ACCA) endorsed by the Heart Rhythm Society (HRS) and Asia-Pacific Heart Rhythm Society(APHRS). European heart journal. 2014 Dec 01;35(45):3155-79. PubMed PMID: 25154388. Epub 2014/08/27. eng.

Table 3: Other conditions associated with cardiac troponin elevation

Table 4: Characteristics of P2Y12 inhibitors

14

atrial fibrillationnovel oral anticoagulentsCase history:A 78-year-old lady was admitted with palpitations. ECG showed atrialfibrillation and average ventricular rate of138 beat per minute. She didnot have any history of renal or hepatic problem. Her blood pressurewas normal. There was no history of previous heart attack, stroke, TIA,peripheral arterial disease. She had osteoarthritis and took codeineand paracetamol on a prn basis. Her blood tests including full bloodcount, renal, liver and thyroid functions, which were normal. Her AFwas treated with a rate control strategy. Her ventricular rate wascontrolled with beta-blocker and she was started on a NOAC aftershe agreed to go ahead with it. Her stroke risk was 3 (CHA2DS2VAScscore) and bleeding risk was 1 (HAASBLED score), indicating inter-mediate risk. She later had an echocardiogram, which showed normalleft ventricular function with mildly dilated left atrium. She wasdischarged home on the next day on the above medications.

Atrial Fibrillation and Novel oral anticoagulants (NOACs)Atrial fibrillation is a common arrhythmia affects 1 to 3% of the generalpopulation. It is associated with thromboembolic risk, which varies from1% or less to more than 20% (1). Those who develop stroke and AF haspoor prognosis compared to those who has stroke without AF. Toprevent stroke, they need anticoagulation. Until recently vitamin Kantagonists (VKAs: warfarin, acenocoumarol, Phenprocoumon) werethe cornerstones of anticoagulation therapy (2). Warfarin showedsignificant reduction in ischaemic stroke and reduction in all-causemortality in different trials. It was better than aspirin alone or acombination of aspirin and clopidogrel while treatment withclopidogrel and aspirin caused increased bleeding incidences. Thereis recent development in the world of anticoagulation therapy andtreatment of venous thromboembolism (3). In 2009, the first trial resultwith dabigatran was published. Following this, results from further trialscomparing the effects of rivaroxaban, apixaban and edoxaban becameavailable. Since the introduction of the NOACs, these have beenincreasingly used as a replacement therapy for the VKAs in thetreatment of venous thromboembolism and treatment for thrombo-prophylaxis in AF. Recent ESC guidelines give preference to NOACsin the management of non-valvular AF (4).

NOACs work on different targets on the coagulation pathwaycompared to the VKAs. There are four of these available and these aredabigatran, rivaroxaban, apixaban, and edoxaban. While dabigatranworks as direct thrombin inhibitor, the others work to prevent factorXa.

Challenges with VKAtherapy VKAs have interactions withmultiple drugs and foods. Theserequire frequent monitoring byblood tests and need adjustment ofdoses. They also have major sideeffects due to bleeding which couldbe intracranial, gastrointestinal,surgical, traumatic or minorbleedings like epistaxis.

Advantages of NOACsTreatment with NOACs usually do not need blood tests for monitoringthe treatment on a routine basis as these have predictable effects andthese have fixed daily doses. However, like VKAs, these also can causebleeding as a major side effect.

NOACs in AFNOACs are recommended for use in non-valvular AF only. As moderateto significant mitral stenosis (mostly rheumatic) or mechanical valveprosthesis are associated with high risk for thromboembolism, AF posesadditional thromboembolic risk and hence require anticoagulation withVKAs. However, AF in patients with other valve diseases or who has tissuevalve prosthesis can be treated with NOACs. All types of AF, paroxysmal,persistent or permanent pose similar stroke risk and require anti-coagulation based on thromboembolic risk. AF in the presence ofcongenital heart disease requires treatment with VKAs.

Different trials showed NOACs are effective in stroke preventioncompared to warfarin.

In a recent meta-analysis NOACs were associated significant reductionsin stroke, intracranial bleeding and mortality but had similar major bleedingrisk compared to warfarin (5). However these were associated withincreased risk of GI bleed.

Another real world observational study found that initiation withdabigatran and apixaban was associated with lower risk of bleeding butthis was high with rivaroxaban (6).

Xarelto for Prevention of Stroke in Patients With Atrial Fibrillation(XANTUS) study reported a reduction of stroke and GI bleeding duringtreatment with rivaroxaban compared to warfarin (7).

Risk scoresAdditional risk factors for stroke present in patients with AF areconsidered in calculating the stroke risk. Based on these, different stroke

Edoxaban30mg o.d.

Non-inferior 53% Reduction

A case of

with focus on


Table summarising the findings of different trials on NOACs

ARISTOTLE (Apixaban for Reduction of stroke and Other Thrombo-embolic Events in Atrial Fibrillation) 2015;132,624-32

RE-LY (Randomised Evaluation of Long-term Anticoagulation Therapy) 2012 125;669-76

ENGAGE AF-TIMI48 (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation--Thrombolysis inMyocardial Infarction 48) New England Journal of Medicine 2013; 369:2093-104

ROCKET-AF (Rivaroxaban Once daily Oral Direct Factor Xa Inhibition) 2014;130:138-46


risks scoring system are available. Most commonly used risk score isCHA2DS2VASc score. Stroke risk of 1% per year is generallyregarded as threshold for treatment with thrombo-prophylaxis. In past,female gender was thought to increase stroke risk. However recentconsensus is, this is NO more a risk factor and it is age dependant. So,if the age is less than 65 years then the stroke risk is minimal and doesnot require thrombo-prophylaxis based on gender only.

Thrombo-prophylaxis is not indicated if the stroke risk is 0 in male and1 in female (if due to female gender under age of 65). This risk scorecan reliably identify those who are at low risk. If Stroke risk 1 in male or2 in females decision to start NOAC should be individualised. If strokerisk is 2 or more anticoagulation is indicated.

ESC guidelines recommend calculating and modifying the bleedingrisks prior to initiating anticoagulation therapy. Multiple risk calculatorsare available (ATRIA, HEMORR2HAGES) but one of these iscommonly used known as HAASBLED score.

HAASBLED score (Hypertension—systolic BP>160; abnormal liverfunction=abnormal LFTs like bilirubin >2 times upper limit of normalwith AST or ALT or ALP >3 times upper limit; abnormal renalfunction=serum creatinine >200micromol or on dialysis or renaltransplant)

Major bleeding is described as intracranial bleeding, any bleedingrequiring blood transfusion or causing a drop in haemoglobin by 2gram per litre.

If the bleeding risk is high, search is made for modifiable risk factors.Modifiable risk factors include hypertension with systolic BP of 160

mmHg or above, Labile INR or time in therapeutic range less than 60%in patients on VKAs, alcohol excess, and medication predisposing tobleeding. Potentially modifiable risk factors include anaemia, impairedrenal or liver function, reduced platelet count or function. Once theserisks are modified, NOACs can be initiated.

Biomarker based bleeding risk factors included high sensitive troponin,serum creatinine and creatinine clearance and growth differentiationfactor 15. Risk scores based on these are available. HAASBLED scoreis still used as biomarker based scores are time consuming whileHAASBLED score is easy to calculate and can be used in a busyclinical setting.

Drug clearance and interactions Dabigatran is 80% renally cleared. Renal clearance for apixaban is25%, for rivaroxaban 35% and for edoxaban is 50%. Apixaban is50% and rivaroxaban is 65% metabolised by CYP3A4.All 4 aresubstrate for P-glycoprotein. So caution is needed when patientsreceive treatment with concomitant inhibitor/inducers of CYP3A4 orp-glycoprotein (e.g., anti-mycotic or HIV protease inhibitors). Cautionis required with the concomitant use of verapamil, amiodarone anddronedarone along with NOAC.

Dose reductionsAll major clinical trials excluded patients with severe renal impairment.Dose reduction is required with reduced creatinine clearance andavoided if creatinine clearance is less than 15ml/min (8).

Dose reductions may be needed in the elderly. A recent trial showedbenefit of dabigatran over warfarin in preventing ischaemic stroke.However, when used in a dose of 150 mg b.d., it was associated withincreased incidence GI bleeding but when administered in a reduceddose of 110 mg bd there was no difference to warfarin. Also, a recentsub study of RE-LY trial found that effects of dabigatran on extra-cranialmajor bleeding are age dependant and supported a dose of 110 mgb.d. for subjects with age of 80 years or more. In elderly patients, otherrisk factors should be taken in to consideration prior to deciding aboutthe dose of the NOAC. These included dementia, frailty, nutritionalstatus, mobility, comorbidities, and life expectancy. As stated above anymodifiable risk factors need to be corrected.

Dr Gautam ChakrabartMRCP

Associate Specialist Cardiology, Royal Blackburn Hospital

Dr SK SinghFRCP

Consultant Cardiology, Royal Blackburn Hospital


Antidotes and monitoringOther than monitoring renal function, blood tests are not needed to assess anticoagulationeffects of the NOACs routinely. Thrombin time and eccarin clotting time (ECT) are used toassess anticoagulant effect of dabigatran and anti -factor Xa assays are used for the effects ofthe others. APTT and PT are prolonged with apixaban and rivaroxaban. PT can be used asrough estimate in treating bleeding with rivaroxaban only.

Only dabigatran has antidote known as Idarucizumab, a monoclonal antibody that reversesthe anticoagulant effect rapidly. For the others, in absence of specific antidote, Andexanet alfa,a recombinant protein that binds factors Xa inhibitors, had been successfully tried in ANEXA-A (apixaban) and ANEXA-R (rivaroxaban) trials (9). Aripazine had been tried to treat bleedingassociated with edoxaban. Four Factor PCCs was used for bleeding due to rivaroxaban.Gastric lavage, platelet and fresh frozen plasma transfusions used as a general measure forall NOACs.

In a recent study in a real-world setting, major bleeding with rivaroxaban was reported to belower as compared to vitamin K antagonists (10). It was also noted that simple measures areoften sufficient to control bleeding associated with rivaroxaban and did not usually requirepro-coagulants.

ConclusionNOACs are being used increasingly in place of VKAs for the treatment and prevention ofthromboembolism. ESC guideline on stroke prevention in AF now prefers NOACs. Thesework on different targets in the coagulation pathway. Different trials showed these arebeneficial in reducing stroke and thromboembolism in patients AF. These have similar sideeffects like VKAs. Guidelines recommend using risk scores prior to initiating therapy withNOACs. These drugs have fixed daily doses and do not require blood tests to monitor anti-coagulation effects routinely. Some of these have specific antidotes but others are treatedcommonly using general measures. Patient education is needed

Possible answers:A: Whipple’s diseaseB: Tropical sprueC: Lactase deficiency D: HIV enteropathyE: Giardiasis F: Cystic fibrosis G: Crohn’s disease H: Coeliac disease I: Chronic alcoholic pancreatitis J: Rotavirus infection Answers on Page 26

Mr Amit SinhaFRCS (Trauma & Ortho)

Consultant Orthopaedic Surgeon,Glan Clwyd Hospital

(North Wales NHS Trust)

For each of these following patientsselect the most likely diagnosis.

Questions:1. 52 Year old gentleman has been admitted to ED with an acuteonset of back pain. He was only recently diagnosed with diabetes.On further questioning he has a long history of chronic epigastricpain as well as a six month history of weight loss and steatorrhoea.Full blood count shows a macrocytic anaemia with low proteins andalbumins.

2. 38 Year old gentleman was seen in the orthopaedic clinic witha history of polyarthralgia. He has recently been diagnosed diabeticand has required insulin. He has been admitted to hospital severaltimes with chest infections. He is a non smoker and there is no historyof asthma. He always had ‘sniffles’ during his childhood and wasdiagnosed as having a ‘weak’ chest. Over the last two years he haslost a lot of weight and admits to having loose motions everydaypassing large and bulky stools.

3. A 21 Year old lady has a history of myalgia affecting joint painsand tiredness and lethargy. She is quite slim and pale looking andhas a several year history of intermittent diarrhoea. She is mentallybright and tries her best to eat a healthy diet. Full blood count showsmacrocytic anaemia. An upper GI endoscopy is normal. Bariumfollow-up study shows multiple small bowel strictures.

4. 25 Year old lady presents to her GP surgery with an acutepresentation of itchy, painful and blistering rash over both her elbows.For the past three months she has developed diarrhoea. White cellcount is normal but albumin and calcium levels are low.

5. 52 Year old gentleman is being investigated in the medical unitfor generalised lymphadenopathy. He also has aching in all his joints;this is associated with tiredness, lethargy and complete lack of energy.Full blood count shows a macrocytic anaemia. Following upper GIendoscopy the duodenal biopsies show numerous macrophages inthe lamina propria.

QuizMedical

References:1. Caterina RDe et al. What is ‘valvular’ atrial fibrillation? A reappraisal. European Heart Journal (2014) 35, 3328–3335

2. Katritsis DG et al. Clinical cardiology Current Practice Guidelines -Updated Editions (OUP)

3. Blann AD et al. Non-vitamin K antagonist oral anticoagulants (NOACs) for the management of venous thromboembolism.Heart 2016; 102:975–983

4. ESC guidelines on management of atrial fibrillation. Eur Heart J (2016) 37 (38): 2893-2962.

5. Ruff CT et al Comparison of the efficacy and safety of the new oral anticoagulants with warfarin in patients with atrial fibrillation-a meta -analysis of the randomised trials, The Lancet 383,No9921:955-962

6 Lip et al. Real-world comparison of major bleeding risk among non-valvular atrial fibrillation patients initiated on apixaban, dabigatran,rivaroxaban, or warfarin. Thrombosis and Haemostasis 116.5:2016

7. Camm AJ. XANTUS Study. Eur Heart 2016;37(14):1145

8. Assessing kidney function in oral anticoagulant prescribing: an aid for safer drug and dose choices.British Journal of Cardiology 2013;20:61–4

9. Siegal DM et al Adenexat alfa for the reversal of factor Xa activity --, New England Journal of medicine 2015;373:511-20

10. Beyer-Westendorf J et al. Rates, management, and outcome of rivaroxaban bleeding in daily care: results from the Dresden NOAC registry,Blood 2014;124:955

atrial fibrillation

novel oralanticoagulents

A case of

with focus on

continued...

Mental Capacity ActNew developments,overview andinteresting facts


Dr BK SinhaBIDA National

Treasurer,

Lead GP intermediate

care inLiverpool for

Knowsley CCG

The mental capacity act (MCA) has been in forcesince 2007 and applies to England and Wales.This is very important for health and social carepractice. It is estimated that around two millionpeople in England and Wales are thought to lackcapacity to make decisions for themselves. Theyare cared for by around six million people,including a broad range of health and social carestaff.

It is essential to understand that the mentalcapacity act has two important functions:

1. It is designed to protect and restore power tothose vulnerable people who lack capacity.

2. It also supports those who have capacity andchoose to plan for their future – this is everyone inthe general population who is over the age of 18.

Causes of lack of mental capacity:

u Stroke or brain injuryu Mental health problemu Dementia u Learning disability u Confusion, drowsiness or unconsciousness

because of an illness or side effect of atreatment

u Substance misuse.

Five key principles applies to MentalCapacity act:

1. A presumption of capacity – every adult hasthe right to make his or her own decisions andmust be assumed to have capacity to do so unlessit is proved otherwise. This means that you cannotassume that someone cannot make a decision forhimself or herself just because they have aparticular medical condition or disability

2. Individuals being supported to make theirown decisions – a person must be given allpracticable help before anyone treats them as notbeing able to make their own decisions. Thismeans you should make every effort to encourageand support people to make the decision forthemselves. If lack of capacity is established, it isstill important that you involve the person as far aspossible in making decisions

3. Unwise decisions – people have the right tomake decisions that others might be regarded asunwise or eccentric. You cannot treat someone aslacking capacity for this reason. Everyone has his

In the last two years I have been heavily involved in intermediate care work as an associate GP. As part of this job I have dealt with a numberof patients who lacked mental capacity. I thought I’d take this opportunity to update BIDA members on the mental capacity act. Not onlythe patient but also all of us should have lasting power of attorney (LPA) for health & welfare as well as finances and property. LPA’s havefully replaced the previous enduring power of attorney. These LPA’s are only valid if registered by the office of the public guardian. Somepeople call LPA’s a living will. I have highlighted in this article the relevant and the salient points from the various acts.

or her own values, beliefs and preferences, whichmay not be the same as those of other people.

4. Best interests – anything done for or onbehalf of a person who lacks mental capacitymust be done in their best interests.

5. Less restrictive option– someone making adecision or acting on behalf of a person who lackscapacity must consider whether it is possible todecide or act in a way that would interfere lesswith the person’s rights and freedoms of action,or whether there is a need to decide or act at all.Any intervention should be weighed up in theparticular circumstances of the case.

Assessment of mental capacity:

In order to decide whether an individual has thecapacity to make a particular decision you mustanswer two questions:

Stage 1. Is there an impairment of or disturbancein the functioning of a person’s mind or brain? Ifso,

Stage 2. Is the impairment or disturbancesufficient that the person lacks the capacity tomake a particular decision?

The MCA states that a person is unable to maketheir own decision if they cannot do one or moreof the following four things:

u Understand information given to them

u Retain that information long enough to beable to make the decision

u Weigh up the information available to makethe decision

u Communicate their decision – this couldbe by talking, using sign language or evensimple muscle movements such as blinkingan eye or squeezing a hand.

The new roles, bodies and powerssupporting the MCA

u Attorneys appointed under Lasting Powersof Attorney (LPAs) – the Act introduces a newform of Power of Attorney which allows peopleover the age of 18 to formally appoint one ormore people to look after their health, welfareand/or financial decisions, if at some time in thefuture they lack capacity to make those decisionsfor themselves.

u Court of Protection and Deputies – theMCA created a new court and a new publicofficial to protect people who lack capacity and tosupervise those making decisions on theirbehalf. The Court is able to appoint a Deputy, forexample, because a person has an ongoing lackof capacity. The Court will tailor the powers of thedeputy according to the circumstances of theindividual.

u The Public Guardian – the role of the PublicGuardian is to protect people who lack capacityfrom abuse. The Public Guardian is supported bythe Office of the Public Guardian (OPG). TheOPG maintains a register of LPAs and EPAs. Italso maintains a register of the Court-appointedDeputies and is responsible for supervising them.

u Independent mental capacity advocate(IMCA) – IMCAs are a statutory safeguard forpeople who lack capacity to make some importantdecisions. This includes decisions about where theperson lives and also for any serious medical orsurgical treatment when the person does not havefamily or friends who can represent them. IMCAscan also represent individuals who are the focus ofadult protection proceedings. The Deprivation ofLiberty Safeguards introduced further roles forIMCAs.

u Advance decisions to refuse treatment– theAct creates statutory rules with clear safeguardsso that people may make a decision in advance torefuse treatment if they should lack capacity in thefuture.

u Criminal offence act– this act introduces anew criminal offence of ill treatment or wilfulneglect of a person who lacks capacity.

Code of Practice

The Code explains how the MCA works on a day-to-day basis and provides guidance to thoseworking with people who may lack capacity. TheCode explains the key features of the MCA inmore detail, as well as some of the practical stepsthat people using and interpreting the law need totake into consideration. If you work with peoplewho lack capacity and you are a professionaland/or you are paid for the work you do then youhave a legal duty to have regard to the Code.

18 British International Doctors’ Association Issue No.2, Volume 23 May 2017

SepsisAbstractSepsis is a syndrome that is best understood as life-threatening organ dysfunc-tion caused by a dysregulated host response to infection. It is an important causeof morbidity, mortality and healthcare utilisation - and its prevalence amonghospitalised patients is significant. This paper reviews the latest revisions to def-initions relating to sepsis and references recently published international andUK guidelines on sepsis identification and management. Lastly, it describes asystem-wide approach taken in one region to the identification and escalationof patients at risk.

IntroductionSepsis….

“The biggest killer you may not know”- BBC News, March 2017 (1)

“Teenager died of meningitis after tweeting ‘Lol… Did not expect to be rushed to hospital’” - TheTelegraph, March 2017 (2)

“Doctor failed to spot sepsis – but is not struck off” - Liverpool Echo, April 2017 (3)

Sepsis is a leading cause of death worldwide (4). In the UK, sepsis is estimatedto account for nearly 40,000 deaths per year, a figure exceeding deaths dueto bowel and breast cancer combined (5). The incidence of sepsis appears tobe rising (6,7) and in the US now consumes more than 5% hospital expenditure(4). The past year (2016/17) has seen the publication of the fourth iteration ofthe Surviving Sepsis Campaign International Guidelines (8) and NICEguidelines on the management of sepsis (9). Furthermore, to judge on the basisof reports in the UK general media – aided by the work of campaigns such asthe UK Sepsis Trust and more recently the endorsement of the Health Secretary(10) - the general public’s exposure to the concept of “sepsis” has almost certainlyincreased in recent years. With rising expectations over standards of care insepsis management, public criticism of sub-optimal care - and in particular thefailure to recognise a life-threatening illness – has been explicit in a number ofrecent cases.

As practitioners in a wider range of medical fields, our contact with patientswith life-threatening “sepsis” may be very variable, and we may have a numberof concerns and questions. For example, what do we actually mean by the term"sepsis"? Can we reliably recognise sepsis at an early stage? What interventionsgenuinely make a difference? And what about the risk of conflicting imperatives,for example, how do we ensure that we treat potential cases of sepsis in a timelyway yet minimise the inappropriate use of antibiotics or the over-zealous fluidresuscitation of patients who do not need it?

Despite its rising profile, “sepsis” is not a concept new to medicine, havingallegedly been used at the time of Hippocrates in ancient Greece (11) and revivedas an idea in Western Europe in the 13th and 14th centuries. Unfortunately, 21stcentury medicine has not identified a specific "magic bullet" able to reverse theorgan dysfunction that defines sepsis, a series of promising interventions havefallen by the wayside in recent years (12). Through necessity, our efforts becomefocussed on the early identification, intervention and escalation of patients withpotentially life-threatening illness.

In the course of this piece, we will review our current understanding of theepidemiology, patho-physiology and clinical features of sepsis. We will discussrecent the recent revisions of definitions of sepsis (4) and international and UKguidelines for the identification of sepsis (9). At the heart of this piece, however,we recognise that the real challenge clinicians is one perfectly captured byMachiavelli in his 16th Century treatise, The Prince:

“As the physicians say it happens in hectic fever, that in the beginning of the maladyit is easy to cure but difficult to detect, but in the course of time, not having beeneither detected or treated in the beginning, it becomes easy to detect but difficultto cure” (13).

DefinitionsIt is important to remember that "sepsis" is not a specific illness, but rather asyndrome (a collection of symptoms and signs) resulting from infection. To use themost recent definitions, those of the Third International Consensus Definitions forSepsis and Septic Shock(4) (Sepsis-3; sepsis should be considered "a life-threatening organ dysfunction caused by a dysregulated host response to infection"(Box 1).

Previous identification ofsepsis using "systemicinflammatory responsesyndrome" (SIRS) criteria(two or more of: tempera-ture <36° or >38°, heartrate 90 per minute,respiratory rate 20 per minute or PaCO2 <4.3 kPa, white blood cell count <4x 109/L > 12x109/L (14)) is no longer felt to be helpful - since SIRS can be presentin a high proportion of patients without life-threatening infection and is absent in asignificant number of critically ill patients with infection and organ dysfunction, whoexperience protracted admission and high mortality(4). Furthermore, since theemphasis in sepsis is the presence of organ dysfunction, any distinction betweenthe historic concepts of "sepsis" and "severe sepsis" (which was understood torepresent infection + 2 or more SIRS criteria + organ dysfunction; (14) is no longerfelt to be relevant. However, the term "septic shock" has been retained in theSepsis-3 definitions, representing a sub-set of patients with a substantially increasedmortality, who may be characterised by persistent low blood pressure or elevatedlactate despite appropriate volume resuscitation (Box 1).

EpidemiologyAlthough we are shortly to discuss an apparent rising incidence of sepsis in thedeveloped world, this should be put into the context of a dramatic decrease ininfection-related mortality over the last two hundred years which pre-dates theeras of antibiotics and intensive care - and reflecting the huge importance of publichealth improvements such as water quality, immunisation and the pasteurisationof milk (11). Most epidemiological data has (predictably) been generated bydeveloped as opposed to developing countries - however, where comparison hasbeen possible, variations in mortality globally can be striking (e.g. 47% mortalitydue to sepsis among ICU patients in Africa vs. 13% in North America (15) with asignificant association between risk of death and national income.

Data from the UK and in the US suggest that the incidence of sepsis is rising (6,16).In the US, the incidence among the general population reportedly increased fromapproximately 100 per 100,000 population to just under 300 per 100,000between 1979 and 2001 (6). In the UK, the numbers of those admitted to ICU withsepsis rose from approximately 45 to 65 per 100,000 between 1996 and 2003(16). Despite some concerns over coding and database extraction methods - andpotential discrepancies over the absolute numbers of cases - such trends havebeen consistently observed using alternative methods along with a rise in nationalmortality rates due to sepsis (7). Globally, it is estimated that the number of cases ofsepsis per year almost certainly exceeds 19 million (17).

Thus, sepsis is increasingly common - presumably at least in part becausepopulations are ageing (18) with consequential morbidity and exposure tomedication and interventions that may increase the risk of developing sepsis.However, despite this, mortality rates on an individual basis - the case fatality rates- are falling. In terms of setting an international bench-mark, the Australian andNew Zealand intensive care community have been able to demonstrate what canbe achieved with a staggering fall in absolute mortality due to sepsis in the criticallyill from 35% to 18% between 2000 and 2012(19).

The biggest, least well-known killer?

Box 1. Definitions of sepsis and septic shock (adapted from Singer 2016 (4))


Dr Richard PughConsultant in Anaesthetics and Intensive Care Medicine

Glan Clwyd Hospital, North Wales

AetiologySepsis may be community- or healthcare- associated. In the hospital setting,pneumonia is the major cause of ICU-acquired and non-ICU acquired sepsisfollowed by abdominal and urinary tract infection (20,21). Appreciating that thereis often (>50% cases) no positive microbiological isolate in sepsis, in the US arecent faster rise in cases has led to Gram-positive organisms (such Staphylo-coccus aureus and Streptococcus pneumoniae) overtaking Gram-negatives(such as Escherichia coli and Pseudomonas aeruginosa) as the leading causeof sepsis (6), though in Western Europe Gram-negative organisms still appearto predominate (21). Historically at least, Gram-negative sepsis has beenassociated with higher mortality than Gram-positive sepsis.

Patho-physiology of SepsisFor more detailed review regarding the pathophysiology of sepsis, readers aredirected to a recent comprehensive review by Angus and Van der Poll (22). Theresponse to an infection appears to depend upon factors relating to the micro-biological pathogen (e.g. bacterial load and virulence) as well as the host (e.g.age, gender, race, comorbidity, nutrition, presence of in-dwelling devices) (22,23).The response may involve pro-inflammatory processes (which are potentiallytissue-damaging) and anti-inflammatory processes (which may predispose tosecondary infection) (24). These inflammatory processes will be determined bythe interaction between elements of the pathogenic organisms (pathogen-associated molecular patterns [PAMPs]) and specific receptors either on thehost cell membrane or within its cytoplasm. However, as well as interacting withPAMPs, such host cell receptors may also interact with damage-associatedmolecular patterns (DAMPs, also referred to as "alarmins") released as aconsequence of tissue injury - which may therefore perpetuate an inflammatoryresponse and in other circumstances initiate an inflammatory response to anon-infectious insult, such as trauma. Pro-inflammatory processes will involvethe activation of inflammatory cells, complement and coagulation pathways.Endothelial cell activation is associated with increased production of nitric oxide(a potent vasodilator) and injury to endothelial cells by proteases, oxidants,prostaglandins and leukotrienes may result in endothelial glycocalyx disruption,increased vascular permeability, further vasodilatation and a prothromboticstate.

Considering pathology at a micro- and macro-scopic level, therefore, theconsequences of sepsis may include poor blood flow in the micro-circulation,relative hypovolaemia, inappropriate vasodilatation and systemic hypotension,with tissue oxygen delivery further compromised by sepsis-induced myocardialdysfunction and sepsis-associated lung injury. Cellular dysfunction and deathmay result in the dysfunction of any organ, which may become manifest, forexample, as acute kidney injury, delirium, septic shock or acute respiratorydistress syndrome.

Clinical featuresThe clinical features of sepsis may be variable depending on host (includingsite of infection) and pathogen factors. However, they may include generalfeatures such as altered mental state, hyperglycaemia, and raised respiratoryand heart rate; there may evidence of inflammation in terms of high or low whitecell count, high or low temperature, and elevated serum C-reactive proteinand serum procalcitonin; there may be evidence of poor tissue perfusion interms of poor capillary refill, mottling and elevated serum lactate (a surrogatemeasure for poor oxygen delivery to tissues which results in anaerobicmetabolism); and there will be evidence of organ dysfunction (according to theSepsis-3 definition; see Table 1. Common Clinical Features of Sepsis) whichmay be a consequence of remote infection (e.g sepsis-induced lung injury, referred to as acute respiratory distress syndrome) or the local source (e.g.impaired oxygenation due to community-acquired pneumonia).

Defining Sepsis and Septic ShockMore formally, organ dysfunction in the context of sepsis can be defined using ascoring system which has been used in critical care for the last two decades as aguide to predicting sepsis-related morbidity and mortality, the Sepsis-relatedOrgan Failure Assessment (SOFA) score (see Box 2 (25)). Recent investigation ofa huge US database (with >1.3 million electronic records) found that SOFA scoreof 2 or more predicted a mortality risk of at least 10% among a general hospitalpopulation, and (depending on baseline risk) a 2- to 25- times increased risk ofdeath compared with patients with SOFA score of less than 2 (4,26). Consequently,the new Sepsis-3 definitions have recommended identifying sepsis by an acuteincrease in SOFA score (appreciating that some patients will have an elevatedbaseline score because of chronic disease) by 2 or more points.

However, since the SOFA score may not lend itself readily to screening patientsfor risk - particularly as it is dependent on the availability of laboratory results -investigators involved with the Sepsis-3 definitions developed a simple screeningtool, the qSOFA ("quick SOFA"), which incorporates just three elements: acutelyaltered mental function (Glasgow Coma Score <14), tachypnoea (respiratory rate22 or more per minute) and hypotension (systolic blood pressure of 100 mm Hgor less; see Box 3 (26). They found that outside of intensive care, a qSOFA score of2 performed predicted poor outcome (hospital mortality) to an even greaterdegree than the full SOFA score - and to a much greater degree than scoring onthe basis of SIRS criteria (26). Having said this, the authors also stressed that failingto meet SOFA or qSOFA definitions of sepsis should never delay appropriateinterventions in the context of suspected sepsis.Furthermore, they acknowledged the risk ofconflict with other methods of identifying thepatient at risk and escalation pathways, forexample early warning scores, which we willdiscuss in greater detail below.

Failure of mean arterial blood pressure or lactate to normalise despite adequatefluid resuscitation indicatesa much higher risk ofmortality (>40%) - and"septic shock" has beenrefined as the term used torefer to those requiringvasopressors to maintain amean arterial bloodpressure greater than orequal to 65 mmHg,together with persistentlyelevated serum lactate(greater than 2 mmol/L).These are thereforepatients who are particu-larly likely to benefit fromprompt escalation to seniorTable 1. Clinical features of sepsis (adapted from Levy 2003 (14))

Box 2. SOFA score (adapted from Vincent 1996 (25))

Box 3. qSOFA (adapted from Singer 2016 (4))


Sepsis

members of the clinical team and / or critical care.

TreatmentThe recent Surviving Sepsis Campaign (SSC) guidelines provide an up-to-dateand extremely comprehensive review of the management of sepsis - and indeed care of the critically ill more generally (8). As mentioned earlier, thereare no "magic bullets" in the treatment of sepsis. After promising initial results,the adjunct which appeared to come closest to a specific treatment for sepsisin recent years, by targeting the inflammatory and coagulation pathways,activated Protein C, was withdrawn for lack of efficacy (12).

Appreciating that early appropriate intervention is likely to provide the best potential for a good outcome, sepsis management becomes more a matter ofmaking early interventions count - and reducing (sub-optimal) variation in thequality of response. With this in mind, the "Sepsis Six" was devised as a simpleset of interventions which should all be achievable within the first hour ofrecognising sepsis (5) - and indeed in their observational study, when achievingSepsis Six was associated with a significantly lower (unadjusted) mortality intheir study (20% vs 44%).

The importance of prompt fluid therapy and antibiotics are emphasised in therecent SSC and NICE guidelines (8,9). Administration of appropriate antibioticsis recommended as soon as possible after the recognition of sepsis or septicshock - again with a target of one hour on the basis of observational studiesdemonstrating a decrease in mortality with earlier administration of earlyantibiotics (27,28). The importance of taking relevant microbiological samples(including blood cultures) is stressed before commencing antimicrobials wherefeasible. In terms of fluid resuscitation, for patients with sepsis-induced hypo-tension, the SSC guidelines recommend (at least) 30 ml/kg of fluid within thefirst 3 hours, guided by haemodynamic parameters (and by urine output) andserial lactate measurement where possible.

Hypoxaemia (low blood oxygen tension) may be a consequence of a primaryrespiratory infection (e.g. pneumonia), the consequence of infection (e.g.atelectasis due to pain and poor mobility associated with abdominal pathology)or a systemic consequence of sepsis (e.g. acute respiratory distress syndrome).Normalising blood oxygen levels is of particular importance for individuals withpoor tissue perfusion, and NICE recommend oxygen saturation targets of 94-98% for healthy individuals and 88- 92% for those at risk of developinghypecapnoeic respiratory failure (9) (NICE 2016).

Source control represents the definitive intervention for the ongoing source ofbacterial contamination (8) - and identifying and managing such as source is likelyto require more senior input. Depending on clinical presentation, further sourceidentification may involve bedside test (e.g. urinalysis), radiography (includingCT of chest, abdomen and pelvis if no obvious source after initial examinationand investigation), and referral to the surgical / gynaecological teams asappropriate. Ideally, source control should adopt the intervention which causesthe least physiological insult, and should be instituted as soon as possible after(or even during) initial efforts to resuscitate, whether this represents, for example,laparotomy for a perforated intra-abdominal viscus, radiological drainage of agallbladder empyema, or removal of an infected vascular device.

The NICE guidelines identify a number of "high risk" criteria which inconjunction with serum lactate can be used as a trigger for critical care referral(high risk sepsis criterion plus either systolic blood pressure less than 90 mmHg or lactate over 4 mmol/L, see Box 1) - and that failure to improve with 1Lfluid (approximately 15 ml/kg for an "average adult") over approximately 30minutes should prompt senior clinical review. However, clearly, any patient inwhom relatively simple interventions fail to reverse significant acute organdysfunction (and in particular fail to correct hypotension or hypoxaemia) shouldbe appropriately considered for escalation of care.

Common critical care interventions may include organ support with vaso-pressor therapy (typically noradrenaline as first line, via a central venous catheterto obtain a target mean arterial pressure of 65 mm Hg (8)), respiratory support(which may be non-invasive, such as nasal high flow oxygen or continuous positiveairways pressure, or invasive ventilation following sedation and tracheal intubation),and/ or renal support (for example, with haemofiltration for life-threatening acutekidney injury). Additional tools such as cardiac output monitoring, echocardiog-raphy and bedside passive leg raise (to detect fluid responsiveness) may provideadditional valuable data to guide further management. However, use of highlyprotocolised (goal-directed) management is not supported by the results recentlarge multi-centre trials (29-31). Appreciating that a proportion of septic patients mayhave relative adrenal insufficiency, the evidence base for the use of steroids haswaxed and waned over the last 2 decades, and recommendations are currentlythat this should be reserved for those patients in whom haemodynamic stabilitycannot be achieved with adequate fluid resuscitation and vasopressor therapyalone (8). Patients requiring such interventions will of course need a higher level ofnursing and medical care, with 1:1 nurse: patient ratio for invasive ventilation ormultiple organ support (an ICU or "Level 3" patient), and 1:2 for a patient with asingle failing organ (who does not require invasive ventilation; an HDU or "Level2" patient).

A system-wide approach to identifying patients with sepsis riskThere is a need for an organised, hospital-wide approach to identifying, treatingand escalating patients with sepsis in a timely manner (32)- but inevitably processeswill vary with resources available, including the presence of a medical emergencyteam and access to critical care, radiology and surgical services.

To provide an example of UK practice, systems operating in Wales now tend tofollow the RRAILS model (Rapid Response to Acute Illness), with the adoption ofa National Early Warning Score (NEWS) track-and-trigger system in secondarycare in 2013 (see Fig 1. (33)). The NEWS score represents a composite measureof abnormal physiological parameters, with thresholds for activation interventionof different members of the local clinical and hospital clinical team. According to aNEWS of 6-8 for example, the nurse-in-charge, the patient's own doctor (unspec-ified seniority), and the critical care "outreach" team should attend within 30minutes; if there is concern or failure to improve, a senior should be contacted;monitoring frequency should be 1-2 hourly (Fig 2). However, the guidelines stressthat concern about a patient should lead to escalation, regardless of the score.

The biggest, least well-known killer?(Continued)

Figure 1:NHS EarlyWarningScore Wales,adapted fromthe BCUHBobservationchart.

Figure 2:Responseto NEWS,adapted fromthe BCUHBobservationchart.


According to the RRAILS recommendations, NEWS of 3 or more shouldprompt consideration of underlying infection - and if in addition 2 or more SIRScriteria are present, the patient is considered to have "sepsis" for purposes ofthe sepsis protocol. The appropriate response should include completion ofthe Sepsis Six within 1 hour, ensuring a member of the medical and critical care"outreach" teams are aware, and that there is consultant review within 24 hours.

A very recent multi-centre study in Wales has shed light on the extent of sepsisoutside of critical care:, according to this protocol definition, the prevalence ofsepsis among 1111 acute in-patient admissions (outside of critical care) was5.5%. Despite the fact that they were (for the most part) managed outside ofcritical care, their 90-day mortality was appreciable at 31%, and only a minorityhad been screened for sepsis (26%), had completed Sepsis Six (12%) or hadbeen referred to critical care (16% (34)).

In this instance,there is clearlystill work to do toimprove clinicalengagement withthe appropriaterecognition andtreatment of sep-sis - and lookingto the future, it isunclear how theqSOFA scoremight identify patients at risk compared with the existing protocol definition ina UK general hospital population (or indeed how a change in the method ofidentifying such patients might itself impact on quality improvement). However,such studies are vitally important since they clearly demonstrate that thesuccess of the quality improvement programme can be tracked sequentiallyamong a population highly representative of acute hospital admissions over alarge region.

OutcomesDespite apparent short-falls in early recognition and management of sepsis, itwould appear that mortality due to sepsis is falling on an individual patient basis(16, 19), and it has been suggested that overall progress of "standard care" of thecritically ill has been one of the factors which determined the lack of efficacy ofhighly protocolised goal-directed therapy in the recent randomised controlledtrials, referred to above (35). However, what is becoming progressively apparentis that sepsis often has adverse consequences for a patient long after he or shehas survived to hospital discharge, in terms of quality of life and indeed long-term mortality (36). If we intend to improve outcomes from sepsis, ultimately, wemust look beyond short-term hospital mortality and longer-term impact ofsepsis on physical and psychological health, function and quality of life.

ConclusionsSepsis is common and, at the very least in secondary care, we will inevitablycome into contact with patients at high risk due to sepsis. It is important that weare able to recognise sepsis whatever our background - but also that we areable to constructively influence the evolution of hospital-wide systems whereverour area of clinical practice. As an already established trigger tool, early warningscores such as NEWS have a potential advantage over the newer qSOFAscore in terms of their existing integration into escalation pathways - thoughtheir relative performance, as predictive tools for outcome in sepsis are still tobe determined. However, at the bedside, the steps required to achieve a goodoutcome are not necessarily complex - and if we raise our index of suspicion(or "Just say sepsis!" to borrow from NCEPOD ) and escalate the care of thoseat risk promptly, we will be given our patients their very best chance.

References:1. Gallagher J. The biggest killer you may not know. BBC News. 2016 10/3/2017.

2. Reporters T. Teenager died of meningitis after tweeting 'Lol... Did not expect to be rushed to hospital, how peak' The Telegraph. 2017 13/3/2017.

3. Belger T. Doctor failed to spot sepsis which killed boy - but is not struck off. Liverpool Echo. 2017 4/4/2017.

4. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus Definitions for Sepsis and SepticShock (Sepsis-3). JAMA. 2016;315(8):801-10.

5. Daniels R, Nutbeam T, McNamara G, Galvin C. The sepsis six and the severe sepsis resuscitation bundle: a prospective observational cohort study.Emerg Med J. 2011;28(6):507-12.

6. Martin GS, Mannino DM, Eaton S, Moss M. The epidemiology of sepsis in the United States from 1979 through 2000. N Engl J Med. 2003;348(16):1546-54.

7. Gaieski DF, Edwards JM, Kallan MJ, Carr BG. Benchmarking the incidence and mortality of severe sepsis in the United States.Crit Care Med. 2013;41(5):1167-74.

8. Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis andSeptic Shock: 2016. Intensive Care Med. 2017;43(3):304-77.

9. NICE. Sepsis: recognition, diagnosis and early management. National Institute for Care and Health Excellence; 2016.

10. Line H. Jeremy Hunt launches nationwide sepsis campaign to help parents spot the signs in children. Independent. 2016 15/12/2016.

11. Marshall JC. Sepsis: current status, future prospects. Curr Opin Crit Care. 2004;10(4):250-64.

12. Opal SM, Dellinger RP, Vincent JL, Masur H, Angus DC. The next generation of sepsis clinical trial designs: what is next after the demise of recombinanthuman activated protein C?*. Crit Care Med. 2014;42(7):1714-21.

13. Machiavelli N. The Prince. London: Penguin; 1961.

14. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003;31(4):1250-6.

15. Vincent JL, Marshall JC, Namendys-Silva SA, Francois B, Martin-Loeches I, Lipman J, et al. Assessment of the worldwide burden of critical illness:the intensive care over nations (ICON) audit. Lancet Respir Med. 2014;2(5):380-6.

16. Harrison DA, Welch CA, Eddleston JM. The epidemiology of severe sepsis in England, Wales and Northern Ireland, 1996 to 2004: secondary analysis ofa high quality clinical database, the ICNARC Case Mix Programme Database. Crit Care. 2006;10(2):R42.

17. Adhikari NK, Fowler RA, Bhagwanjee S, Rubenfeld GD. Critical care and the global burden of critical illness in adults. Lancet. 2010;376(9749):1339-46.

18. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013;369(9):840-51.

19. Kaukonen KM, Bailey M, Suzuki S, Pilcher D, Bellomo R. Mortality related to severe sepsis and septic shock among critically ill patients in Australiaand New Zealand, 2000-2012. JAMA. 2014;311(13):1308-16.

20. Vincent JL, Sakr Y, Sprung CL, Ranieri VM, Reinhart K, Gerlach H, et al. Sepsis in European intensive care units: results of the SOAP study.Crit Care Med. 2006;34(2):344-53.

21. Vincent JL, Rello J, Marshall J, Silva E, Anzueto A, Martin CD, et al. International study of the prevalence and outcomes of infection in intensive care units.JAMA. 2009;302(21):2323-9.

22. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013;369(21):2063.

23. Mayr FB, Yende S, Angus DC. Epidemiology of severe sepsis. Virulence. 2014;5(1):4-11.

24. Hotchkiss RS, Monneret G, Payen D. Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy. Nat Rev Immunol. 2013;13(12):862-74.

25. Vincent JL, Moreno R, Takala J, Willatts S, De Mendonca A, Bruining H, et al. The SOFA (Sepsis-related Organ Failure Assessment) score to describeorgan dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine.Intensive Care Med. 1996;22(7):707-10.

26. Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, et al. Assessment of Clinical Criteria for Sepsis: For the Third InternationalConsensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):762-74.

27. Kumar A, Roberts D, Wood KE, Light B, Parrillo JE, Sharma S, et al. Duration of hypotension before initiation of effective antimicrobial therapy is thecritical determinant of survival in human septic shock. Crit Care Med. 2006;34(6):1589-96.

28. Ferrer R, Martin-Loeches I, Phillips G, Osborn TM, Townsend S, Dellinger RP, et al. Empiric antibiotic treatment reduces mortality in severe sepsis and septicshock from the first hour: results from a guideline-based performance improvement program. Crit Care Med. 2014;42(8):1749-55.

29. ARISE, Group ACT, Peake SL, Delaney A, Bailey M, Bellomo R, et al. Goal-directed resuscitation for patients with early septic shock.N Engl J Med. 2014;371(16):1496-506.

30. PROCESS, Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA, et al. A randomized trial of protocol-based care for early septic shock.N Engl J Med. 2014;370(18):1683-93.

31. Mouncey PR, Osborn TM, Power GS, Harrison DA, Sadique MZ, Grieve RD, et al. Trial of early, goal-directed resuscitation for septic shock.N Engl J Med. 2015;372(14):1301-11.

32. NCEPOD. Just Say Sepsis! A review of the process of care received by patients with sepsis. 2015.

33. Hancock C. A national quality improvement initiative for reducing harm and death from sepsis in Wales. Intensive Crit Care Nurs. 2015;31(2):100-5.

34. Szakmany T, Lundin RM, Sharif B, Ellis G, Morgan P, Kopczynska M, et al. Sepsis Prevalence and Outcome on the General Wards and EmergencyDepartments in Wales: Results of a Multi-Centre, Observational, Point Prevalence Study. PLoS One. 2016;11(12):e0167230.

35. Marik PE. The demise of early goal-directed therapy for severe sepsis and septic shock. Acta Anaesthesiol Scand. 2015;59(5):561-7.

36. Winters BD, Eberlein M, Leung J, Needham DM, Pronovost PJ, Sevransky JE. Long-term mortality and quality of life in sepsis: a systematic review.Crit Care Med. 2010;38(5):1276-83.

Box 4. The Sepsis Six (adapted from Daniels 2011 (5))

Box 5. High risk factors (adapted from NICE 2016 (9))


IntroductionNecrotizing soft tissue infection (NSTI) is a rare and sometimes deadlyinfective condition affecting the subcutaneous tissue and fascia, with orwithout involvement of the muscle. Early diagnosis of NSTI is often achallenge due to inconsistent features of necrosis at presentation however;features of necrosis can also develop within hours.

Necrotizing soft tissue infections (NSTI) which include necrotizing fasciitis(NF) are potentially deadly. They more commonly affect men, the elderlyand diabetics. Diagnosis remains primarily clinical but adjuncts likeLRINEC (Laboratory Risk Indicator score for Necrotizing fasciitis) andMRI scanning may be useful. Early definitive debridement within 24 h ofadmission reduces mortality.

HistoryNSTIs are not new, having been described in the 5th century B.C. byHippocrates, as a complication of erysipelas (2). Modern descriptions firstappeared in 1871, when Joseph Jones, a confederate army surgeon namedit ‘‘Hospital gangrene’’; a rapidly progressing fascial necrosis of bacterialcauses. Since then it has been labeled as “Necrotising Erysipelas”,“Suppurative Fasciitis” and “Acute Dermal Gangrene”. Fournier in 1883-84 gave a classic description of gangrenous infection of perineum andmale genitalia. Meleney in 1908 made a more detailed study and isolatedan organism, naming the infection haemolytic streptococcal gangrene. In1924, he published a detailed description of progressive necrotizing “AcuteHemolytic Streptococcus Gangrene”, exclusively due to Beta HemolyticStreptococcus. Later He described synergistic association of AnaerobicStreptococcus and Staphylococcus. The term “Necrotizing Fasciitis” wasfirst coined by Wilson in 1952, who realized a consistent feature of thisinfection was necrosis of the fascia and subcutaneous tissue with relativesparing of the underlying muscle. He observed that cutaneous gangreneis not invariably present but fascial necrosis is a constant feature. In 1977,Giuliano determined the polymicrobial infection involvement.

Epidemiology and aetiology It remains relatively rare in the UK, with an incidence, although difficult toassess, of approximately 500 new cases each year (3). The aetiology ofnecrotising fasciitis is not fully understood, and in many cases no identifiablecause can be found.

It appears to occur more often in men, and in patients older than 50 years.The risk factors have not yet been fully determined, probably due to itsrarity, problems with definition, and its diverse nature. However, there area number of conditions that are almost certainly related. Patients withdiabetes appear to be particularly at risk. Other common associationsinclude obesity, hypertension, peripheral vascular disease, alcoholism,smoking, chronic liver disease, immunosuppression, end stage renal

disease and intravenous drug abuse.

In children, there is a relationship between recent varicella zoster infectionand severe muskuloskeletal infections including NF, particularly with groupA beta-haemolytic streptococcus. It is thought that the varicella vesicleprovides a portal of entry for the bacteria, with subsequent scratching of theskin contributing to the spread of the infection.

Some authors have suggested that Non-Steroidal Anti- Inflammatory Drugs(NSAIDs) may be a risk factor for NF caused by group A streptococcusinfections. It is suggested that NSAIDs may suppress the symptoms of NF,leading to delayed diagnosis, or they may suppress the immune response andenhance the virulence of the disease. Some have suggested that NSAIDs maydelay appropriate treatment due to symptom suppression.

While NSTIs may affect any part of the body, they are most common in theextremities, particularly the lower limb. Fournier’s gangrene is a specific formof NF of the perineal, genital or perianal regions. Taviloglu et al found perinealdisease was an independent risk factor for idiopathic NF (4).

Some of the predisposing risk factors are listed below in the table.

Pathophysiology The pathogens responsible for NSTI are known to cause infections thatgenerally are not normally life threatening. Regardless of the type of micro-organism, a common pathway ensues following inoculation. The pathogenesisof NSTI involves a three-staged attack with i) local angiothrombotic bacterialinvasion, ii) local tissue necrosis and iii) release of toxins. The exotoxins areresponsible for early systemic features. Bacterial invasion leads to secretionof local cytokines, leading to activation of platelets. Along with activated whitecells, these platelet clumps lead to microvascular occlusion. Cutaneous bloodsupply and lymphatic channels undergo thrombosis. Subsequent localhypoxia and local inflammatory marker release, including TNF alpha and IL-6, lead to cellular dysfunction and death. Early local ischaemia encouragesnecrosis as well as preventing access to antibiotic therapy. This local anoxialeads to progressive cutaneous nerve damage, leading to severe pain followedby local anaesthesia. Rapid thrombosis oflocal vasculature explains lack of lymphaticspread of these conditions. This may alsoexplain the low incidence of NSTIstravelling across the fascia to deepermuscular compartments. Spread ofinfection is therefore contiguousand horizontal. Group AStreptococcus also displayssurface proteins M1 and M3,which resist phagocytosis.The presence of superanti-gens leads to excessive activationof T-cells, leading to an acceleratedimmune response.

Necrotizing Fasciitis:Strategies for management


Clinical featuresNecrotising fasciitis can affect any part of the body but the extremities, theperineum, and the truncal areas are the most commonly involved. Mostpatients present with signs of inflammation such as erythema, swelling, andpain at the affected site. Severe pain disproportionate to local findings andin association with systemic toxicity should raise the suspicion of necrotisingfasciitis. However, these symptoms may be non-specific at first, which oftencauses the diagnosis to be missed. As the infection progresses, the skinbecomes increasingly tense and erythematous with indistinct margins. Itmay change colour sequentially from a red-purple to a dusky blue beforeprogressing to necrosis and formation of bullae and eventually becominghaemorrhagic. Crepitus of the affected area may be palpated and may evenbe seen as soft tissue air on a plain radiograph. Symptoms may develop overa period of hours to several days, and presentations are varied. Patientspresenting at an advanced stage may show signs of systemic shock andsepsis, and it is these patients that often pose diagnostic difficulties sincethey may be confused, agitated, or even have a reduced level ofconsciousness.

DiagnosisCertain diagnostic signs that have come to associate with necrotisingfasciitis are not always present. The findings of crepitus can be seen as softtissue air on plain radiograph. Even though they are pathognomonic forthe disease, their absence should not exclude the diagnosis (5). Otherfindings that are common in necrotising fasciitis include a raised white cellcount as well as raised concentrations of glucose, urea, and creatinine.Hypoalbuminaemia, acidosis, and an altered coagulation profile may alsobe present. Other tests, such as fine needle aspiration and incisional biopsyhave been used to aiddiagnosis since they providetissue samples for culture andhistological analysis. However,their usefulness is limited byfalse negative results. Similarly,computed tomography andmagnetic resonance imagingare useful in cases where signsare equivocal or the diagnosisis in doubt.

The diagnosis thereforeremains a clinical one, and theinformation drawn from all theinvestigations should be usedin conjunction.

Wall et al developed the firstlaboratory based diagnostictool for NSTI (6). The presence

of either a WBC >15.4 x 109/L or a serum Na<135 mmol/L was shown to be have 90%sensitivity and 76% specificity for NSTI. Thepositive predictive value (PPV) was 26% andthe negative predictive value (NPV) was99%, meaning that this is a good tool to ruleout NSTI, but not useful to confirm an NSTIdiagnosis. Serum lactate >2.0 mmol/L atpresentation identifies the tissue necrosis ofNSTI, with a sensitivity of 100% and specificityof 76%. Lactate in isolation has not been vali-dated in other papers, but has been integratedin other biochemical prediction tools (7).

In 2004, Wong et al published the results oftheir Laboratory Risk Indicator forNecrotizing Fasciitis (LRINEC) (8). This was amulticenter observational study thatperformed a univariate and multivariatelogistical regression analysis to identify themost useful blood tests to differentiatebetween NSTI and severe (non-necrotizing)soft tissue infections. The serum bloodparameters for the LRINEC scoring and theirassociated weighting are seen in tables, witha maximum LRINEC score of 13.Despite its limitations, the LRINEC index isused widely to escalate the response tosevere infections. An LRINEC score of 6had a PPV of 92% and NPV of 96% todiagnose NSTI, a significant improvement onthe initial predictive modelsuggested by Wall et al. Analysisof the LRINEC scoring tool wasbased on 89 consecutive NSTIcases and it demonstrated thatLRINEC is a statistically strongmodel. However, a validationassessment of LRINEC from anindependent unit by Liao et al, (who assessed 233 NSTI patients) foundthat an LRINEC score of 6 had a sensitivity of just 59%, a specificity of84%, a likelihood ratio of 3.89, a positive predictive ratio of 38% and anegative predictive ratio of 93% (9). The conclusion of this secondaryvalidation assessment was that the LRINEC is a useful diagnostic adjunct,but less useful in achieving an early diagnosis.

Dr Amit GoelClincal Fellow,

Department of Trauma& Orthopaedics

Glan Clwyd HospitalRhyl LL18 5UJ

Risk stratification of LRINEC Score


TreatmentThe treatment of NSTIs is early definitive surgery with supportive care withfluid and electrolyte resuscitation and intravenous antibiotics. The infectionmust be assumed to be polymicrobial until the results of sensitivities areavailable and empirical antibiotic therapy should cover both aerobic andanaerobic bacteria.

Surgery remains the only definitive treatment for NSTI/NF. Operativefindings include grey necrotic fascia, the presence of murky ‘‘dish water’’pus, a lack of bleeding and less resistance of the fascia to digitalexamination. Debridement should be continued following the necroticplane proximally to where subcutaneous tissue no longer lifts easily off thefascia and healthy bleeding tissue is identified. It must be remembered thatthe infection extends beyond the margin of apparently healthy skin. Initialsurgery must be aggressive. Following the initial surgery, patients shouldbe returned to theatre every 24 to 48 hours for re-examination to ensureadequate control of the infection. The patient will recover only when allinfected tissue has been removed.

A clear pre-operative surgical strategy is important, as with all surgery.Harrison and Kapoor suggested the zone approach to debridement (10).The zones must be marked as clearly as possible prior to surgery.

Zone I is an area of clearly defined necrosis. Zone II is the reactionary zonesurrounding the area of necrosis and can be defined by areas of indurationand erythema. Zone III is considered healthy tissue; however, the marginswith Zone II may be compromised on a microscopic level.

The advised stages for surgeryare as follows:

Zone I: Must be completelyexcised, including the fascia.This may include amputation ifappropriate, for instancewhere digits are involved.

Zone III: Following Zone Idebridement, recommendsexploratory incisions in ZoneIII with a fresh set ofinstruments. This is helpful notonly to confirm the extent of

the infection but it also expedites laboratory confirmation of completeclearance. The site needs to be near but not adjacent to a markedboundary of Zone II. As some of these debridement may take a numberof hours, samples sent at the end of the procedure may delay an essentialreturn to theatre. Samples should be sent for gram stain, culture andsensitivity as well as frozen section, if this is available.

Zone II: Complete dermofasciectomy must be performed in this zone.Muscle should form the bed where possible, due to the superior vascularityof this tissue, with resultant high concentration of antibiotics. The ‘Fingersweep test’ aids surgical debridement. This test is performed by thesurgeon running a finger between the fascia and subcutaneous tissue in afirm forward sweeping manner. If the subcutaneous tissue has undergone

necrosis, it will peel away easily from the fascia. This should not occur innormal, unaffected tissue. Foul smelling ‘dishwasher fluid’, althoughpathognomonic of necrotizing fasciitis, may not necessarily be present.

Following complete surgical debridement, highly absorbent dressing padsare used with large steriderm sheets as a dressing. The use of VAC dressingsfollowing the first debridement is not recommended. This is for multiplereasons; continued ooze from the wound bed increases the blood loss, thereis a need for wound review in theatre within 24 hours, and extremely largeareas of wounds are often present following debridement.

Following large soft tissue debridement a patient will be in state of extremeprotein catabolism. Therefore aggressive nutritional support should becommenced as soon as possible to improve healing. Some authors havesuggested maggot debridement therapy to clean the wound of necrotic tissuefollowing initial surgical debridement. Once the wound has been satisfactorilycleared, traditional treatment of the wound involves multiple dressing changes,allowing for slow granulation of the wound base for later skin grafting. Topicalnegative pressure with a VAC dressing to reduce wound oedema, dischargeand to stimulate granulation tissue formation can be used. Topical anti-microbials guided by swab sensitivities have been used to prevent furtherbacterial infection of the wound. Once the surgeon is satisfied with that theinfection has been eliminated, wound closure depends on the size of thedefect and if there are exposed bone or neurovascular structures. Delayedwound closure, skin grafts or flaps may be necessary for final soft tissuereconstruction.

The use of hyperbaric oxygen (HBO) is an area of ongoing investigation. Thetheoretical benefits of an oxygen rich environment are in promoting angio-genesis, improving the function of neutrophils (by increasing local free oxygenradicals) and increasing collagen formation. Improved tissue perfusion resistsinfection, especially when the causative organism is anaerobic (e.g.Clostridium species). HBO has been shown to significantly reduce thechance of amputation and reduces the time for wound stabilization andgranulation formation.

ConclusionNSTI are rare but devastating infections. Necrotizing fasciitis is an uncommonbut potentially fatal condition. It can affect any part of the body. Aetiology isnot clear but most patients have pre-existing conditions that render themsusceptible to infection. Diagnosis remains primarily clinical and requires highindex of suspicion, but diagnostic adjuncts such as LRINEC may help stratifypatients’ risk. MRI remains the best imaging modality if practical and available.However the corner stone of diagnosis and treatment is rapid surgicaldebridement within a maximum of 24 hours of admission. Managementshould consist of immediate resuscitation, early aggressive surgicaldebridement and broad spectrum intravenous antibiotics.

References:1. Hutchison R et al. Necrotizing soft tissue infections for the orthopaedic surgeon. Elsevier 2010; 24(5): 355-62.2 Sadasivan J et al. Necrotizing fasciitis. Indian Journal of Plastic Surgery 2013; 46: 472-8.3 Hasham S et al. Necrotising fasciitis. BMJ 2005; 330: 830.4. Taviloglu K et al. Idiopathic necrotizing fasciitis: risk factors and strategies for management. The American Surgeon 2005; 71(4): 315-20.5 Anaya DA et al. Necrotizing soft-tissue infection: diagnosis and management. Clinical infectious diseases 2007; 44(5): 705-10.6. Wall D et al. A simple model to help distinguish necrotizing fasciitis from nonnecrotizing soft tissue infection.

Journal of the American College of Surgeons 2000; 191(3): 227-31.7. Murphy G et al. Raised serum lactate: a marker of necrotizing fasciitis? Journal of Plastic, Reconstructive & Aesthetic

Surgery 2013; 66(12): 1712-6.8. Wong C et al. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis

from other soft tissue infections. Critical Care Medicine 2004; 32(7): 1535-41. 9 Liao CI et al. Validation of the laboratory risk indicator for necrotizing fasciitis (LRINEC) score for early diagnosis of necrotizing fasciitis.

Elsevier 2012; 24: 73-6.10. Harrison W et al. Necrotizing soft tissue infection: principles of diagnosis and management. Elsevier 2016; 30(3): 223-31.


The Merseyside and Cheshire Division ofBIDA organised an interactive financial meeting atMayur Restaurant of Liverpool, which wasattended by approximately sixty BIDA membersof Merseyside & Cheshire Division. This meetingwas sponsored by Thind financial services. Themeeting was opened by Dr Birendra Sinha thepresident of the division, who welcomed themembers and Mr Jay Thind, Director of Thindfinancial services along with Mr Steve Moy, WealthManagement Consultant of St James Place. DrSinha also announced and welcomed the fourNEW members who joined BIDA on the day. Themeeting was very informative for the financialhealth of BIDA members, Thind financial serviceshas been sponsoring similar meetings in variousother divisions of BIDA nationwide.

Dr Anurag Gupta, the divisional secretary gavethe vote of thanks.

Many congratulations toProf. Nirmal Kumar,Consultant Otolaryngolo-gist and Director of MedicalEducation at the WWLNHS Foundation Trust.

He has been elected asPresident elect ENT UKstarting from March 2017. He would take over asPresident in 2019 for 2 years.

He also holds the post of being an HonoraryProfessor at Edge Hill University, Vice ChairmanSAC Otolaryngology UK JCST and is the ENTResearch Lead in the National Institute of healthresearch, Greater Manchester Clinical ResearchNetwork.

Many Congratulations toDr Kailash Chand OBE,one of the senior most GPsfrom the British AsianCommunity. He wasconferred the post of theHonorary Vice President ofthe British Medical Associ-ation for his lifetime servicesto the fraternity and the NHS. He is the first Asianto achieve this honour.

BIDA Journal, February 2017, page25 – BIDA International Congress,Abstract presentations).

The Joint editors of BIDAJournal express their utmostregret and apology to Dr BK Jha. whose photographshould have been printedbeside his abstract presentation entitled:“Orthostatic hypotension in the elderly".

The WIgan and Leigh Division of BIDA haselected new Officers. In addition to beinghonoured as the Division’s ‘Patron’, Dr Alka Trivedi(pictured above, left) will also serve as its President.The new Chairman of Wigan and Leigh is DrLeena Saxena (right), and Dr Shikha Pitalia(centre) was elected as Divisional Secretary.

DivisionalNews

BIDAAchievements

Erratum

BIDA

On Sunday 21st May 2017 the third BIDANational Badminton and table tennis tournamenttook place. The tournament was hosted byMerseyside & Cheshire division and was held atthe Ian Robinson Sports Centre, Crosby,Liverpool. Merseyside, Wigan, Blackburn, NorthEast and Wolverhampton divisions participated.The event was well attended by local members;also in attendance were BIDA National PresidentDr Bachi Sarker, National Treasurer Dr B K Sinhaand Merseyside Divisional Chairman Dr BiplabDas. It was an exciting event, which all theparticipants enjoyed thoroughly.

The following is the outcome of the tournament:

Badminton: Singles Nalin Attanayake - Blackburn (Winner) Rahim Khan - North-East (Runner Up) Doubles Chakra Pani Kulluri & Rahim Khan - North East (Winner) Nalin Attanayake & Narsimha Rao Kalla - Blackburn (R)

Table Tennis: Singles Sarang Sapre - Merseyside (Winner) Mikhil - Wigan (Runner Up) Doubles Prathish Thakkar & Aninda Saha - North East (Winner) Sunil Sapre & Sarang Sapre - Merseyside (Runners Up).

Sports EventsBIDA

Merseyside and Cheshire

Wigan & Leigh

Keep in touch! For all the BIDA news, views, reviews and much more, simply go to www.bidaonline.co.uk

1: I Chronic Alcoholic Pancreatitis: Long standing epigastric painand back pain is suggestive ofchronic pancreatitis.Macrocytosis indicatesexcessive alcohol.

3: G Crohn’s Disease

Small bowel strictures aretypical of the condition.Macrocytosis is due to Vit.B12 malabsorption at theterminal ileum.

4: H Coeliac Disease

May present at any age.Rash is dermatitis herpeti-formis, which is a rare butpersistent immunobullousdisease linked to Coeliacdisease.

5: A Whipple’s DiseaseCaused most likely by a gm +ive cocci, Tropherymawhippelii. It has features of malabsorption and affectsjoints, central nervous system and the cardiovascularsystem. PAS +ive macrophages in the lamina propriain duodenal biopsy is pathognomonic.

2: F Cystic fibrosis:

Caused by a mutation in the gene Cystic fibrosis transmembraneconductance regulator (CFTR). May present at any age. May have mild features in childhood. Recurrent chest infections together with bothendocrine (diabetes) and exocrine (malabsorption due to pancreatic failure)features are strongly suggestive of the diagnosis.

AnswersMedical Quiz

Mr Amit SinhaFRCS (Trauma & Ortho)

Consultant Orthopaedic Surgeon, Glan Clwyd Hospital (North Wales NHS Trust)


l National President (1 Post)l National Chairman (1 Post)l National Treasurer (1 Post)l National General Secretary (1 Post)l ARM Chairman (1 Post)l ARM Vice Chairman (1 Post)l National Vice President (1 Post)l National Vice Chairman (1 Post)l Deputy Treasurer (1 Post)l Deputy Secretary (1 Post)l Hospital Doctors Forum Chairman (1 Post)l General Practitioners’ Forum Chairman (1 Post)l Doctors’ in Training Forum Chairman (1 Post)l Women Doctors’ Forum Chairlady (1 Post)l Public Health & Community Health Medicine Forum (1 Post)l Executive Committee Members (10 Posts)

As per BIDA Constitution, the BIDA National Elections are due to be held in July2017. The Constitution entitles only fully paid members of the Association toparticipate in this election, either for contesting or voting purposes. As per theNational Executive Committee decision only those with valid membership on28th April 2017 will be eligible. Every nomination must include consent fromthe nominee and be proposed and seconded by a fully paid member and dulysigned by all three. Any nomination which does not comply with theserequirements will be invalidated. The posts of Chairmen of the Craft Committeesare only applicable to those whose main craft of current practice is in that field.

Nomination forms have already been posted to all BIDA members.

The last date for nominations to be received at Central Office, addressed to theChairman of the Election Commissioners, is before 5.00pm Friday 2nd June2017 accompanied by a brief CV of the nominee (not more than 30 words forExecutive Committee posts and 60 words for Officer’s posts). Any nominationsreceived late for whatever reason, or received in the form of faxes and e-mailswill not be accepted.You can if you so wish, send a separate nomination for thepost of one Officer as well as an Executive Committee Member. If you are electedfor the post of Officer, your nomination for the post of EC Member will be deemedto be invalidated.

After the closing date of receipt of nominations i.e. 5.00pm 2nd June 2017, a listof those candidates contesting for the same position will be sent to the nomineesand they will have the opportunity to withdraw (if they so wish in writing, dulysigned) before 5.00pm 20th June 2017. The final list of nominees will beforwarded to the Election Commissioners on that date and no further requestsfor withdrawals can be accommodated. Ballot papers will be posted out to theregistered address of all fully paid members by Central Office with a reply paidenvelope by Friday 7th July 2017 and returned to the Central Office by Friday28th July 2017.

Yours sincerely,

Dr U M Pati Chairman of the Election Commissioners, BIDA

Please note the National Executive Committee has decided to advise thatwritten canvassing by individual candidates will not be encouraged.

Dear Members,

I hereby invite nominations for the following posts:

2017 BIDA

NationalElections

Dr U M PatiChairman of the Election

Commissioners, BIDA


When you’ve passed, book a place at thefree Welcome to UK practiceworkshop

99% of doctors said theywould change their practice as aresult of attending the course.

You are invited to a free half-day workshop called Welcometo UK practice.

Are you takingPLAB part 2?

If you are a new doctor, or a doctor who isnew to working in the UK, the workshop willhelp you understand the ethical issues thatwill affect you and your patients on a day-to-day basis.

What does the workshop cover?■ Find out about the role of the General Medical Council, including the standards that all doctors working in the UK need to follow.

■ Learn from the real life experiences of other doctors through the video Things I wish I’d known.

■ Work through interactive scenarios on the issues regularly faced by doctors new to working in the UK, including consent, confidentiality, raising and acting on concerns, caring for patients aged 0–18 years, and prescribing.

■ Use your own learning log to capture tips and reflections to take away with you.

How does the workshop help you?Over 1,000 doctors have taken part in theworkshop across the UK and feedback has beenuniversally positive. From a sample of doctorsattending the programme:

■ 98% of doctors said it helped them to reflect on their practice

■ 99% said they would change their practice as a result of attending the workshop.

Book your place!We hold sessions every month across the UK.Events are very popular and places go quickly!

“”

I gained confidence and myawareness increased“ ”For more information about the workshop, and to book your place, go to

Join theconversation youtube.com/gmcuktv

linkd.in/gmcuk@/gmcuktvfacebook.com/gmcuk

www.gmc-uk.org/welcomeUKTelephone

0161 923 6602

The British International Doctors Association (BIDA) is a professional doctors' association. Its soleobjective is promoting Equalityand Fairness for all doctors and dentists working throughout the UK.

BIDA’s mission is to achieve equal treatment of all doctors and dentists based on their competence andmerit, irrespective of their race, gender, sexual orientation, religion, country of origin or school ofgraduation.

If you believe in this mission and would like to be part of this endeavour, join us!

u You will make professional contacts, gaining the opportunity to network with people who can impact your profession, and giving you access to new opportunities, friends and information.

u In addition to being part of a group of like-minded professionals, and having the recognition of your peers, specific member benefits include:l Attending BIDA-organised international, national and regional conferences, seminars, meetings and many other educational and social activitiesl Constant access to pastoral supportl Nominations for excellence awardsl BIDA Journal, our Scientific journal, complete with news, interviews and much more.

If you are interested in joining BIDA, or would simply like to know more about us, please either write toBIDA, ODA House, 316A Buxton Road, Great Moor, Stockport, SK2 7DD

or e-mail us at [email protected], or contact us through our website at the address below.

We look forward to hearing from you!

www.bidaonline.co.uk

Documents

BIDA Journal May2017 A4x28pp FINAL...Dr S Kumar Dr P Sarkar Dr S Sarker Mr C Selvasekar Dr S Senapati Any photographs offered for publication become the property of BIDA Journal and