Muniesh Muthaiyan Shanmugam has completed a MSc (Integrated) in Biomedical Sciences , and now studying for a Post Graduate Advance Diploma in Molecular Diagnosis at Bharathidasan University, Tamil Nadu. He has accepted this week’s TLS challenge to complete the 10-point medical school questionnaire. Read on to find out more, and don’t forget to look here for more information on how YOU can take up the 10 question challenge.

1) Why did you decide to study medicine?
From early high school, I have admired the way the living system is organised & the way it functions. I am fascinated by the science underlying pathological condition and how the living system can be aided to restore its homeostasis? Such admiration and profound interest in gaining knowledge about the basic organisation of living being paved way to study medicine.

2) Can you share some things that you wish that someone had told you before you applied to study medicine?
I wish to share one of the invaluable advice provided by one of the Professor who taught me good laboratory practice and various techniques in molecular biology. “Always make a note of the protocol, conditions, incubation timings etc. exactly as you carry out the experiment. It is important to have good record of the work you are doing, so that when the results seem impossible, you can look back and discover where you may have gone wrong”.

3) What profession would you be in if you weren’t in medicine?
I would have been in the field of Aeronautics as I am fascinated by the science of flight. I had an equal passion for Aeronautics, like that of medical science. More realistically I would have been doing Master of Technology in Aeronautics if I weren’t in medical science.

4) What is your biggest motivation?
It is my profound interest in this subject that motivates me. The challenge of science to test the capacity of my brain to deeply understand, analyze and creatively think has kept my enthusiasm towards biology than any other subjects during my high school days.

5) What are you most interested in so far and why?
I am interested in molecular biology, and understanding various mechanisms such as physiological signal transduction/signals and their outcome or events which helps to maintain homeostasis. However, I like applying my knowledge of cellular integrity and pathological conditions towards understanding the development of therapeutic strategies devouring molecular biology.
The reason for my desire towards molecular biology is because of the fact, that I had enough exposure to research laboratories employing techniques in molecular biology that address problems in biology both through my course work and internships where I learnt to plan, execute and troubleshoot experiments efficiently.

6) What has been your most difficult module so far and why?
In my view, the most difficult module in my medical studies was to plan and successfully execute “Short term Project” (first independent research experience), for around 3 months that was a mandatory component of my masters curriculum. Department of Biomedical Science, being one of the newly started centers at my university, was equipped only with infrastructure that can sustain few pilot experiments.However with these substructure students of my class were provided a chance to plan on their own project work, yet unique, and complete it within the deadline. This period of my study was more challenging to bring the best in me, both intellectually and physically.

7) What is the most memorable positive moment in your medical studies so far?
Persistent positive moment is the successful completion of “short term Project” (mentioned earlier). This project gave me a strong positive hope that I can satisfy my quest in a systematic way taking research as future career.

8 ) What is the worst horror story in your medical studies to date?
The way I missed the placement for clinical medical studies, after my higher secondary schooling, is the worst horror story. I had just missed it on 3 marks less than the cut-off that had been set during the selection process. And finally I decided to graduate in non-clinical studies though I did not lose momentum being at biomedical science.

9) Where do you see yourself in 10 years time?
a) The wishful thinking version
I would wish to see myself as a Professor guiding more than 10 student in my research in a premier research institute at one corner of the world

b) The perhaps slightly more realistic version
More realistically I will be carrying out my second post-doctoral fellowship, because I feel that at least three post-doctoral stints should be carried out to gain sufficient professional experience to successfully establish a laboratory of my own and guide students very efficiently.

10) Can you share some tips/advice for others
a) wanting to study medicine
I request everyone to feel from within. Studying medical science is not a fantasy or a way to make money, it is as a service to the well being of mankind. Stick to ethical rules when doing research and be more ‘Human’ when dealing with patients.

b) already studying medicine
I request everyone to understand the subjects from the basic principles & concepts to high fidelity concepts and realistically apply your understanding to take a logically worth-full decision, have more patience towards research, and try to convert the failure into a positive troubleshooting energy. And finally don’t forget to enjoy your life and studies.

By Elliot Davis

King’s College London
elliot.davis(a)kcl.ac.uk

In 2005, the World Health Organisation (WHO) estimated that three quarters of all HIV positive individuals in Malaysia contracted the virus through intravenous drug use. Described by the UN as a “concentrated epidemic”, the result was a country failing in its Millennium Development Goal of reversing the spread of HIV/AIDS. Since 2005, however, the Malaysian government has radically altered its approach to managing intravenous drug use in the country. Its previously tough stance has been softened, while needle exchange and methadone maintenance programmes have been piloted and are now starting to be rolled-out across the country. These schemes remain in their infancy, yet recent evidence suggests they are already starting to have a positive impact on HIV infection rates.

HIV and AIDS continue to represent a significant public health risk across South and South-east Asia. Recent estimates by the WHO suggest that there are now around 3.8 million children and adults living with HIV in the region. This means only sub-Saharan Africa has a greater burden of infection, with an estimated 22.4 million individuals being HIV positive [1].

In several South and South-east Asian countries, HIV prevalence rates exceed 1 per cent of the 15 to 49-year-old population. Cambodia (1.6 per cent), Thailand (1.4 per cent) and Burma (Myanmar, 1.3 per cent) are among those most severely affected [2]. In Malaysia, which is often lauded for the quality of its healthcare service, the HIV prevalence rate is much lower at 0.5 per cent. But while this figure is below that of even the United States (0.6 per cent), the country faces its own serious challenge. This is because three quarters of the estimated 69,000 HIV positive individuals living inMalaysia contracted the virus through intravenous drug use [2-3].

The extent of the problem was brought into sharp focus by a United Nations (UN) report in 2005. Reflecting on the country’s progress towards achieving its Millennium Development Goals (MDGs), the UN stated that: “Malaysia has achieved commendable successes towards all the MDGs except in halting and reversing the spread of HIV/AIDS” [4-5]. Branding the problem a “concentrated epidemic”, the report went on to point out that, although the general population was perceived to be at low risk, infection rates among high-risk groups – specifically intravenous drug users (IDUs), sex workers and prison inmates – were bordering on 20 per cent. This figure is forty times higher than the 0.5 per cent prevalence rate reported for the Malaysian population as a whole [2-5].

With its MDG of reversing the rise in HIV prevalence by 2015 under threat, the Malaysian government acted swiftly in a bid to stem the tide of rising infections, sparking a rapid and dramatic turnaround in the country’s previous drug policy.

Prior to 2005, Malaysia had exercised a zero tolerance approach when it came to drug use, declaring it “public enemy number one” and hailing 2003 as a “year of total war against drugs” [6-7].

This tough stance extended beyond mere rhetoric, with one of the government’s main aims being the creation of a drug free society by 2015 [7]. Previous attempts to introduce needle exchange schemes had been dismissed out of hand [6] and drug rehabilitation programmes were overseen not by the Ministry of Health but by the Internal Affairs Ministry, which had a wider remit for national security [8]. Capitalpunishment remained the maximum penalty for anyone convicted of trafficking [9]. Meanwhile, any individual recording a positive urine test for either opiate or cannabis use was likely to face a mandatory two year sentence in a government-run drug rehabilitation centre, followed by a further two years’ probation [6, 10].

To many commentators, this hard line stance resulted in a disjointed approach to not only HIV management but also to health policy in general. First and foremost, there was good evidence that the programmes in place simply didn’t work – with up to 90 per cent of those attending rehabilitation centres going on to relapse [7]. In addition, government policy marked a dangerous precedent in a country where various studies have suggested that up to 43.9 per cent and 89.9 per cent of IDUs are respectively HIV and hepatitis C positive [10-11].

Encouragingly, the evidence to date already suggests that the change in approach is starting to yield results. The Malaysian government has worked with a number of Non-Government Organisations (NGOs) to introduce harm reduction schemes, namely methadone maintenance and needle-exchange projects.

From an initial pilot scheme of three centres in 2006, the needle exchange programme had extended to cover eight of the country’s 13 states by 2008. In the same year, some 1.8 million needles were distributed to more than 12,000 users. Meanwhile, over 7,000 individuals are now registered with central government-run methadone clinics, with a further 10,000 people receiving opiate replacement therapy through private practices [6].

The introduction of methadone maintenance schemes, in particular, seems to have had a major knock-on effect in terms of health benefits. A number of studies from around the world have already suggested that individuals involved in these schemes are more compliant with anti-retroviral treatment (ART) regimens, resulting in improved healthcare outcomes [12-13]. By 2007, up to 25 per cent of Malaysian ART patients were IDUs, marking a sharp rise from the figure of 7 per cent reported in 2003 [6].

Although harm reduction programmes remain a relatively new invention in Malaysia, the progress made so far has been heralded as a step in the right direction. Research from UNICEF suggests that the number of new HIV infections occurring in the country each day has fallen from 17 to ten between 2004 and 2009. There has also been a noticeable drop in the number of these infections associated with intravenous drug use, from the previous 75 per cent to 57 per cent [14] (see Figure 1).

Figure 1: HIV infection rates in Malaysia [2, 14]

Yet there remain problems. A recent article in The Lancet pointed out that IDUs continue to drive the epidemic in Malaysia. Around 1.3 per cent of the population are believed to be IDUs. And although HIV testing is now almost universal amongst these individuals (at close to 100 per cent), just 5.1 per cent said they used a condom during their last sexual encounter. Less than 30 per cent, meanwhile, reported using sterile equipment [15].

Compare these figures with the Ukraine, which is frequently cited as the country in the world with the most significant IDU-driven HIV epidemic, and the extent of the task still facing the Malaysian government becomes clear. Although only 27.6 per cent of Ukrainian IDUs had been tested for HIV in the past 12 months, over 80 per cent use sterile equipment and almost 60 per cent used a condom the last time they had sex [15-16].

The importance of these statistics cannot be over-stated. One recent survey of 526 IDUs not involved in drug treatment programmes across five cities in Peninsula Malaysia reported that 68.6 per cent of those questioned continued to share equipment and that 34 per cent were regularly involved in paid sex. Presciently, the study also identified the sharing of injecting equipment and having multiple sexual partners as the two most significant risk factors for HIV infection [11].

There have also been reports that, initially at least, local anti-drug legislation was slow to catch up with the new approach. Writing in 2007, one group of researchers reported that some pilot methadone maintenance and needle exchange projects had been raided by police with attendees beingarrested [7].

Though there is much work still to do in Malaysia, the results achieved so far do suggest that introducing simple measures like needle exchange programmes and methadone maintenance therapy can have a significant impact on HIV infection rates.

As a result of the initial success of these schemes there appears to be increasing goodwill towards them. Last year alone, the number of government-run health clinics operating needle exchange programmes increased from seven to 12, with RM43.1 million (£9.3 million) being invested in the scheme over a five-year programme. In the coming years, the president of the Malaysian AIDS Council has set a target of granting access to these schemes to a minimum of 60 per cent of IDUs [17].

Time will tell how successful these measures are long-term. However, it could well be that Malaysia emerges as a model of just how effective harm reduction measures can be in curbing the spread of HIV/AIDS in developing nations.

References

1. Joint United Nations Programme on HIV/AIDS and World Health Organisation (2009). AIDS epidemic update: December 2009. Geneva, UNAIDS.
2. United Nations Children’s Fund (2007). The state of the world’s children 2008. New York, UNICEF.
3. World Health Organisation (2007). Country cooperation strategy at a glance: Malaysia [online]. Available:http://www.who.int/countryfocus/cooperation_strategy/ccsbrief_mys_en.pdf [accessed 30 March 2010].
4. United Nations Country Team: Malaysia (2005). Achieving the millennium development goals: successes and challenges. Kuala Lumpur, United Nations Development Programme.
5. United Nations General Assembly (2005). Monitoring the declaration of commitment of HIV/AIDS. New York, United Nations.
6. Kamarulzaman A. (2009). Impact of HIV prevention programs on drug users in Malaysia. Journal of Acquired Immune Deficiency Syndrome 52(S1):17-19.
7. Reid G, Kamarulzaman A, Sran SK. (2007). Malaysia and harm reduction: The challenges and responses. The International Journey of Drug Policy18(2): 136-140.
8. Scorzelli JF. (1992). Has Malaysia’s antidrug effort been effective? Journal of Substance Abuse Treatment 9(2): 171-176.
9. Mazlan M, Schottenfield RS, Chawarski MC. (2006). New challenges and opportunities in managing substance abuse in Malaysia. Drug and Alcohol Review 25(5): 473-478.
10. Chawarski MC, Mazlan M, Schottenfeld RS. (2006). Heroin dependence and HIV infection in Malaysia. Drug and Alcohol Dependence 82(S1): 39-42.
11. Vicknasingam B, Narayanan S, Navaratnam V. (2009). The relative risk of HIV among IDUs not in treatment in Malaysia. AIDS Care 21(8): 984-991.
12. Palepu A, Tyndall MW, Joy R, Kerr T, Wood E, Press N, Hogg RS, Montaner JS. (2006). Antiretroviral adherence and HIV treatment outcomes among HIV/HCV co-infected injection drug users: the role of methadone maintenance therapy. Drug and Alcohol Dependence 84(2): 188-194.
13. Roux P, Carrieri MP, Villes V, Dellamonica P, Poizot-Martin I, Ravaux I, Spire B; MANIF2000 cohort study group. (2008). The impact of methadone or buprenorphine treatment and ongoing injection on highly active antiretroviral therapy (HAART) adherence: evidence from the MANIF2000 cohort study. Addiction 103(11): 1828-1836.
14. United Nations Children’s Fund (2009). HIV and AIDS in Malaysia: Fact sheet. Kuala Lumpur, UNICEF Malaysia Communications.
15. Arasteh K, Jarlais DCD. (2008). Injecting drug use, HIV, and what to do about it. The Lancet 372: 1709-1710.
16. United Nations Regional Task Force on Injecting Drug Use and HIV/AIDS for Asia and the Pacific. (2009). Malaysia country advocacy brief: injecting drug use and HIV. Geneva, UNAIDS.
17. Edwards A. (2009). Needle syringe exchange programme injects hope. The Star, May 2009.

Chun Yat, a third year medical student at the University of Cape Town, has accepted this week’s TLS challenge to complete the 10-point medical school questionnaire. Read on to find out more, and don’t forget to look here for more information on how YOU can take up the 10 question challenge.

1) Why did you decide to study medicine?
The ways that the human body functions really intrigue me. I like a discipline in which there is practical application. Medicine was the natural choice. I enjoy the interaction with people too.

2) Can you share some things that you wish that someone had told you before you applied to study medicine?
Dissection is really not that bad or scary, however, the embalming fluid does smell a little offensive. When people say studying medicine is hard-work – it’s not a lie. Having said that, it’s a lot of fun too.

2) What profession would you be in if you weren’t in medicine?
I would have been studying music to become a pianist. I’ve always been passionate about music. I sometimes wonder if there might be some connection between medicine and music because there are many fellow students and lecturers in my faculty who play musical intruments or sing.

4) What is your biggest motivation?
I want to become a good doctor who practises good medicine. It’s also very motivating when you watch medically-related dramas on television and know what they’re talking about.

5) What are you most interested in so far and why?
Internal medicine has been fascinating. The scope of the practice is so big and the different conditions of patients encountered in this field is unique to each patient. I see it as a challenge.

6) What has been your most difficult module so far and why?
I find Embryology difficult because it is very hard to conceptualise the developments of the embryo and foetus in three dimensions. Some anatomical parts in embrology also have very long names which can be difficult to memorise.

7) What is the most memorable positive moment in your medical studies so far?
Towards the end of my second year, when I was interviewing and examining patients in groups of two people. I identified an ejection-systolic murmur on auscultation in a patient with aortic stenosis. We presented our patient to the consultant who was teaching us and he confirmed it. The feeling was very rewarding because there are many moments where murmurs are just seem like noise – something I’m still in the process of learning to appreciate.

8 ) What is the worst horror story in your medical studies to date?
We had to go on an ambulance shift in our emergency medicine module. The ambulance staff and I transported a trauma patient to casualty. When someone took off the patient’s shoe, a pool of blood spluttered onto the floor at casualty. The patient had a stab wound on his feet and blood had been collecting in his shoe.

9) Where do you see yourself in 10 years time?
a) the wishful thinking version
It would be great to be one of the people who helped discover the cure for HIV/AIDS in ten years time. In South Africa, I see many patients who arrive at our academic hospital with HIV/AIDS related conditions. It’s my wish everyday to see this world free of this pandemic.

b) the perhaps slightly more realistic version
After completing my internship and community service, I would love to specialise in the field of internal medicine. Many physicians from my academic hospital (Groote Schuur Hospital) are truly inspiring doctors who are passionate, knowledgeable and caring. I strive to be a doctor like them someday.

10) Can you share some tips/advice for others
a) wanting to study medicine
Many years ago, I’ve always been overwhelmed by the thought of becoming a doctor. It seems like a fantasy that would unlikely to come true because the sheer amount of knowledge and skills that one is suppose to grasp in a few years is just insurmountable. In actual fact, nobody expects a medical student to gather all this knowledge and skills in a single day. Learning is a continuous process that takes place over a long period of time extending well beyond your graduation. Take things a step at a time, and eventually you’ll be studying medicine before you know it (assuming that’s what you really want).

b) already studying medicine?
Sometimes I might feel that what I am learning or doing is completely irrelevant to becoming a doctor. Often later I realise that what I was doing actually helped me develop personally and professionally, therefore be inquisitive and take every situation as a learning opportunity. Be compassionate to your patients because most people will get sick some time in their lives including yourself and me. Become a doctor that you and others will want to seek help from. Enjoy and experience the process of becoming what you want to be because it’s truly a privilege.

By Kevin Gillmann
University of Newcastle
kevin.gillmann(a)wanadoo.fr

“Is it legal for employment to be refused as a result of the outcome of a 3 station OSCE devised by a Trust when a 5 year programme, quality assured by the GMC has provided evidence that the applicant is fit for purpose?” [1]

Such was Professor Tony Weetman, Chair of the Medical Schools Council’s comment, reflecting on the pitfalls underlying the British Government decision to reform the medical career pathway.
Medical Career Pathway in the UK

Since the introduction of the Modernising Medical Careers programme, in 2005, British medical careers are made up of 4 steps. The medical degree, typically consists of 5 years of study in one of the 32 medical schools of  United Kingdom. After graduating, junior doctors enter a 2-year multidisciplinary clinical training called the foundation program. Once they have completed this, doctors can apply for specialty registrar positions, and train to a specialty. This training varies  in length depending on the chosen specialty, and gives access to hospital consultancy or general practice.

Figure 1: Modernising Medical Careers’ organisation with average duration of each step.

A flawed selection process?

While the Modernising Medical Careers programme has made transitions between career steps more harmonious, it is now the access to foundation programme positions that is questioned. The issue was raised in 2008, when a NHS study “The Next Stage Review: A High Quality Workforce” stated that “New work needs to be undertaken to develop more reliable and valid selection tools for recruitment”. Following this declaration, the British department of health took immediate action, committing a panel of international experts to analyse and reflect upon the current selection methods. [2]

The current selection is based upon 2 scores. The first one, a knowledge score, is obtained by ranking medical students on the basis of their medical school results. From this sorted list, each medical school divides its own students into four quartiles, and scores are allocated to students of each quartile. Students from the first quartile receive 40 points, and all those from the second, third and fourth quartiles receive 38, 36 and 34 points respectively. This allocating method has been depicted unfair and two crucial issues were highlighted. First, since students from the first quartile of any medical school get the same amount of points, some students may theoretically be lead to choose a less competitive medical school to rank in the first quartile more easily and thus be more likely to obtain the foundation placement of their choice. [3] Then, there are currently enough foundation positions to ensure employment to every junior doctor. However, it may not always be the case, and the day the ever-increasing number of junior doctors will overcome the number of posts available, some will ultimately be refused. And refusing employment on the basis of a selection process, which is not considered as sound, transparent and fair would open the way to a myriad of potential legal challenges. [2, 4]

The second part of the current selection process is a professionalism score. Students’ professional traits are assessed by a series of open-ended ‘white space’ questions they answer during their spare time at the end of their final year. Their answers are marked by a panel of doctor from the applicant’s first choice base unit. The criticisms on this method are numerous. Firstly, it has been identified that the ‘white space’ format for answers compromised the objectivity of the assessment. [4] Then, despite the fact a random selection of 10% of applicants is asked to provide evidences of their answers, this method is said to open the way to cheating and plagiarism. [4, 5] Finally, the panels responsible for the marking of the forms complain about the time-consuming aspect of the task. [6]

Options study

During the 9 months following these findings, the panel of experts assessed various selection methods, and proposed the “Improving Selection to the Foundation Programme Project”. In order to define the ideal selection criteria, they firstly raised the crucial question of what expectations hospitals have of ‘good doctors’. Three attributes were retained: clinical knowledge, clinical skills and professional traits. [7] They then considered the traditional options available to assess such criteria: structured interviews, multiple-mini interviews, a national examination of clinical skills and knowledge, a national test of professional traits, and a standardised score from medical schools. All these selection methods were assessed upon several criteria, ranging from transparency to fairness and cost. As a result of this feasibility study, interviews were dismissed for their inherent lack of objectiveness and their cost, just like national examinations of which the OSCE component was considered to be too expensive, and the assessment of knowledge too redundant with students’ finals. [8]

Figure 2: Results of the feasibility study showing the cost of every method over five years on the ordinate and their reliability score in arbitrary units on the abscissa. (Adapted from Option Review in Paul O’Neil’s presentation: Pilots for FP Recruitment and Selection 2013)  [8]

Proposed selection process : what is going to change?

At the end of the study, the panel reached a conclusion and proposed a recommendation framework. As other methods to assess clinical knowledge and skills had been ruled out, experts decided that medical school should keep the responsibility of this assessment. However, the quartile distribution would be replaced by a more granular process allowing standardisation of every student’s grades in a fair and reliable way: the Educational Performance Measure (EPM).

As far as ‘white space’ questions are concerned, they would be replaced by another professionalism assessment, which would this time be a national computer-marked test: the Situational Judgement Test (SJT). The Medical Schools Council describes it as “similar to GP short-listing tests”, and it is very likely to be on the form of small scenarios and identifying the most appropriate action to take. It should also put an emphasis on solving ethical and professional dilemma rather than focusing on students’ extra-curricular achievements. The rest of the process should on the whole not be reformed. [8] In practical terms, for students this reform would mainly replace the professionalism “take-home essays” by a National Situational Test, and change the way their medical school achievements are converted into a standardised score.

Figure 3: Proposed Selection Process. (Adapted from «Proposed Selection Process» in Denis Shaughnessy’s presentation: Improving the Selection Process) (7)

Figure 4:  Situational Judgement Test, sample question. A suggested answer to the above question is: A-D-C-B-E. (2)

This new selection process is currently in its stage of development and still has to be tested, legally reviewed and approved by the ministry before it can go live.

Dr Richard Price, careers coordinator at Newcastle University adds: “All we know currently is that the planned changes will be piloted  in selected medical schools alongside the existing system for the next two years, and  will  be  thoroughly evaluated prior to their full introduction.”

These trials are to start in October 2010 on a sample of a few hundred applicants, before expanding to a few thousand by March 2011. These pilots will be followed by a legal review, an approval, and a preparation phase that could last until autumn 2012. This last stage is an unavoidable part of the process since it is during this preparation that will be decided how to combine the EPM and SJT to produce a representative overall score.

Thereby, the new selection process should not go live until the academic year 2012-2013, at the earliest. However, experts recommend to continue with the current method unless the pilots show sound reasons for change. [8]

Figure 5: Introducing the changes: a timing overview. (Adapted from “Timing Overview” in Denis Shaughnessy’s presentation: Improving the Selection Process) [7]

So how do other countries sort the matter?

Generally, four main methods are broadly accepted internationally to determine selection of junior doctors’ first placements after graduation. Most countries opt for one of these solutions, or a close alternatives.

1. A national examination ranks applicants according to their results and allocates everyone to his first available choice, starting from the top of the list. [9]
2. Applicants get systematically appointed to the university hospital the graduated from. [10]
3. The government decides where junior doctors are appointed to, depending on current needs. [11]
4. Applicants are scored against various criteria before an algorithm matches them with to their most highly ranked choice. [12]

In France, students do not graduate until they have finished their internship. But the 6-years lecture-based studies are separated from the clinical internship by an examination. This latter is a national examination after which students are ranked upon their score. Students may then choose their positions in the order of their ranking.  There are generally more positions than applicants, however applicants with the lowest scores may not have the choice of their specialty. [9]

In Italy, after graduation junior doctors complete a three-month unpaid supervised placement. It consists of two months in the university hospital they graduated from and a month shadowing a general practitioner in a local surgery. After they successfully complete these, a national examination must be passed to obtain full license to practise. [10]

India : Compulsory Rural Service

In India, the degree of Bachelor of Medicine and Bachelor of Surgery (MBBS) is awarded to students once they have completed five years and a half at medical school. However, in an attempt to improve health care standards in the most rural communities, some states have decreed that junior doctors should, as a priority, be appointed to tribal areas. Thereby, young doctors are now bound to practice medicine in rural settings for a year after graduation, before they can apply to any other post. [11]

During their last year of medical school, American students apply to residency programmes via the online Electronic Residency Application Service (ERAS). These programmes then short-list the applicants they want to interview. Criteria used for such a selection can vary widely. A study undertaken in 2000 shows these variations as 94% residency programmes reported to base their selection on examination scores, 87% on potential letters from deans, 85% on application forms, and only 61% on personal statements. [13] After the interview stage, programmes rank their interviewee by order of preference, and applicants similarly rank the programmes they applied to. An algorithm, the National Residency Matching Program, is then responsible to match programmes and applicants with their most highly ranked choice. In 2008, of the almost 36,000 applicants, 20,940 matched. [14] For the unmatched applicants, it is during a period known as the ‘Scramble’, during which the applicants who did not match try to secure a remaining available position. But this process is barely structured and offers minimal chances of success. Dr. Freedman, an American leader in medical education, describes the situation: “Jammed fax machines and lines of communication make this process challenging. […] In 2008 by 6pm the day after the Scramble, only 179 positions of the 1,388 positions remained open.” The Association of American Medical Colleges has, however, acknowledged the issue and is currently leading a study to give a more defined structure to the Scramble. [12]

References

1- Pr. Weetman T., Written Evidence Submission – The Evaluation Of the Foundation Programme, Medical Education England.

2- Improving Selection to Foundation Programme Briefing Pack – Stage 2 of Project, Medical Schools Council: 2010.

3- Kelly C., Should UK Medical Students Sit a National Qualifying Exam?, Student BMJ: 2008 – 16:184|17.

4- Pr. Paice E., Dr. Rainsberry A., House of Commons, Health Committee, Modernising Medical Careers, Volume II, Written evidence: October 2007 – p127.

5- Medical Schools Council, Characteristics of the Current System for Selection into the Foundation Programme, Appendix B.

6- KSS FP Evaluation Final Report from KSS Deanery: 2006 – p25-28.

7- Shaughnessy D., Improving The Selection Process, Presentation: March 2010.

8- O’Neill P., Pilots For FP Recruitment and Selection 2013, Presentation, UKFPO: 2010.

9- Postes et Rangs Pour l’Examen National Classant, Journal Officiel, Direction de l’Information Légale et Administrative: 2009.

10-Pr. Torre G.C., Corso di Laurea in Medicina e Chirurgia, Facoltà di Medicina e Chirurgia, Università degli Studi di Genova.

11- Sai Gopal M., Opinion Divided Over Compulsory Rural Service, The Hindu: February 2010.

12- Freedman J. MD, The Residency Scramble: How It Works and How It Can Be Improved,  The Student Doctor Network: March 2009.

13- Adams L. J. MSW, Brandenburg S. MD, Blake M. MS, Factors Influencing Internal Medicine Program Directors’ Decisions about Applicants, Academic Medicine: May 2000 – Volume 75 – Issue 5 – p 542-543.

14- Advance Data Tables For The 2008 Main Residency Match, National Residency Matching Program, March 2008 – p3.

Prof Eric AP Steegers MD,  Peter von Dadelszen MBChB, Johannes J Duvekot MD, Prof Robert Pijnenborg PhD.

Summary 

Pre-eclampsia remains a leading cause of maternal and perinatal mortality and morbidity. It is a pregnancy-specific disease characterised by de-novo development of concurrent hypertension and proteinuria, sometimes progressing into a multiorgan cluster of varying clinical features. Poor early placentation is especially associated with early onset disease. Predisposing cardiovascular or metabolic risks for endothelial dysfunction, as part of an exaggerated systemic inflammatory response, might dominate in the origins of late onset pre-eclampsia. Because the multifactorial pathogenesis of different pre-eclampsia phenotypes has not been fully elucidated, prevention and prediction are still not possible, and symptomatic clinical management should be mainly directed to prevent maternal morbidity (eg, eclampsia) and mortality. Expectant management of women with early onset disease to improve perinatal outcome should not preclude timely delivery—the only definitive cure. Pre-eclampsia foretells raised rates of cardiovascular and metabolic disease in later life, which could be reason for subsequent lifestyle education and intervention.

Introduction

Complicating 2—8% of pregnancies, pre-eclampsia, along with the other hypertensive disorders of pregnancy, is a major contributor to maternal mortality worldwide.1, 2 In Latin America and the Caribbean, hypertensive disorders are responsible for almost 26% of maternal deaths, whereas in Africa and Asia they contribute to 9% of deaths. Although maternal mortality is much lower in high-income countries than in developing countries, 16% of maternal deaths can be assigned to hypertensive disorders.1 The incidence of pre-eclampsia has risen in the USA. 3, 4 This finding might be related to an increased prevalence of predisposing disorders, such as chronic hypertension, diabetes, and obesity.3 Some ethnic groups (eg, African-American and Filipino women5, 6) and low socioeconomic status are associated with a heightened risk.7 Furthermore, severe pre-eclampsia is a major cause of severe maternal morbidity (eg, stroke and liver rupture) and adverse perinatal outcomes, such as prematurity and intrauterine growth restriction.2 Although the generalised seizures of eclampsia complicate 2—3 cases per 10 000 births in Europe, eclampsia is 10—30 times more common in developing countries than in high-income countries. 2

Other hypertensive disorders in pregnancy are pre-existing hypertension and gestational hypertension. Pre-eclampsia is generally defined as new hypertension (diastolic blood pressure of ≥90 mm Hg) and substantial proteinuria (≥300 mg in 24 h) at or after 20 weeks’ gestation.8 However, how best to define the maternal syndrome of pre-eclampsia, and how to differentiate mild from severe disease is being debated.9—12Table 1 shows recent classification frameworks, evolving from previous work of the American College of Obstetricians and Gynecologists13 and the International Society for the Study of Hypertension in Pregnancy.14 The main differences between the classification systems are: (1) inclusion or exclusion of complicated non-proteinuric gestational hypertension as pre-eclampsia; (2) differentiation between clinical and research definitions in the Australasian guideline; (3) use of early-onset pre-eclampsia as a severity criterion in Canada (<34 weeks) and the USA (<35 weeks); (4) clinical importance of assessing white-coat hypertension; and (5) definition of severe hypertension. Although perinatal risks have long been recognised to be highest remote from term, the 20-fold increase in maternal mortality that is associated with pre-eclampsia arising at less than 32 weeks (compared with that at ≥37 weeks)15 seems not to have been, emphasising the importance of early-onset pre-eclampsia as a severity criterion. The debate between setting the systolic blood pressure definition of severe hypertension at either 160 mm Hg or 170 mm Hg needs to be resolved because of rising concerns about lethal maternal stroke risks at the lower threshold for blood pressure.16, 17 None of these classification systems seems to have been independently assessed for the ability to identify women and fetuses at heightened risk of the adverse events that make pre-eclampsia so important.

Table 1 International comparison between recent classification systems

Pathogenesis

Although the cause of pre-eclampsia remains largely unknown, the leading hypotheses strongly rely on disturbed placental function in early pregnancy (figure). Impaired remodelling of the spiral artery has especially been considered as an early, but not necessarily the primary, defect causing pre-eclampsia.19 Remodellingis a multistep process20 in which the first decidua-associated step should be initiated around implantation. Disturbances at this stage could increase risk of pre-eclampsia, and might explain its higher incidence in women with unexplained subfertility or recurrent miscarriage.21, 22 Decidua-associated vascular changes also arise in the inner (junctional zone) myometrium, followed by trophoblast invasion with associated remodelling.23 Interaction of trophoblastic HLA-C, HLA-E, and HLA-G with uterine natural killer cells or dendritic cells, or both, is thought to be important in regulation of invasion,24—26 and some combinations of HLA-C and killer cell immunoglobulin-like receptor isoforms predispose to pre-eclampsia.27

 

Figure 1 Possible pathophysiological processes in pre-eclampsiaAV=anchoring villus. COE=coelomic cavity. CY=cytotrophoblast. DB=decidua basalis. DC=decidua capsularis. DP=decidua parietalis. EN=endothelium. ET=extravillous trophoblast. FB=fetal blood vessel. FV=floating villus. GL=gland. IS=intervillous space. JZ=junctional zone myometrium. MB=maternal blood, leaving the intervillous space with various components such as antiangiogenic factors. MV=maternal vein. SA=spiral artery. SM=smooth muscle. ST=stroma. SY=syncytiotrophoblast. TM=tunica media. UC=uterine cavity. sFlt-1=soluble form of the vascular endothelial growth factor receptor. Centre panel of figure adapted from Karumanchi et al,18 with permission from Elsevier.

Intervillous flow seems to start 7—8 weeks of gestation by the appearance of connecting channels between spiral arteries and lacunae in the wall of the implanted blastocyst.28 Early trophoblast plugging might protect the embryo against high oxygen concentrations. Researchers29 have postulated that premature loss of these plugs could result in early miscarriage, or, dependent on timing, pre-eclampsia. Gradually plugs are resolved by intravascular migration of the trophoblast. Intervillous flow is thought to start in lateral regions,29 whereas trophoblast invasion and associated deplugging of spiral artery outlets starts in the centre and spreads to the periphery. Peripheral onset of intervillous flow should result in high local oxidative stress, leading to villous regression and formation of the chorion leave. Insufficient lateral spread of endovascular plugging could therefore result in extensive chorionic regression and a small placenta,29 contributing to intrauterine growth restriction, early-onset pre-eclampsia, or both.

Overlaying trophoblast invasion and spiral artery remodelling steps on Jauniaux’s placental oxygen curve 30 shows that decidua-associated remodelling in decidua and junctional zone myometrium develops during the steep rise in placental oxygen (10—12 weeks), whereas at 10 weeks some decidual arteries are already filled with endovascular trophoblast over their entire length.31 Placental flow defects can be detected as early as 12 weeks in women who subsequently develop pre-eclampsia.32 Deep invasion of the myometrial arterial segments comes after the steep rise in placental oxygen from 15 weeks onwards, and can therefore be triggered by increased flow.31 Thus, impaired invasion of myometrial spiral arteries in pre-eclampsia might result from, rather than cause, maternal flow defects. As myometrial spiral arteries have a more pronounced muscular coat and elastica than do the corresponding decidual vessels, failed remodelling at this level leadsto reduced uteroplacental arterial flow and episodesof irregular placental perfusion. Such hypoxia or reoxygenation episodes in some cases generate reactive oxygen species,33 leading to placental oxidative stress and placental dysfunction, with endoplasmic reticulum stress and impaired protein synthesis.34 We believe that the unidentified causes of the first (placental) stage of pre-eclampsia35 might include excessive or atypical maternal immune response to trophoblasts,36 and either impaired decidualisation or failure of proper uterine preconditioning.37 Thus, pre-eclampsia is a disease of failed interaction between two genetically different organisms. As such, Haig’s maternal-fetal conflict hypothesis could be relevant.38

The second stage (figure) of systemic maternal disease is associated with an exaggerated endothelial activation and a generalised hyperinflammatory state compared with normal pregnancy.39 Episodes of placental hypoxia or reperfusion result in oxidative stress, subsequent apoptotic and necrotic disruption of syncytial architecture,40 and release of various components from the intervillous space into the maternal circulation, stimulating production of inflammatory cytokines.41 The circulating bioactive trophoblast debris includes syncytiotrophoblast membrane microparticles41 and an excess of syncytiotrophoblast-derived antiangiogenic factors, such as soluble endoglin and the soluble form of the vascular endothelial growth factor (VEGF) receptor (sFlt-1).18 Increased production of anti-angiogenic factors by trophoblasts was also recently shown in molar pregnancy, a disorder known to pre-dispose women to pre-eclampsia.42, 43 The excessive systemic inflammatory response of pre-eclampsia44 results in endothelial dysfunction and associated increased vascular reactivity, preceding onset of symptomatic clinical disease.45 Loss of endothelial integrity contributes to derangements of sodium-volume homoeostasis and reversal of many cardiovascular changes (eg, increased cardiac output and intravascular volume) accompanying normal pregnancy. Thus, pre-eclampsia is a low-output, high-resistance state with paradoxically decreased aldosterone and renin activity.46

Linking mechanisms between stages 1 and 2 can be different for several phenotypes of pre-eclampsia, including haemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome,47 and sometimes varies between individuals. Whether pre-eclampsia will be of early (often complicated by intrauterine growth restriction) or late onset can be dependent on whether the placenta in stage 1 becomes phenotypically small because of a greater angiogenic imbalance.48 Poor placentation should not be regarded as the cause of pre-eclampsia, because not all of such pregnancies have poor outcomes, but instead as a powerful predisposing factor.39 In the presence of a placenta with an appropriate size for gestational age, predisposing cardiovascular and metabolic syndrome-like disorders might also be able to set off a cascade of placental and systemic inflammation and oxidative stress, resulting in late onset pre-eclampsia (also called maternal pre-eclampsia).49 This view is substantiated by findings of normal villous morphology in late-onset pre-eclampsia, by contrast with early-onset pre-eclampsia,50 although no such data seem to exist for the placental bed.

Although interactions between maternal genetic and constitutional factors with environmental factors contribute to the second stage, such factors are now thought to have an effect on the first stage of the disease.49 Decreased antioxidant and phase I and phase II biotransformation activities in the maternal blood and decidual and placental tissue probably contribute to an increased risk of pre-eclampsia.51 The protective effect of smoking against pre-eclampsia52 could result from beneficial carbon monoxide effects on trophoblast invasion and spiral artery remodelling, increased stage 1 placental blood flow, and decreased stage 2 inflammatory responses.53 Decreased placental release of sFlt-1 is possibly associated with this protective effect.54

Screening

Table 2 shows factors that can easily be measured at the first prenatal appointment and that increase the likelihood of pre-eclampsia in any pregnancy.8, 55 In risk assessments done after 20 weeks’ gestation, attention should be paid to the possible onset of pre-eclampsia by identification of any of the following signs and symptoms: new hypertension, new proteinuria, symptoms of headache, visual disturbance, epigastric pain, vomiting, reduced fetal movements, and an infant that is small for gestational age.56 Such risk assessment before and after 20 weeks can be used in the community to offer referral for specialist input.

 

Table 2 Risk markers for pre-eclampsia at antenatal booking according to the PRE-eclampsia Community Guidelines (PRECOG8)

Next to history taking, physical examination including measurement of blood pressure and assessment for presence of proteinuria, are the cornerstones of screening in antenatal care. Blood pressure should be measured as for non-pregnancy, with the woman at rest, sitting upright, with the arm supported, and the sphygmomanometer cuff at the level of the patient’s heart.11 Korotkoff sound V (disappearance of turbulence) should be used to define diastolic blood pressure and values recorded to the nearest 2 mm Hg. Thigh cuffs (18×36 cm) should be used for women with an arm circumference of 41 cm or more.56 Of the automated blood pressure measuring devices on the market, only the Microlife 3BTO-A and Microlife WatchBP Home57 have met the British Hypertension Society’s criteria for accuracy. Mean arterial blood pressure might be a better predictor for pre-eclampsia than is systolic or diastolic blood pressure or an increase in blood pressure.58 Although dipstick testing for screening of proteinuria is prone to issues of intraobserver and interobserver variability and limited sensitivity and specificity,59 it is readily available, widely used, and might be the only test available in low-income and middle-income countries. Although 24 h urine collection is still used to confirm and quantify a substantial amount of proteinuria,56 this method seems vulnerable to issues of overcollection, undercollection, and large coefficients of variation between tests in the same women.60 The spot urinary protein-to-creatinine ratio, often used as a screening method,56 is less cumbersome than is 24 h urine collection, and is suggested to be an equivalently accurate measure of clinically significant proteinuria in pregnancy.61 Still to be established, however, is whether this ratio remains constant throughout a 24 h period.62

Prediction

Early prediction of pre-eclampsia would allow for close surveillance and preventive strategies. Many tests have been assessed for their relation to placental perfusion, vascular resistance, and placental products, including tests for Down’s serum screening analytes and hormones, renal and endothelial dysfunction, oxidative stress, and fetal-derived products. Of 27 tests reviewed by Meads and colleagues,63 only a few reached specificities above 90%. These were body-mass index of 34 kg/m2 or higher, α-fetoprotein, and bilateral uterine artery Doppler notching. Sensitivity of higher than 60% was achieved only by uterine artery Doppler resistance index and combinations of indices. Kallikreinuria (sensitivity >80% and specificity >90%) and cellular and total fibronectin (specificity >90%) seem worthy of further investigation. No single test, however, met the clinical standards for a predictive test—a conclusion also drawn by authors of another systematic review.64Because any single biomarker is unlikely to be effective in prediction of the onset of a disorder as heterogeneous as pre-eclampsia, researchers65 have suggested that combinations of tests such as ultrasound assessment of uterine artery Doppler waveforms, placental thickness and homogeneity, and serum markers raise the effectiveness of history and physical-based screening. Logistic regression analysis combining information on uterine artery pulsatility index, mean arterial pressure, serum pregnancy-associated plasma protein-A, serum-free placental growth factor, body-mass index, and presence of nulliparity or previous pre-eclampsia showed promising high sensitivity and specificity in prediction of early pre-eclampsia.66 Similarly, ratios of antiangiogenic and proangiogenic factors (eg, ratio of sFlt-1 to placental growth factor)67, 68 might have better discriminatory power than do other methods.69 However, whether or not these tests will also be useful across the range of placenta-related complications remains unknown.

Clinical presentation

Maternal organ systems that are susceptible to excessive inflammation and endothelial damage are the CNS, lungs, liver, kidneys, systemic vasculature, coagulation, and the heart—the placenta and fetus are also at risk. The more organ systems that are affected, the more maternal and perinatal complications arise. Clinicians should take caution not to undervalue clinical signs and symptoms in (severe) pre-eclampsia (table 1) because they can be non-specific (eg, nausea and vomiting). Caregivers should always remember that pre-eclampsia can potentially fulminate, and therefore they should not be given a false sense of security because mild disease has been designated. Some risks pertain to development of the HELLP syndrome of microangiopathic haemolysis and platelet consumption, and hepatocellular damage from periportal or focal parenchymal necrosis. Patients frequently (40—90%) have epigastric or right upper quadrant pain.70 These clinical symptoms, along with headache, visual changes, and nausea or vomiting seem to be more predictive than are laboratory parameters for adverse maternal outcomes.71

HELLP syndrome complicates 10—20% of cases of severe pre-eclampsia, and develops mostly preterm (50%). In 20% of women, however, it presents in late gestation, or in 30% post partum.72 HELLP without hypertension or proteinuria is reported in 10—20% of cases. Direct complications of HELLP syndrome are abruptio placentae (9—20%), disseminated intravascular coagulation (5—56%) and acute renal failure (7—36%). Less frequent complications are eclampsia (4—9%), pulmonary oedema (3—10%), and subcapsular liver haematoma (less than 2%).72 Estimates of complication rates can be quite high because they are derived mainly from tertiary care centres. Overall, significant maternal morbidity is encountered in about 15% of women with severe pre-eclampsia,73 including retinal detachment and cerebrovascular bleeding, and complications related to HELLP syndrome, but with lowered frequencies. The brain is at risk because of impaired cerebral autoregulation due to endothelial damage together with decreased sympathetic innervation in the posterior cerebral circulation, and a lessened ability for neurogenic response to increase blood pressure. Cortical blindness and some cases of eclampsia could evolve from the acute cerebral illness, posterior reversible leukoencephalopathy syndrome (PRES).74

Eclampsia, complicating 1—2% of severe pre-eclampsia,75 is defined as the occurrence of tonic-clonic seizures in a pregnant or recently delivered woman that cannot be attributed to other causes. Although difficult to predict, in 79% of cases promonitory signs and symptoms are present during the week before the first eclamptic seizure: headache (56%), visual disturbances (23%), epigastric pain (17%), hypertension (48%), proteinuria (46%), and concurrent hypertension and proteinuria (38%).76 Hypertension and proteinuria can last for several weeks post partum.77 Pre-eclampsia can also deteriorate or present de novo after delivery, occasionally evolving into severe forms that are similar to eclampsia.78 Women with symptoms and signs of pre-eclampsia might have other maternal diseases,79 and therefore differential diagnoses should be considered and excluded (panel 1). Perinatal concerns in women with pre-eclampsia relate to risks of placental abruption (0—6%), intrauterine growth restriction (5—18%), and perinatal mortality (0—9%), dependent on severity and gestational onset of disease.80

Management

For women with pre-eclampsia, dependent on severity, review at day assessment units or admission to hospital is indicated according to local guidelines.56Table 3 and panel 2 show our suggested management paradigms according to gestational age at presentation. Although we recognise that there is no universally accepted standard of care, which is dependent on local facilities, we believe that risk reduction for women with pre-eclampsia needs a series of strategies—namely standardised assessment and surveillance, avoidance and management of severe systolic and diastolic hypertension, prevention and treatment of seizures of eclampsia, and avoidance of use of aggressive rehydration in women admitted with severe pre-eclampsia. Although debate exists about routine use of some individual tests, standardised assessment and surveillance of all vulnerable organ systems in women with pre-eclampsia has been associated with reduced adverse maternal outcomes,86 and proposals for blood tests have been developed.56 Tests for uric acid is one of the controversial tests that has been suggested. Although researchers have suggested that uric acid is as important as proteinuria for identification of fetal risk in women with gestational hypertension,93 it is a poor predictor of maternal and fetal complications in women with pre-eclampsia.94 In a review,62 researchers concluded that the amount of proteinuria is not a good marker of severity of pre-eclampsia, and that this measure should not guide management.

 

Table 3 Antepartum management options for women with pre-eclampsia by gestational age at diagnosis.

NICU=neonatal intensive care unit.

For women who are remote from term (<34 weeks’ gestation), there is both randomised controlled trial and cohort-based evidence81 that expectant management (compared with stabilisation and delivery, which is the sole cure for pre-eclampsia) confers some perinatal benefit with a minimum amount of additional maternal risk. However, insufficient data are available for straightforward recommendations for either expectant or interventionist care,82 and policies could differ for women cared for in low-resource settings. For women who present before 24 weeks’ gestation, expectant management is unlikely to offer any perinatal advantages, although maternal risks accumulate.81, 83 Women at term with pre-eclampsia (and non-proteinuric gestational hypertension) are best managed by a policy of induction of labour.95 In the case of women with HELLP syndrome at or near term, expedited delivery should be standard management. Remote from term, clinicians could consider expectant management in some cases with vigilant expectancy, but no evidence exists to advise for which women such policy can be applied without substantial maternal risks.81, 82 Such practices should only be attempted in institutions with much experience in management of pre-eclampsia. Failure to exhibit due clinical care in combination with a policy of expectant management can prove lethal.96 Corticosteroids have not been shown to benefit primary maternal and perinatal outcomes in women with HELLP.72, 97, 98

The present Cochrane review99 does not support the choice of any one antihypertensive agent over another for management of severe pregnancy hypertension, concluding that the choice should depend on the clinician’s experience with a specific drug. It does, however, advise against use of diazoxide because, although more effective for reduction of blood pressure than is hydralazine,100 diazoxide might result in increased rates of maternal hypotension. Ketanserin seems to be less effective than is hydralazine. Neither magnesium sulphate (MgSO4) nor nimodipine are recommended as antihypertensive agents.99 In another systematic review,89 nifedipine (within the class of calcium-channel blockers) seemed to be more effective in bringing blood pressure within the target range, with less hypotension, than was hydralazine. By comparison, labetalol was less effective but was associated with fewer adverse maternal and perinatal events than was hydralazine.89 Nifedipine capsules (5 mg or 10 mg) are no longer available in all markets, and should not be used in women with known coronary artery disease, those who have had diabetes mellitus for more than 15 years, or those who are older than 45 years because of the risks of sudden cardiac death.101 Clinicians who choose the alternative of intermediate-acting nifedipine tablets should recognise the slow onset of action so that women are not over-treated because of an expectation of a rapid blood pressure response.102 Nifedipine and MgSO4 can be used together effectively and safely.103 Antihypertensives for use in women with non-severe hypertension, although generally not related to improved pregnancy outcome except for less severe hypertension,90, 104 are also shown in panel 2.

Prevention and management of eclampsia seizures is based on giving MgSO4.87, 88 Women with severe pre-eclampsia should be considered for MgSO4 prophylaxis.104 Findings from randomised controlled trials87, 88 support a regimen of MgSO4 given as a 4 g intravenous loading dose during a 15—20 min period, followed by an infusion of 1 g/h, with a first or recurrent seizure treated with another 2—4 g intravenous loading dose. This regimen does not need testing of blood concentrations of MgSO4 because clinical effect can be monitored with deep tendon reflexes. Additionally, it adds a wider therapeutic index between effect and toxicity risk than does the historical 2 g/h regimen. Despite a reduced intravascular volume in pre-eclampsia, plasma volume expansion has not proven to provide any benefit.91

Timing of delivery should be designed to keep perinatal outcomes at an optimum while obviating maternal risks. In pre-eclampsia, this timing should be based on criteria of fetal wellbeing and gains to be made in terms of perinatal outcomes by achievement of additional intrauterine time. Fetal wellbeing is assessed by ultrasound (biometry, umbilical artery Doppler, ductus venosus Doppler, and amniotic fluid) and cardiotocography (preferably computerised).105 Antenatal corticosteroids for fetal lung maturation should be given to all women at risk of delivery at less than 34 weeks of gestation.84 Previable fetuses can be delivered with misoprostol induction.85 In early-onset pre-eclampsia and often concurrent intrauterine growth restriction and placental pathology, the fetus is unlikely to tolerate labour. However, the closer the pregnancy gets to term, the more reasonable an attempt at induction of labour is for women with pre-eclampsia who require timely, but not emergency, delivery.

When women have severe disease, issues of peripartum management of thrombocytopenia and HELLP syndrome arise.11, 72 Although routine prophylactic platelet transfusions are not recommended, ordering blood products, including platelets, should be considered when platelet counts are fewer than 50×109 platelets per L, falling rapidly, or when coagulopathy is present. Platelet transfusion is always indicated before, during, or after either caesarean section or vaginal delivery when platelet counts are fewer than 20×109/L or in case of significant bleeding (eg, ecchymosis, bleeding from gums or wound).70 Preanaesthetic assessment of a woman with pre-eclampsia is essential, including an airway examination and assessment of coagulation status (such as platelet count). There is no role for tests of platelet function.9, 11, 106 Use of regional analgesia or anaesthesia, or both, is not contraindicated in women when platelet counts are higher than 75×109/L in the absence of a coagulopathy, falling platelet count, or concomitant use of either an antiplatelet agent (eg, aspirin) or anticoagulant (eg, heparin).

Regional anaesthesia (epidural, spinal, or combined spinal-epidural) is appropriate for women taking low-dose aspirin (without either coagulopathy or platelets <75×109/L), and those given low-molecular-weight heparin at least 12 h after a prophylactic dose or 24 h after a therapeutic dose.107 Early insertion of a spinal or epidural catheter for obstetric or anaesthetic indications should be considered (in the absence of contraindications) to reduce the need for general anaesthesia in case of caesarean section. A difficult airway due to pharyngolaryngeal oedema should always be anticipated. Intubation could increase risk of severe hypertension (and subsequent cerebral events) and aspiration. Measures should be taken to avoid a speed that compromises maternal safety, even in the presence of acute fetal compromise. Central venous access or pulmonary artery catheterisation should only be used for specific disorders (ie, pulmonary oedema and cardiac disease) in a high dependency setting. Ergot alkaloids should be omitted for active management of the third stage of labour if the mother is hypertensive.16

Preconception care and future health

Women at high risk for pre-eclampsia, including those with a history of the disease or other complications in their obstetric history, should be offered preconception care by obstetricians with experience in management of the disorder. If present, severity of chronic hypertension, diabetes, connective tissue, or renal disease should be assessed and pharmacological treatment adjusted for safety in pregnancy. Risks of occurrence and recurrence (10% for previous mild disease and up to 40% for severe disease) and perinatal mortality and morbidity should be explained and a management plan, available for all associated caretakers, should be drawn up. Obesity and an increase in body-mass index between pregnancies108 increases risk of (recurrent) pre-eclampsia,109 and partly neutralises the protective effect of smoking.52 Although preconception weight loss has not yet been properly investigated, studies after bariatric surgery suggest positive effects.110 Other risk factors (table 2), should also be discussed.

Nutritional preventive measures should not be advised for management of the occurrence or recurrence of pre-eclampsia in women at high risk or the general population. Neither diets low in energy or salt, nor supplementation with either antioxidants vitamins C or E, fish oil, garlic, zinc, selenium, folic acid, or magnesium are effective.63, 111, 112 An evidence-based review113 showed no relation between calcium supplementation and risk reduction of pre-eclampsia, although supplementation might have some effects in high-risk populations that are calcium-deficient. Low-dose aspirin prophylaxis has long been of interest because it is thought to correct an imbalance in the ratio of thromboxane A2 to prostacyclin that is associated with increased vasoreactivity. Findings from a meta-analysis114 of individual patients’ data from 31 randomised trials showed that asprin was associated with a 10% reduction in pre-eclampsia and prematurity (less than 34 weeks’ gestation), and that aspirin seemed to be safe. The number needed to treat to obtain these results was, however, very large. Low-dose aspirin should be offered on an individual basis and decisions made on the basis of the woman’s risk profile from their obstetric and medical history. Neither progesterone or diuretics nor antihypertensives in women with chronic hypertension reduce risk of pre-eclampsia.111 The damaging effects of smoking on general health and perinatal outcomes especially115 outweigh its incidence-lowering effects on pre-eclampsia.52

Inherited or acquired thrombophilias are a heterogeneous group of coagulation disorders that predispose women to an extra risk of thromboembolic events during pregnancy and puerperium.116 Although pre-eclampsia is related to reduced uteroplacental blood flow, its direct correlation with thrombophilia remains controversial. Placental thrombotic and inflammatory lesions associated with early-onset pre-eclampsia or fetal growth restriction do not arise more often in women with thrombophilia or hyperhomocysteinaemia than in those without these disorders.117 Meta-analyses118 often showed positive, though mostly weak, associations of thrombophilia with pre-eclampsia, although there were instances of heterogeneity between studies. Results from three large, prospectively designed studies119—121 showed no associations with any of the inherited thrombophilias for mild or severe pre-eclampsia. In small studies,122, 123 investigation of recurrence rates of pre-eclampsia in women with thrombophilias showed conflicting results. Associations with hyperhomocysteinaemia are often biased by delivery to test-time interval and maternal age.124 There are no completed trials to establish the effects of heparin on pregnancy outcomes for women with a thrombophilia.125 Therefore, in view of WHO criteria by Wilson and Jungner,126 routine screening of women who had pre-eclampsia and treatment when they were positive for thrombophilia does not yet seems justified, unless the intent is to randomly assign women in definitive randomised controlled trials. Thrombophilia testing, however, should be recommended for those with a personal or family history of thrombosis.127

Pre-eclampsia, especially of early onset, can be followed by symptoms of maternal post-traumatic stress.128, 129 Timely recognition of those women at risk and referral reduces the duration of treatment necessary.129 Women with pre-eclampsia are at increased risk for future cardiovascular disease. Pooled relative risks for hypertension, fatal and non-fatal ischaemic heart disease, and fatal and non-fatal stroke are 3·70 (95% CI 2·70—5·05), 2·26 (1·86—2·52), and 1·81 (1·45—2·27), respectively, 10—14 years after the index pregnancy.130 Early-onset disease and other additional concurrent placental pathology confer cumulative risk.131 Increased pre-pregnancy serum concentrations of triglycerides, cholesterol, LDL cholesterol, non-HDL cholesterol, and blood pressure are positively associated with risk of subsequent pre-eclampsia and could explain, together with abdominal obesity, the link with future cardiovascular disease.132, 133 Identification of such young women possibly offers opportunities for strategies to decrease remote cardiovascular risk.130 As the absolute risk for disease within 12 years is low (less than 0·5—1·5% dependent on pre-eclampsia severity)130 a first focus might be on lifestyle modifications, including smoking cessation, weight reduction, healthy diet, and exercise,134 in individualised intervention programmes, including use of the internet. Because the risk of developing chronic hypertension could be higher than 20%,130 blood pressure should be checked regularly. Other individual cardiovascular risk factors should be treated as indicated, but there seems to be no place for further screening or preventive drug interventions until further evidence is available. Pre-eclampsia has been suggested to predispose to reduced thyroid function in later years.135

Perspectives

Although genetic contributions to the risk of pre-eclampsia are recognised by familial clustering of this disorder, underlying mechanisms remain uncertain.136 Maternal constitutional and environmental risk factors for pre-eclampsia could be implicated by interference with the epigenetic programming of the gametes, placenta, and fetus.137 Derangements in genomic imprinting in placental tissue, resulting in disturbed paternal versus maternal gene expression, have additionally been suggested to contribute to pre-eclampsia.137, 138 Therefore, high priority will be given in the near future to elucidation of gene-gene and gene-environment interactions and underlying epigenetic mechanisms139 that are associated with the programming of trophoblast cells and how they relate to placental causes and systemic linkages of different phenotypes of pre-eclampsia. Such phenotypes include that for HELLP syndrome and other placental complications such as isolated intrauterine growth restriction. These insights could direct future specific preconception and early pregnancy preventive measures to favourably affect placentation in women at high risk. Such measures might also be targeted at decreasing excessive inflammatory and oxidative stress (eg, by statins or metformin) or improvement of endothelial health.

A lowered incidence of hypertensive disease in pregnancy was suggested after periconception low-dose aspirin treatment.140 Trophoblast complement inhibitory therapy with heparin might seem beneficial in some subgroups of patients.141 However, to be able to keep spiral artery remodelling at an optimum with prophylactic treatment, a need for more comparative research to understand the placental bed remains. Additionally, pharmacological approaches to counteract the anti-angiogenic state in the second stage of the disease could be promising. Epigenetic modification of fetal vascular tissue during a pregnancy that is complicated by pre-eclampsia might also relate to future reproductive status and cardiovascular health.137, 142 Men and women exposed to pre-eclampsia as a fetus,143 and women born small for gestational age,144 have an increased risk of having (or fathering) a future pregnancy that is complicated by pre-eclampsia. These children also have a heightened risk of high blood pressure, features of metabolic syndrome, and cardiovascular diseases at relative early age.145, 146

In preconception care, development of simple rules for prediction of recurrent early-onset hypertensive disease in pregnancy is important.147 During pregnancy, proteomics-based identification of clinically useful predictive biomarkers might become feasible.148, 149 Furthermore, development and validation of disease severity criteria that objectively identify women at incremental risk of adverse outcomes need to be developed. Randomised controlled trials are much needed to establish recommendations for management of early-onset severe pre-eclampsia. In the UK, substandard care contributes to 72% of maternal deaths that are related to hypertensive disease in pregnancy,16 and to 96% of those in the Netherlands.96 In the Dutch enquiry,96 no instructions about danger signs to women had been documented in 80% of cases. Therefore, patient education is of major importance. The need for drills and simulations for obstetric emergencies such as severe hypertension and eclampsia, and for audits of pre-eclampsia-related maternal mortality and severe morbidity should be further advocated.

Search strategy and selection criteria

We searched PubMed and the Cochrane Library with the search terms “pre-eclampsia” and “hypertension and pregnancy”, and cross-referenced them with the following terms: “epidemiology”, “definition”, “aetiology”, “pathophysiology”, “prediction”, “prevention”, “management”, “clinical trials”, “preconception care”, and “thrombophilia”. We mainly restricted our search to studies done in human beings. We largely selected publications from the past 5 years, but did not exclude commonly referenced and highly regarded older publications. We also searched the reference lists of articles identified by this search strategy and selected those that we judged to be relevant. Review articles and book chapters are cited to provide readers with more details and references than this Seminar provides. Our reference list was modified on the basis of comments from peer reviewers.

Contributors

EAS designed the structure of the review and coordinated writing of the Seminar. All authors contributed to the literature search, writing of the Seminar, and addressing of reviewers’ comments.

Conflicts of interest

We declare that we have no conflicts of interest.

Acknowledgments

No funding was used for the preparation or submission of this report. We thank the PhD fellows Durk Berks, Meeke Hoedjes, Nienke Bergen, and Evelyne van Uitert for assisting in the literature search; Jolanda Claessens for her secretarial support; and Frits Wilbrink for his contribution to the graphics of the figure. Peter von Dadelszen receives funding support from WHO, the Canadian Institutes of Health Research, the Michael Smith Foundation for Health Research, and the Child and Family Research Institute.

1 Khan KS, Wojdyla D, Say L, Gulmezoglu AM, Van Look PFA. WHO analysis of causes of maternal death: a systematic review. Lancet 2006; 367: 1066-1074. Summary | Full Text | PDF(2367KB) | CrossRef | PubMed

2 Duley L. The global impact of pre-eclampsia and eclampsia. Semin Perinatol 2009; 33: 130-137. CrossRef | PubMed

3 Berg CJ, Mackay AP, Qin C, Callaghan WM. Overview of maternal morbidity during hospitalization for labor and delivery in the United States: 1993—1997 and 2001—2005. Obstet Gynecol 2009; 113: 1075-1081. PubMed

4 Wallis AB, Saftlas AF, Hsia J, Atrash HK. Secular trends in the rates of preeclampsia, eclampsia, and gestational hypertension, United States, 1987—2004. Am J Hypertens 2008; 21: 521-526. CrossRef | PubMed

5 Caughey AB, Stotland NE, Washington AE, Escobar GJ. Maternal ethnicity, paternal ethnicity, and parental ethnic discordance: predictors of preeclampsia. Obstet Gynecol 2005; 106: 156-161. PubMed

6 Rao AK, Cheng YW, Caughey AB. Perinatal complications among different Asian-American subgroups. Am J Obstet Gynecol 2006; 194: e39-e41. CrossRef | PubMed

7 Silva LM, Coolman M, Steegers EA, et al. Low socioeconomic status is a risk factor for preeclampsia: the Generation R Study. J Hypertens 2008; 26: 1200-1208. CrossRef | PubMed

8 Milne F, Redman C, Walker J, et al. The pre-eclampsia community guideline (PRECOG): how to screen for and detect onset of pre-eclampsia in the community. BMJ 2005; 330: 576-580. PubMed

9 Tuffnell DJ, Shennan AH, Waugh JJS, Walker JJ. The management of severe pre-eclampsia/eclampsia, guideline number 10(A). London: Royal College of Obstetricians and Gynaecologists, 2006.

10 Lowe SA, Brown MA, Dekker GA, et alfor the Society of Obstetric Medicine of Australia and New Z. Guidelines for the management of hypertensive disorders of pregnancy 2008. Aust N Z J Obstet Gynaecol 2009; 49: 242-246. CrossRef | PubMed

11 Magee LA, Helewa ME, Moutquin JM, et al. SOGC guidelines; diagnosis, evaluation and management of the hypertensive disorders of pregnancy. J Obstet Gynaecol Can 2008; 30 (suppl): 1-48. PubMed

12 Lindheimer MD, Taler SJ, Cunningham FG. ASH position article: hypertension in pregnancy. J Am Soc Hypertens 2008; 2: 484-489. PubMed

13 ACOG Committee on Obstetric Practice. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. Number 33, January 2002. American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet 2002; 77: 67-75. CrossRef | PubMed

14 Brown MA, Lindheimer MD, de Swiet M, Van Assche A, Moutquin JM. The classification and diagnosis of the hypertensive disorders of pregnancy: statement from the International Society for the Study of Hypertension in Pregnancy (ISSHP). Hypertens Pregnancy 2001; 20: IX-XIV. CrossRef | PubMed

15 MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol 2001; 97: 533-538. CrossRef | PubMed

16 National Institute for Clinical Excellence, Scottish Executive Health Department, Department of Health, Social Services and Public Safety, Northern Ireland. Saving mothers’s lives; 2003—2005. The seventh report of the confidential enquiries into maternal deaths in the United Kingdom. London: CEMACH, 2007.

17 Martin JN, Thigpen BD, Moore RC, Rose CH, Cushman J, May W. Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure. Obstet Gynecol 2005; 105: 246-254. PubMed

18 Karumanchi SA, Stillman IE, Lindheimer MD. Angiogenesis and preeclampsia. In: Lindheimer MD, Roberts JM, Cunningham FG, eds. Chesley’s hypertensive disorders in pregnancy. Amsterdam: Academic Press, Elsevier, 2009: 87-103.

19 Brosens I, Robertson WB, Dixon HG. The role of spiral arteries in the pathogenesis of preeclampsia. In: Wynn RM, ed. Obstetrics and Gynecology Annual. New York: Appleton-Century-Crofts, 1972: 177-191.

20 Pijnenborg R, Vercruysse L, Hanssens M. The uterine spiral arteries in human pregnancy: facts and controversies. Placenta 2006; 27: 939-958. PubMed

21 Pandian Z, Bhattacharya S, Templeton A. Review of unexplained infertility and obstetric outcome: a 10 year review. Hum Reprod 2001; 16: 2593-2597. CrossRef | PubMed

22 Trogstad L, Magnus P, Moffett A, Stoltenberg C. The effect of recurrent miscarriage and infertility on the risk of pre-eclampsia. BJOG 2009; 116: 108-113. CrossRef | PubMed

23 Ng EH, Chan CC, Tang OS, Yeung WS, Ho PC. The role of endometrial and subendometrial vascularity measured by three-dimensional power Doppler ultrasound in the prediction of pregnancy during frozen-thawed embryo transfer cycles. Hum Reprod 2006; 21: 1612-1617. CrossRef | PubMed

24 Hanna J, Goldman-Wohl D, Hamani Y, et al. Decidual NK cells regulate key developmental processes at the human fetal-maternal interface. Nat Med 2006; 12: 1065-1074. CrossRef | PubMed

25 Goldman-Wohl DS, Ariel I, Greenfield C, et al. Lack of human leukocyte antigen-G expression in extravillous trophoblasts is associated with pre-eclampsia. Mol Hum Reprod 2000; 6: 88-95. CrossRef | PubMed

26 Le Bouteiller P, Pizzato N, Barakonyi A, Solier C. HLA-G, pre-eclampsia, immunity and vascular events. J Reprod Immunol 2003; 59: 219-234. CrossRef | PubMed

27 Moffett A, Hiby SE. How Does the maternal immune system contribute to the development of pre-eclampsia?. Placenta 2007; 28 (suppl A): 51-56. PubMed

28 Burton GJ, Jauniaux E, Watson AL. Maternal arterial connections to the placental intervillous space during the first trimester of human pregnancy: the Boyd collection revisited. Am J Obstet Gynecol 1999; 181: 718-724. CrossRef | PubMed

29 Burton GJ, Jauniaux E. Placental oxidative stress: from miscarriage to preeclampsia. J Soc Gynecol Investig 2004; 11: 342-352. CrossRef | PubMed

30 Jauniaux E, Watson AL, Hempstock J, Bao YP, Skepper JN, Burton GJ. Onset of maternal arterial blood flow and placental oxidative stress. A possible factor in human early pregnancy failure. Am J Pathol 2000; 157: 2111-2122. PubMed

31 Pijnenborg R, Brosens I. Deep trophoblast invasion and spiral artery remodelling. In: Pijnenborg R, Brosens I, Romero R, eds. Placental bed disorders: basic science and its translation to obstetrics. Cambridge: Cambridge University Press, 2010: 97-107.

32 Plasencia W, Maiz N, Bonino S, Kaihura C, Nicolaides KH. Uterine artery Doppler at 11 + 0 to 13 + 6 weeks in the prediction of pre-eclampsia. Ultrasound Obstet Gynecol 2007; 30: 742-749. CrossRef | PubMed

33 Burton GJ. Oxygen, the Janus gas; its effects on human placental development and function. J Anat 2009; 215: 27-35. CrossRef | PubMed

34 Burton GJ, Yung HW, Cindrova-Davies T, Charnock-Jones DS. Placental endoplasmic reticulum stress and oxidative stress in the pathophysiology of unexplained intrauterine growth restriction and early onset preeclampsia. Placenta 2009; 30 (suppl A): 43-48. PubMed

35 Redman CW. Current topic: pre-eclampsia and the placenta. Placenta 1991; 12: 301-308. PubMed

36 Jauniaux E, Poston L, Burton GJ. Placental-related diseases of pregnancy: Involvement of oxidative stress and implications in human evolution. Hum Reprod Update 2006; 12: 747-755. CrossRef | PubMed

37 Brosens JJ, Parker MG, McIndoe A, Pijnenborg R, Brosens IA. A role for menstruation in preconditioning the uterus for successful pregnancy. Am J Obstet Gynecol 2009; 200: 615. PubMed

38 Haig D. Altercation of generations: genetic conflicts of pregnancy. Am J Reprod Immunol 1996; 35: 226-232. PubMed

39 Redman CW, Sacks GP, Sargent IL. Preeclampsia: an excessive maternal inflammatory response to pregnancy. Am J Obstet Gynecol 1999; 180: 499-506. CrossRef | PubMed

40 Huppertz B. Placental origins of preeclampsia: challenging the current hypothesis. Hypertension 2008; 51: 970-975. CrossRef | PubMed

41 Redman CWG, Sargent IL, Roberts JM. Immunology of normal pregnancy and preeclampsia. In: Lindheimer MD, Roberts JM, Cunningham FG, eds. Chesley’s hypertensive disorders in pregnancy. Amsterdam: Academic Press, Elsevier, 2009: 129-142.

42 Koga K, Osuga Y, Tajima T, et al. Elevated serum soluble fms-like tyrosine kinase 1 (sFlt1) level in women with hydatidiform mole. Fertil Steril 200910.1016/j.fertnstert.2009.02.015. published online March 6. PubMed

43 Kanter D, Lindheimer MD, Wang E, et al. Angiogenic dysfuction in molar pregnancy. Am J Obstet Gynecol 2010; 202: 184.e1-184.e5. CrossRef | PubMed

44 Redman CW, Sargent IL. Placental stress and pre-eclampsia: a revised view. Placenta 2009; 30 (suppl A): 38-42. PubMed

45 Myers J, Mires G, Macleod M, Baker P. In preeclampsia, the circulating factors capable of altering in vitro endothelial function precede clinical disease. Hypertension 2005; 45: 258-263. CrossRef | PubMed

46 Irani RA, Xia Y. The functional role of the renin-angiotensin system in pregnancy and preeclampsia. Placenta 2008; 29: 763-771. PubMed

47 Buimer M, Keijser R, Jebbink JM, et al. Seven placental transcripts characterize HELLP-syndrome. Placenta 2008; 29: 444-453. PubMed

48 Wikstrom AK, Larsson A, Akerud H, Olovsson M. Increased circulating levels of the antiangiogenic factor endostatin in early-onset but not late-onset preeclampsia. Reprod Sci 2009; 16: 995-1000. PubMed

49 Roberts JM, Hubel CA. The two stage model of preeclampsia: variations on the theme. Placenta 2009; 30 (suppl A): 32-37. PubMed

50 Egbor M, Ansari T, Morris N, Green CJ, Sibbons PD. Morphometric placental villous and vascular abnormalities in early- and late-onset pre-eclampsia with and without fetal growth restriction. BJOG 2006; 113: 580-589. CrossRef | PubMed

51 Zusterzeel PL, Peters WH, Burton GJ, Visser W, Roelofs HM, Steegers EA. Susceptibility to pre-eclampsia is associated with multiple genetic polymorphisms in maternal biotransformation enzymes. Gynecol Obstet Invest 2007; 63: 209-213. CrossRef | PubMed

52 Stone CD, Diallo O, Shyken J, Leet T. The combined effect of maternal smoking and obesity on the risk of preeclampsia. J Perinat Med 2007; 35: 28-31. CrossRef | PubMed

53 Bainbridge SA, Sidle EH, Smith GN. Direct placental effects of cigarette smoke protect women from pre-eclampsia: the specific roles of carbon monoxide and antioxidant systems in the placenta. Med Hypotheses 2005; 64: 17-27. CrossRef | PubMed

54 Jeyabalan A, Powers RW, Durica AR, Harger GF, Roberts JM, Ness RB. Cigarette smoke exposure and angiogenic factors in pregnancy and preeclampsia. Am J Hypertens 2008; 21: 943-947. CrossRef | PubMed

55 Duckitt K, Harrington D. Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies. BMJ 2005; 330: 565. PubMed

56 Milne F, Redman C, Walker J, et al. Assessing the onset of pre-eclampsia in the hospital day unit: summary of the pre-eclampsia guideline (PRECOG II). BMJ 2009; 339: 626-628. PubMed

57 Chung Y, de Greeff A, Shennan A. Validation and compliance of a home monitoring device in pregnancy: Microlife WatchBP Home. Hypertens Pregnancy 2009; 28: 348-359. CrossRef | PubMed

58 Cnossen JS, Vollebregt KC, de Vrieze N, et al. Accuracy of mean arterial pressure and blood pressure measurements in predicting pre-eclampsia: systematic review and meta-analysis. BMJ 2008; 336: 1117-1120. PubMed

59 Brown MA, Buddle ML. Inadequacy of dipstick proteinuria in hypertensive pregnancy. Aust N Z J Obstet Gynaecol 1995; 35: 366-369. CrossRef | PubMed

60 Cote AM, Firoz T, Mattman A, Lam EM, von Dadelszen P, Magee LA. The 24-hour urine collection: gold standard or historical practice?. Am J Obstet Gynecol 2008; 199: 625. PubMed

61 Cote AM, Brown MA, Lam E, et al. Diagnostic accuracy of urinary spot protein:creatinine ratio for proteinuria in hypertensive pregnant women: systematic review. BMJ 2008; 336: 1003-1006. PubMed

62 Lindheimer MD, Kanter D. Interpreting abnormal proteinuria in pregnancy. The need for a more pathophysiological approach. Obstet Gynecol 2010; 115: 365-375. CrossRef | PubMed

63 Meads CA, Cnossen JS, Meher S, et al. Methods of prediction and prevention of pre-eclampsia: systematic reviews of accuracy and effectiveness literature with economic modelling. Health Technol Assess 2008; 12: iii-iiv. 1—270. PubMed

64 Conde-Agudelo A, Romero R, Lindheimer MD. Tests to predict pre-eclampsia. In: Lindheimer MD, Roberts JM, Cunningham FG, eds. Chesley’s hypertensive disorders in pregnancy. Amsterdam: Academic Press, Elsevier, 2009: 189-211.

65 Toal M, Chan C, Fallah S, et al. Usefulness of a placental profile in high-risk pregnancies. Am J Obstet Gynecol 2007; 196: 363. PubMed

66 Poon LCY, Kametas NA, Maiz N, Akolekar R, Nicolaides KH. First-trimester prediction of hypertensive disorders in pregnancy. Hypertension 2009; 53: 812-818. CrossRef | PubMed

67 Verlohren S, Galindo A, Schlembach D, et al. An automated method for the determination of the sFlt-1 / PIGF ratio in the assessment of pre-eclampsia. Am J Obstet Gynecol 2010; 202: 161.e1-161.e11. CrossRef | PubMed

68 Sunderji S, Gaziano E, Wothe D, et al. Automated assays for sVEGF R1 and PIGF as an aid in the diagnosis of preterm pre-eclampsia: a porspective clinical study. Am J Obstet Gynecol 2010; 202: 40.e1-40.e7. CrossRef | PubMed

69 Kusanovic JP, Romero R, Chaiworapongsa T, et al. A prospective cohort study of the value of maternal plasma concentrations of angiogenic and anti-angiogenic factors in early pregnancy and midtrimester in the identification of patients destined to develop pre-eclampsia. J Matern Fetal Neonatal Med 2009; 22: 1021-1038. CrossRef | PubMed

70 Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Obstet Gynecol 2004; 103: 981-991. PubMed

71 Cavkaytar S, Ugurlu EN, Karaer A, Tapisiz OL, Danisman N. Are clinical symptoms more predictive than laboratory parameters for adverse maternal outcome in HELLP syndrome?. Acta Obstet Gynecol Scand 2007; 86: 648-651. CrossRef | PubMed

72 Haram K, Svendsen E, Abildgaard U. The HELLP syndrome: clinical issues and management. A Review. BMC Pregnancy Childbirth 2009; 9: 8. PubMed

73 Tuffnell DJ, Jankowicz D, Lindow SW, et alfor the Yorkshire Obstetric Critical Care G. Outcomes of severe pre-eclampsia/eclampsia in Yorkshire 1999/2003. BJOG 2005; 112: 875-880. CrossRef | PubMed

74 Zeeman GG. Neurologic complications of pre-eclampsia. Semin Perinatol 2009; 33: 166-172. CrossRef | PubMed

75 Sibai BM. Preeclampsia as a cause of preterm and late preterm (near-term) births. Semin Perinatol 2006; 30: 16-19. CrossRef | PubMed

76 Knight MUkoss. Eclampsia in the United Kingdom 2005. BJOG 2007; 114: 1072-1078. CrossRef | PubMed

77 Berks D, Steegers EAP, Molas M, Visser W. Resolution of hypertension and proteinuria after preeclampsia: a 2-year follow-up study. Obstet Gynecol 2009; 14: 1307-1314. PubMed

78 Sibai BM, Stella CL. Diagnosis and management of atypical preeclampsia-eclampsia. Am J Obstet Gynecol 2009; 200: 481. PubMed

79 Sibai BM. Imitators of severe pre-eclampsia. Semin Perinatol 2009; 33: 196-205. CrossRef | PubMed

80 Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol 2003; 102: 181-192. CrossRef | PubMed

81 Magee LA, Yong PJ, Espinosa V, Cote AM, Chen I, von Dadelszen P. Expectant management of severe preeclampsia remote from term: a structured systematic review. Hypertens Pregnancy 2009; 28: 312-347. CrossRef | PubMed

82 Churchill D, Duley L. Interventionist versus expectant care for severe pre-eclampsia before term. Cochrane Database Syst Rev 2002; 3. CD003106. PubMed

83 Gaugler-Senden IP, Huijssoon AG, Visser W, Steegers EA, de Groot CJ. Maternal and perinatal outcome of preeclampsia with an onset before 24 weeks’ gestation. Audit in a tertiary referral center. Eur J Obstet Gynecol Reprod Biol 2006; 128: 216-221. CrossRef | PubMed

84 Brownfoot FC, Crowther CA, Middleton P. Different corticosteroids and regimens for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev 2008; 4. CD006764. PubMed

85 Allen R, O’Brien BM. Uses of misoprostol in obstetrics and gynecology. Rev Obstet Gynecol 2009; 2: 159-168. PubMed

86 Menzies J, Magee LA, Li J, et alfor the Preeclampsia Integrated Estimate of RiSk (PIERS) Study Group. Instituting surveillance guidelines and adverse outcomes in preeclampsia. Obstet Gynecol 2007; 110: 121-127. PubMed

87 The Eclampsia Trial Collaborative Group. Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial. Lancet 1995; 345: 1455-1463. Summary | PubMed

88 The Magpie Trial Collaboration Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet 2002; 359: 1877-1890. Summary | Full Text | PDF(157KB) | CrossRef | PubMed

89 Magee LA, Cham C, Waterman EJ, Ohlsson A, von Dadelszen P. Hydralazine for treatment of severe hypertension in pregnancy: meta-analysis. BMJ 2003; 327: 955-964. PubMed

90 Abalos E, Duley L, Steyn DW, Henderson-Smart DJ. Anihypertensive drug therapy for mild to moderate hypertension during pregnancy. Cochrane Database Syst Rev 2007; 1. CD002252. PubMed

91 Ganzevoort W, Rep A, Bonsel GJ, et al. A randomised controlled trial comparing two temporising management strategies, one with and one without plasma volume expansion, for severe and early onset pre-eclampsia. BJOG 2005; 112: 1358-1368. CrossRef | PubMed

92 Nelson-Piercy C. Thromboprophylaxis during pregnancy, labour and after vaginal delivery. Guideline number 37. London: Royal College of Obstetricians and Gynaecologists, 2004.

93 Roberts JM, Bodnar LM, Lain KY, et al. Uric acid is as important as proteinuria in identifying fetal risk in women with gestational hypertension. Hypertension 2005; 46: 1263-1269. CrossRef | PubMed

94 Thangaratinam S, Ismail KMK, Sharp S, Coomarassamy A, Khan KS. Accuracy of serum acid in predicting complications of pre-eclampsia: a systematic review. BJOG 2006; 113: 369-378. CrossRef | PubMed

95 Koopmans CM, Bijlenga D, Groen H, et al. Induction of labour versus expectant monitoring for gestational hypertension or mild pre-eclampsia after 36 weeks’ gestation (HYPITAT): a multicentre, open-label randomised controlled trial. Lancet 2009; 374: 979-988. Summary | Full Text | PDF(215KB) | CrossRef | PubMed

96 Schutte JM, Schuitemaker NW, van Roosmalen J, Steegers EA, Dutch Maternal Mortality C. Substandard care in maternal mortality due to hypertensive disease in pregnancy in the Netherlands. BJOG 2008; 115: 732-736. CrossRef | PubMed

97 Katz L, de Amorim MM, Figueiroa JN, Pinto e Silva JL. Postpartum dexamethasone for women with hemolysis, elevated liver enzymes, and low platekets (HELLP) syndrome: a double-blind, placebo-controlled, randomized clinical trial. Am J Obstet Gynecol 2008; 198: 283. PubMed

98 Matchaba PT, Moodley J. Corticosteroids for HELLP syndrome in pregnancy. Cochrane Database Syst Rev 2009; 3. CD002076. PubMed

99 Duley L, Henderson-Smart DJ, Meher S. Drugs for treatment of very high blood pressure during pregnancy. Cochrane Database Syst Rev 2006; 3. CD001449. PubMed

100 Hennessy A, Thornton CE, Makris A, et al. A randomized comparison of hydralazine and mini-bolus diazoxide for hypertensive emergencies in pregnancy: the PIVOT trial. Aust N Z J Obstet Gynaecol 2007; 47: 279-285. CrossRef | PubMed

101 Grossman E, Messerli FH, Grodzicki T, Kowey P. Should a moratorium be placed on sublingual nifedipine capsules given for hypertensive emergencies and pseudoemergencies?. JAMA 1996; 276: 1328-1331. PubMed

102 Magee LA, von Dadelszen P. The management of severe hypertension. Semin Perinatol 2009; 33: 138-142. CrossRef | PubMed

103 Magee LA, Miremadi S, Li J, et al. Therapy with both magnesium sulfate and nifedipine does not increase the risk of serious magnesium-related maternal side effects in women with preeclampsia. Am J Obstet Gynecol 2005; 193: 153-163. CrossRef | PubMed

104 Leveno KJ, Cunningham FG. Management. In: Lindheimer MD, Roberts JM, Cunningham FG, eds. Chesley’s hypertensive disorders in pregnancy. Amsterdam: Academic Press, Elsevier, 2009: 389-414.

105 Freeman RK. Antepartum testing in patients with hypertensive disorders in pregnancy. Semin Perinatol 2008; 32: 271-273. CrossRef | PubMed

106 Turner JA. Severe preeclampsia: anesthetic implications of the disease and its management. Am J Ther 2009; 16: 284-288. CrossRef | PubMed

107 Horlocker TT, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient: defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med 2003; 28: 172-197. CrossRef | PubMed

108 Getahun D, Ananth CV, Oyelese Y, Chavez MR, Kirby RS, Smulian JC. Primary preeclampsia in the second pregnancy: effects of changes in prepregnancy body mass index between pregnancies. Obstet Gynecol 2007; 110: 1319-1325. PubMed

109 Mostello D, Kallogjeri D, Tungsiripat R, Leet T. Recurrence of preeclampsia: effects of gestational age at delivery of the first pregnancy, body mass index, paternity, and interval between births. Am J Obstet Gynecol 2008; 199: 55. PubMed

110 Maggard MA, Yermilov I, Li Z, et al. Pregnancy and fertility following bariatric surgery: a systematic review. JAMA 2008; 300: 2286-2296. CrossRef | PubMed

111 Duley L, Meher S, Abalos E. Management of pre-eclampsia. BMJ 2006; 332: 463-468. PubMed

112 Barton JR, Sibai BM. Prediction and prevention of recurrent preeclampsia. Obstet Gynecol 2008; 112: 359-372. PubMed

113 Trumbo PR, Ellwood KC. Supplemental calcium and risk reduction of hypertension, pregnancy-induced hypertension, and preeclampsia: an evidence-based review by the US Food and Drug Administration. Nutr Rev 2007; 65: 78-87. CrossRef | PubMed

114 Askie LM, Duley L, Henderson-Smart DJ, Stewart LAon behalf of the PARIS Collaborative Group. Antiplatelet agents for prevention of pre-eclampsia: a meta-analysis of individual patient data. Lancet 2007; 369: 1791-1798. Summary | Full Text | PDF(142KB) | CrossRef | PubMed

115 Rogers JM. Tobacco and pregnancy. Reprod Toxicol 2009; 28: 152-160. CrossRef | PubMed

116 Pabinger I. Thrombophilia and its impact on pregnancy. Thromb Res 2009; 123 (suppl 3): 16-21. PubMed

117 Sikkema JM, Franx A, Bruinse HW, van der Wijk NG, de Valk HW, Nikkels PG. Placental pathology in early onset pre-eclampsia and intra-uterine growth restriction in women with and without thrombophilia. Placenta 2002; 23: 337-342. PubMed

118 Robertson L, Wu O, Langhorne P, et alfor the Thrombosis: Risk and Economic Assessment of Thrombophilia Screening Study. Thrombophilia in pregnancy: a systematic review. Br J Haematol 2006; 132: 171-196. PubMed

119 Dizon-Townson D, Miller C, Sibai B, et alfor the National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. The relationship of the factor V Leiden mutation and pregnancy outcomes for mother and fetus. Obstet Gynecol 2005; 106: 517-524. PubMed

120 Kahn SR, Platt R, McNamara H, et al. Inherited thrombophilia and preeclampsia within a multicenter cohort: the Montreal Preeclampsia Study. Am J Obstet Gynecol 2009; 200: 151. PubMed

121 Kocher O, Cirovic C, Malynn E, et al. Obstetric complications in patients with hereditary thrombophilia identified using the LCx microparticle enzyme immunoassay: a controlled study of 5,000 patients. Am J Clin Pathol 2007; 127: 68-75. CrossRef | PubMed

122 Facchinetti F, Marozio L, Frusca T, et al. Maternal thrombophilia and the risk of recurrence of preeclampsia. Am J Obstet Gynecol 2009; 200: 46. PubMed

123 van Rijn BB, Hoeks LB, Bots ML, Franx A, Bruinse HW. Outcomes of subsequent pregnancy after first pregnancy with early-onset preeclampsia. Am J Obstet Gynecol 2006; 195: 723-728. CrossRef | PubMed

124 Steegers-Theunissen RP, Van Iersel CA, Peer PG, Nelen WL, Steegers EA. Hyperhomocysteinemia, pregnancy complications, and the timing of investigation. Obstet Gynecol 2004; 104: 336-343. PubMed

125 Walker MC, Ferguson SE, Allen VM. Heparin for pregnant women with acquired or inherited thrombophilias. Cochrane Database Syst Rev 2003; 2. CD003580. PubMed

126 Wilson JMG, Jungner G. Principles and practice of screening for disease. Public health papers, no 34. Geneva: World Health Organization, 1969.

127 Silver RM, Warren JE. Preconception counseling for women with thrombophilia. Clin Obstet Gynecol 2006; 49: 906-919. CrossRef | PubMed

128 Rep A, Ganzevoort W, Bonsel GJ, Wolf H, de Vries JI. Psychosocial impact of early-onset hypertensive disorders and related complications in pregnancy. Am J Obstet Gynecol 2007; 197: 158. PubMed

129 Poel YH, Swinkels P, de Vries JI. Psychological treatment of women with psychological complaints after pre-eclampsia. J Psychosom Obstet Gynaecol 2009; 30: 65-72. CrossRef | PubMed

130 Bellamy L, Casas JP, Hingorani AD, Williams DJ. Pre-eclampsia and risk of cardiovascular disease and cancer in later life: systematic review and meta-analysis. BMJ 2007; 335: 974. PubMed

131 Newstead J, von Dadelszen P, Magee LA. Preeclampsia and future cardiovascular risk. Expert Rev Cardiovasc Ther 2007; 5: 283-294. CrossRef | PubMed

132 Magnussen EB, Vatten LJ, Lund-Nilsen TI, Salvesen KA, Davey Smith G, Romundstad PR. Prepregnancy cardiovascular risk factors as predictors of pre-eclampsia: population based cohort study. BMJ 2007; 335: 978. PubMed

133 Berends AL, de Groot CJ, Sijbrands EJ, et al. Shared constitutional risks for maternal vascular-related pregnancy complications and future cardiovascular disease. Hypertension 2008; 51: 1034-1041. CrossRef | PubMed

134 Mosca L, Appel LJ, Benjamin EJ, et al. Evidence-based guidelines for cardiovascular disease prevention in women. American Heart Association scientific statement. Arterioscler Thromb Vasc Biol 2004; 24: 29-50. CrossRef | PubMed

135 Levine RJ, Vatten LJ, Horowitz GL, et al. Pre-eclampsia, soluble fms-like tyrosine kinase 1, and the risk of reduced thyroid function: nested case-control and population based study. BMJ 2009; 339. b4336. PubMed

136 Mutze S, Rudnik-Schoneborn S, Zerres K, Rath W. Genes and the preeclampsia syndrome. J Perinat Med 2008; 36: 38-58. CrossRef | PubMed

137 Nafee TM, Farrell WE, Carroll WD, Fryer AA, Ismail KM. Epigenetic control of fetal gene expression. BJOG 2008; 115: 158-168. CrossRef | PubMed

138 Oudejans CB, van Dijk M. Placental gene expression and pre-eclampsia. Placenta 2008; 29 (suppl A): 78-82. PubMed

139 Arngrimsson R. Epigenetics of hypertension in pregnancy. Nat Genet 2005; 37: 460-461. CrossRef | PubMed

140 Lambers MJ, Groeneveld E, Hoozemans DA, et al. Lower incidence of hypertensive complications during pregnancy in patients treated with low-dose aspirin during in vitro fertilization and early pregnancy. Hum Reprod 2009; 24: 2447-2450. CrossRef | PubMed

141 Hossain N, Schatz F, Paidas MJ. Heparin and maternal fetal interface: Why should it work to prevent pregnancy complications?. Thromb Res 2009; 124: 653-655. CrossRef | PubMed

142 Krause B, Sobrevia L, Casanello P. Epigenetics: new concepts of old phenomena in vascular physiology. Curr Vasc Pharmacol 2009; 7: 513-520. CrossRef | PubMed

143 Wu CS, Nohr EA, Bech BH, Vestergaard M, Catov JM, Olsen J. Health of children born to mothers who had preeclampsia: a population-based cohort study. Am J Obstet Gynecol 2009; 201: 269. PubMed144 Zetterstrom K, Lindeberg S, Haglund B, Magnuson A, Hanson U. Being born small for gestational age increases the risk of severe pre-eclampsia. BJOG 2007; 114: 319-324. CrossRef | PubMed

145 Oglaend B, Forman MR, Romundstad PR, Nilsen ST, Vatten LJ. Blood pressure in early adolescence in the offspring of preeclamptic and normotensive pregnancies. J Hypertens 2009; 27: 2051-2054. CrossRef | PubMed

146 Tenhola S, Rahiala E, Halonen P, Vanninen E, Voutilainen R. Maternal preeclampsia predicts elevated blood pressure in 12-year-old children: evaluation by ambulatory blood pressure monitoring. Pediatr Res 2006; 59: 320-324. CrossRef | PubMed

147 Sep SJ, Smits LJ, Prins MH, Spaanderman ME, Peeters LL. Simple prepregnant prediction rule for recurrent early-onset hypertensive disease in pregnancy. Reprod Sci 2009; 16: 80-87. PubMed

148 Blankley RT, Gaskell SJ, Whetton AD, Dive C, Baker PN, Myers JE. A proof-of-principle gel-free proteomics strategy for the identification of predictive biomarkers for the onset of pre-eclampsia. BJOG 2009; 116: 1473-1480. CrossRef | PubMed

149 de Groot CJ, Guzel C, Steegers-Theunissen RP, et al. Specific peptides indentified by mass spectrometry in placental tissue from pregnancies complicated by early onset preeclampsia attained by laser capture dissection. Proteomics Clin Applic 2007; 1: 325-335. PubMed

Over the past three decades community-based public health programming focused on promoting the wellbeing of women and children in East Africa have created positive partnerships between local governments and western NGOs. Together, these organisations have primarily focused on improving the health of children in East Africa by supporting women through educational programming and empowering their independence. These organizations are working in communities and societies where men have traditionally perpetrated, and continue to perpetuate, the very gender inequalities that compromise the health of women and children. Through focusing early efforts on direct partnership with women, these initiatives have greatly improved health equality. However, this approach has led to the inadvertent exclusion of men within many child health projects. Involving men has not been overlooked, but rather it has been greatly underutilised.

Improvements that will build upon past successes of such programs should include targeted curriculum focused on empowering men to become more involved in maternal and child health issues. Moreover, these programs would benefit from actively supporting and encouraging the positive roles men do fill within their communities. In doing so, international public health organizations would be able to more effectively utilize the familial and social resources within the communities that they serve.

The role of men within community-based Integrated Management of Childhood Illness (c-IMCI) programs throughout East Africa has traditionally been through their training as community health volunteers, as their status as community leaders has important influence on the success of these projects. A recent Lancet World Report on child health in Uganda reports on how expanding the role of men within these programs has positively influenced the c-IMCI underway in the Mbarara district [1]. By framing the roles that men play as resource gatekeepers in these communities and emphasizing how they could become more proactive in the area of maternal health, this project has successfully expanded its volunteer base and has encouraged many men to lead the way in areas of child health education and promotion. The importance of this direct partnership with men in the areas of child health became clear to me on a recent trip to Tanzania.

After finishing my first year of medical school, I spent the summer of 2009 working with a US-based public health NGO conducting a mid-term project evaluation of a USAID-funded c-IMCI program in the Karatu district of Northwest Tanzania. My time there brought me into the lives of many families and gave me a brief, but broad, perspective on the various social, cultural, and economic factors that have both positively and negatively influenced the impact of the health education initiatives of this c-IMCI project. One experience, in particular, emphasized the emerging need for international public health agencies to become more proactive in engaging men within the area of maternal health.

After a day of interviews in the small farming village of Rhotia, a few dozen miles east of Karatu, we agreed to squeeze in the eldest of the midwives into our land cruiser and give her a lift into town. On our way home, she told us a story of a recent, and in her view, potentially avoidable disaster. A few weeks prior to our visit, she had been working with a young first time mother-to-be as she prepared for delivery. The midwives in this village serve as support during the delivery and liaisons between local health facilities. When the day came for this young mother to deliver the midwives helped prepared her house for the arrival of the new baby and took care of the mother after her water broke. At this first sign of delivery, the young husband was so unsettled that he quickly gathered his up his cell phone and money and fled, leaving the women stranded. Without the phone they couldn’t coordinate a car to pick them up to take them to health facility, without the money they couldn’t pay for the car, and without him, she emphasized, they couldn’t experience this important event in their lives together as a family. Fortunately, the midwives delivered the baby safety at home. The lesson, she wanted to impress upon us, was that it was time that we start teaching fathers about child delivery and supporting them in becoming more involved in this process.

Similar stories of injustice and societal complications were narrated by my friend, a fellow public health student who recently worked with a women’s group on a mosquito net distribution program in the Masaka district of Uganda. All of these issues are leaving lasting negative impact on child health. There is an opportunity for western-based NGOs implementing the Maternal and Child Health (MCH) and c-IMCI in these regions to rethink how they are integrating men into their programming to improve health outcomes.

The evidence exists to support the involvement of men in MCH programming. In Tanzania, a study found that pregnant women were more likely to deliver in a healthcare facility if both partners were involved in the decision-making process of the delivery location [2]. In Uganda, a UNFPA led program focused on including male elders in the decision making-process was able to reduce female genital cutting by roughly 35% [3]. New doors of opportunity could open for men to expand their responsibilities within the healthcare of their children, as has already been found to be working in Haiti and Kenya in areas such as breastfeeding and neonatal care [4,5].

The acceptance and response of integrating these gender-inclusive training programs will certainly vary from region to region depending on cultural differences and educational resource availability. These successful programs noted above demonstrate the balance between preserving the sensitive culture-specific gender dynamic while focusing on making changes to improve the health of young women and children through education-base interventions. With knowledge comes responsibility. The education and involvement of men in MCH issues may consequently increase the call for men to become more specifically invested in the health of mothers and infants.

The idea of involving men in MCH issues is not new. In 1994, the International Conference on Population and Development in Cairo, men were beginning to be included in the conversation surrounding reproductive health [6]. A snowballing effect has occurred since, and now there are a number of organizations and programs that highlight the need to include men in the area of MHC.

A global alliance of NGOs and UN agencies emerged over the past decade to promote the role of men in gender equality and women’s health. These organizations include: the International Center for Research on Women, International Planned Parenthood Federation, WHO, UNFPA, UNDP. Moreover, many useful web-based resources such as EngenderHealth.org and MenEngage.org have been created to outline actionable strategies that organizations can adopt to expand their current programs. The formation of MenEngage.org has made it clear that there is a growing call for the inclusion of men and fathers in MCH issues. Taking advantage of these resources and proven models will be essential for future MCH programming throughout the world.

Beyond improving safe delivery and rearing practices, such programming can empower men in other important and new ways. When interviewed about his experience with one such program in northwest Tanzania one husband’s response was:

“What I have appreciated most is accompanying my wife to the health centre for her antenatal clinic visits. That way, I will know if she has complications, and I can budget in advance to take her to a bigger hospital. I never went with my wife to the antenatal clinic when she was pregnant with our other children. I think I missed out. But in the past, men were not allowed. Now, if you go with your wife, the clinic staff treat you like someone important.”

Joseph, age 42, a resident of northwestern Tanzania’s Geita District [5]

In East Africa and across the globe, there is an opportunity to start recognizing men as partners in the health of women and children. This need is slowly being addressed in pockets of East Africa; perhaps the most recently successful is an on-going USAID-supported breastfeeding campaign started in 2009 in Western Kenya that has encouraged men to support their wives as they breastfeed [6]. By reshaping MCH programming with the aid of such successful models and available resources, we may hope to include more men like Joseph in MCH interventions. This will consequently facilitate a greater and more widespread dissemination of information and skills. To continue improving the health and wellbeing of the women and children who benefit from MCH and c-IMCI project we need to begin integrating creative and meaningful ways that engage both parents in a manner that empowers women and men to work together on the shared goal of improving the health of the next generation.

Ben Pederson* & Tyler Weber T.W.

University of Minnesota School of Public Health, MPH2; B.P. University of Minnesota School of Medicine, MS2. *corresponding author: ben.pederson(a)gmail.com

References

1. Webster PC. Uganda registers successes with child-health volunteers. Lancet. 2009; 374: 1735-6.

2. Danforth EJ, Kruck ME, Rocker PC, Mbaruku G, Galea S. Household Decisions-making about Delivery in Health Facilities: Evidence form Tanzania. J Health Popul Nutr. 2009; 27(5): 696-703.

3. United Nations Population Fund. Partnering with Men in Reproductive and Sexual Health. 1st ed. New York: United Nations Population Fund; 2003.

4. Martin S, Maeor P. 5th Breastfeeding and Feminism Symposium; 2010 [cited 2010 May 14]. Engaging men to increase support for optimal infant feeding in Western Kenya. Available from: http://www.iycn.org/InfantandYoungChildNutritionProjectEvents.php

5. Sloand E, Gebrain B. Fathers Clubs to Improve Health in Rural Haiti. Public Health Nurs. 2006; 23(1): 46-51.

6. Earth Negotiations Bulletin [homepage on the internet]. Cairo: Proceedings of the International Conference on Population and Development; 1994 [cited 2010 Apr 10]. Reproductive Rights and Reproductive Health; [one screen]. Available from: http://www.iisd.ca/vol06/0639016e.html.

7. United Nations Population Fund. UNFPA at Work: Six Human Rights Case Studies. New York, NY; United Nations Population Fund; 2008.

Anil Joshi has accepted this week’s TLS challenge to complete the 10-point medical school questionnaire. Read on to find out more, and don’t forget to look here for more information on how YOU can take up the 10 question challenge.

Here are his answers:

1. Why did you decide to study medicine?

At school I studied a combination of both arts and sciences and I viewed medicine as encompassing both. Along with science there was sociology, ethics, philosophy, history, language and many  more. Furthermore the fact that this lead into a career where everyday will present with new challenge really attracted me! A medical career for me was more than a single subject which stays in the workplace. It was applied knowledge and skills which you can use globally for the rest of your life.

2. Can you share some things that you wish that someone had told you before you applied to study medicine?

I was actually quite well informed before I applied and not much came as a surprise to me. Which emphasises the point of researching the course, the city, the university, the career choice and the job itself very well before applying. Work experience is invaluable. Make sure you speak to doctors of all levels to know what to expect and then decide if its for you or not. You really need to be fully dedicated as it’s a massive life choice to study medicine, and well worth it.

3. What profession would you be in if you weren’t in medicine?

I always enjoyed learning new languages and can speak French and Gujarati, so I would have tried for a career utilising this skill. This would have also given me the prospect of travelling as well. Fortunately, medicine still gives me the opportunity to use my language skills and travel which is an added bonus, so I’m happy!

4. What is your biggest motivation?

The variety. Everyday is not the same, from psychiatry to orthopaedic surgery. The patients you see, their families, the pathology you witness, the different hospitals, and the different doctors who teach you are always changing. Also there are so many opportunities to do whatever interests you outside the scope of the curriculum, such as research and option modules. This way if you’re anything like me who cannot decide when there is so much choice, you can try things out and see how you feel.

5. What are you most interested in so far and why?

Since the beginning I have always been fascinated by the heart, and subsequently all my option modules have been based around cardiology. The doctors we work with on our placements tend to be our role models and we often associate our own characters with theirs. I associated mine with cardiologists and consequently really enjoyed working with them

6. What has been your most difficult module so far and why?

I found paediatrics the most challenging module. Although fascinating, there were a lot of things to learn, and it proved difficult to revise it in such a small time. It was the whole of medicine again but for children under 16 to 30 weeks premature babies. Furthermore it was emotionally difficult with the amount of child abuse witnessed in the hospital in which I was based. Nevertheless I really enjoyed the module and added social aspect of it.

7. What is the most memorable positive moment in your medical studies so far?

My elective in East Timor allowed me to work in an environment where not all the usual medical resources were accessible. It was a turning point in my academia, which obliged me to focus on my patient histories, improve clinical decision making, and develop my skills in diagnosing and formulating a management plan in all specialities. I feel a lot more confident for my fast approaching final exams, and my foundation years thereafter.

8. What is the worst horror story in your medical studies to date?

I was doing my first ever delivery on my obstetric placement, after waiting so long to do one. As the baby’s head came out, his shoulders got stuck and it turned out to be shoulder dystocia. I was holding a blue head in my hands, midwife panicking and alarms screaming which caused about 10 people to rush in order to help save the baby and mother. Luckily we got the baby out in time by performing the McRobert’s manoeuvre on the mother. Everyone lived happily ever after but it was a moment of fear and panic I will never forget it.

9. Where do you see yourself in 10 years time?

a. Wishful thinking version: I’d like to be working abroad in a developing setting or as a humanitarian doctor.

b. Perhaps slightly more realistic version: I know it’s not the easiest thing to do but I’ll try my hardest to get there and I hope I do! There is no easy route for anything in medicine; it’s just a matter of trying your hardest. I believe if you want something enough, you will get it.

10. Can you share some tips/advice for others

a. Wanting to study medicine: As well as being a part of  medical school you will also be part of a larger university with a whole array of extracurricular activities. If you are not already, make sure you get involved in something outside medicine and academia.This will give you means to relax at times and will prevent you from cracking under the pressure as the course can be really demanding at first.

If you haven’t applied to med school yet then being involved in extracurricular activities often works in favour of your application. Don’t forget the prospect of a gap year too, contrary to belief, it’s not frowned upon  and is even commended. It gives you enough time to mature and prepare yourself before starting the 5 year course. To study medicine is a massive choice and a life changing one, so make sure you’re certain and mentally prepared.

b. Already studying medicine: Intercalating is a great idea. As well as developing your interest in a particular area, it gives you a midpoint in your medical studies. Personally, I changed city for a year after my 2nd year and this turned out to be a great personal and professional experience. It will give a more rounded approach to the rest of the course. Personally, I was more focused after.

Anil Joshi
mda05aj@sheffield.ac.uk

Health, famously defined by the WHO as “a state of complete physical, mental and social well being” [1], is arguably one of the most fundamental entitlements of life. Tragically for millions of people around the globe this basic right is not realised due to lack of access to health care, a fundamental determinant of health in a population through its roles in preventing and treating illness and promoting good health practices.

Fractured health care

Disparities in health care availability, access and quality are entrenched internationally between developed and developing nations as well as within countries, both between urban and rural regions and affluent and poorer areas. Thus from the outset of life, in terms of health outcomes, where you live matters. In London, a baby born today would expect to survive to the grand old age of 80. Compare this to Malawi, one of the poorest nations in the world, where the average life expectancy at birth is just 50 years [2].

The distorted allocation of human capital to deliver heath care services is one situation which fuels these gross inequities in health outcomes. Malawi has a huge deficit in health care professionals, with less than one doctor per 10,000 citizens [3]. Despite the fact that only 18% of the population reside in urban areas [4], a disproportionate number of doctors work at central referral hospitals in these regions. Consequently, some district hospitals serving rural populations do not employ a single doctor. This leaves medical assistants, nurses and clinical officers (akin to specialist nurse practitioners in the UK) to provide the medical care [5].

This fractured state of heath provision in Malawi is further exacerbated due to acute shortages of specialists in many areas within the medical profession itself. This includes orthopaedic surgeons of which there are only nine to serve the entire population [6]. With the huge focus on communicable diseases such as HIV/AIDS in the developing world, it is easy to forget the significant contribution of musculoskeletal conditions to morbidity and mortality in these countries. Although this burden is not well documented in Malawi, the fact that motor vehicle accidents are the eighth commonest cause of death amongst adults [7] argues for increased resource allocation to the orthopaedic specialty.

Local solutions – the Orthopaedic Clinical Officer

The desperate state of orthopaedic care in Malawi was observed by Dr Edward Blair whilst working as a Rotary International volunteer orthopaedic surgeon in the mid 1980s. At the time Malawi was completely reliant on expatriates, having no orthopaedic specialists of its own. Compelled to improve the situation, he developed an 18 month programme to educate existing clinical officers to manage common orthopaedic problems, reserving the expertise of orthopaedic surgeons for more serious cases. The significantly lower input costs and training time in comparison to full orthopaedic surgical education enabled the rapid deployment of specially trained paramedical professionals, now known as Orthopaedic Clinical Officers (OCOs), to expand orthopaedic facilities, particularly in rural areas [6].

Professor Chris Lavy restarted the course in 1990s after it had fallen into financial hardship, obtaining funding from the United Kingdom Department for International Development and the Nuffield Foundation through THET (Tropical Health Education Trust). He says of the OCOs, “They are great at what they can do, which is the delivery of conservative care to people with common fractures and dislocations. These common conditions make up the vast majority of injuries that present at district hospitals in Malawi.” The OCO impact on access to orthopaedic care has been remarkable. Collectively, by the mid 1990s actively practicing OCOs were seeing approximately 150,000 patients per year, the majority of diagnoses being trauma related. Furthermore, with over 50% employed by District and Mission Hospitals, this goes some way to fill the void of musculoskeletal expertise in rural areas [6].

An additional advantage of the scheme has been that the OCO profession has not been subject to the migratory ‘brain drain’ that occurs in other healthcare sectors, with all practicing OCOs still working within the county [6]. The exodus of healthcare workers out of Malawi to nations with stronger economic prospects has been particularly damaging to the nursing and midwifery pool, with over 100 personnel per year emigrating to countries such as the UK. This exacerbates an already critical situation, where over 60% of nursing posts are vacant nationally [5]. As their qualification is not recognised outside Malawi the OCO specialty triumphs by being exempt from this phenomenon, which keeps indispensible frontline healthcare staff in the country and means the investment in their training is fully realised.

Looking to the future

Currently the programme has an annual intake of 10-15 students per year but because OCOs will continue to be the key deliverers of primary orthopaedic care for the foreseeable future, the need for expansion remains [6]. Of course this is dependent on the concomitant amplification of financial backing which has changed in recent years, when income from its major donor THET ended in 2007 [6]. Alternative sources have had to be sought to allow training to continue as Stuart Palmer, the current course director in Malawi, explains. “The Ministry of Health is now on board here in Malawi as a core funder for the course but we still need to keep working with them and others to see it grow further.” The dependence on external bodies for the support of the course highlights the need for continued awareness, both inside and outside Malawi, of the importance of the multifaceted benefits OCOs deliver to ensure that care of musculoskeletal conditions is not put on the back-burner. 

Despite the apparent successes of the scheme it is important to recognise the limitations of the care that can be provided by OCOs. Their role is no replacement for the expertise of orthopaedic surgeons that is required to manage more complex presentations. Current postgraduate arrangements aim to produce between one and three graduate orthopaedic specialist doctors per year but an escalation in training places will be required to produce enough surgeons for equitable nationwide coverage [6]. The existence of OCOs should not detract from the need to train more orthopaedic surgeons.

As shown by the success of the OCO course in Malawi, it is possible for low cost programmes utilising existing paramedical professionals to rapidly meet the needs of side-lined specialties such as orthopaedics. Stakeholders in public health in developing countries need to recognise the potential of such interventions as an important tool in redressing the gross urban-rural inequity in healthcare access that prevents so many from receiving the care that they deserve.

Tamsin Cargill

4th Year Medical Student, Imperial College London

tnc06(a)ic.ac.uk

 References 

1. Constitution of the World Health Organization. Basic Documents, Forty-fifth edition, Supplement, October 2006. World Health Organization Web site. Available at: http://apps.who.int/gb/bd/PDF/bd47/EN/constitution-en.pdf Accessed: June 2010

 2. WHO World Health Statistics Report 2009. World Health Organization Web site. Available at: http://www.who.int/whosis/whostat/EN_WHS09_Table1.pdf Accessed: November 2009

 3. World Health Statistics Report 2009. World Health Organization Web site. Available at: http://www.who.int/whosis/whostat/EN_WHS09_Table6.pdf Accessed: November 2009

 4. World Health Statistics Report 2009. World Health Organization Web site. http://www.who.int/whosis/whostat/EN_WHS09_Table9.pdf Accessed: November 2009

 5. Record, R., & Mohiddin, A. (2006). An economic perspective on Malawi’s medical “brain drain”. Globalization and Health, 2, 12.

6. Mkandawire, N., Ngulube, C., & Lavy, C. (2008). Orthopaedic clinical officer program in malawi: A model for providing orthopaedic care. Clinical Orthopaedics and Related Research, 466(10), 2385.

7. WHO Country Health System Fact Sheet 2006 – Malawi. World Health Organization Web site. Available at: http://www.who.int/whosis/mort/profiles/mort_afro_mwi_malawi.pdf Accessed: November 2009

By Carlos Fioravanti

State University of Campinas

chfioravanti(a)gmail.com

A versatile new drug candidate called P-Mapa along with a new proposal to fight infectious diseases have emerged in Brazil. They are the result of collaboration among non-academic and academic groups in Brazil, Chile and the US led by the non-profit research network Farmabrasilis.

Figure 1. Crystals (300 x) and nanocrystals (37,000 and 80,000 x) of P-Mapa: an immunomodulator derived from Aspergilus orizae  (Credit: Courtesy Farmabrasilis)

P-Mapa, a proteinaceous aggregate of ammonium and magnesium phospholinoleate-palmitoleate anhydride, is a biotechnological compound derived from Aspergilus orizae [1]. It is an immunomodulator, which can rebuild the organism’s natural defence system against tumours, viruses, bacteria and other disease-causing microbes.

P-Mapa has demonstrated anti-tumor activity, with no relevant signs of toxicity, on studies performed on rodents, non-human primates and on HIV-positive patients-phase I clinical trial [2,3,4]. The compound was shown to induce proliferation of lymphocyte T, increase cytokine production and natural killer cell activity, and stimulate nitric oxide release by macrophages [5,6,7].

Scientists from the Brazil-based Farmabrasilis and the US National Institute of Allergy and Infectious Diseases (NIAID) have confirmed the potential of P-Mapa to treat infectious diseases. In 2009, Farmabrasilis and NIAID teams showed that P-Mapa can protect against Punta Toro Virus (PTV), which produces a fatal hepatic disease in animals and is closely related to the Rift Valley fever virus, endemic in sub-Saharan Africa. In these experiments P-MAPA was compared to the antiviral Ribavirin. Both were able to protect 100% of all infected animals with no signs of hepatic damage, strengthening the possibility of using P-Mapa as adjuvant to treat hepatitis B and C, mainly when the first-choice medicine has limited use or with adverse effects [7,8].

The latest tests carried out by Brazilian and American teams have demonstrated that P-Mapa is active against Mycobacterium tuberculosis in vivo. Wild-type C57BL/6 mice were exposed to an aerosol of M. tuberculosis and later treated with P-Mapa and the antimicrobial Moxifloxacin, used both alone and together. The P-Mapa acted alone to deter the bacterial proliferation in the lung and spleen at levels above the minimum standards required. P-Mapa may have synergized with Moxifloxacin, as the combination of the two drugs provide wider protection than each when used alone [9].

A plan to fight infectious diseases

Based on these data, the Farmabrasilis team proposed the use of P-Mapa to fight infectious diseases. Launched in 2009 at 3^rd Stop TB Partners Forum, the proposal focuses on the re-establishment of the patients’ natural defenses (immunocompetence) by using P-Mapa as an adjuvant medicine with antiviral and antimicrobial drugs. This approach could help to prevent or treat diseases such as tuberculosis and malaria in patients, including those co-infected with HIV.

The Farmabrasilis proposal includes the possibility of sharing all data and methods of production, free of charge, with governments, institutions or groups interested in using the P-Mapa to treat neglected diseases and disadvantaged populations. In such cases, partners cannot sell the medicines or the technologies associated with them, and must also offer the medicine free of charge to people who most need them, as detailed on the Farmabrasilis website [10].

Broader than other approaches from other Public-Private Partnerships, Farmabrasilis’ call for a collective, open task force against infectious diseases represents a way to reduce the cost of drug development whilst engaging civil society organizations in the search for new models of medicine research and production [11,12].

A collective effort

In its use of non-academic and academic groups, from discovery to the first human trials, the P-Mapa course illustrates innovative ways to produce scientific knowledge. This approach can reduce the time and the money usually required to develop a new drug, as well as to conciliate interests from different groups and help to solve public health needs.

This strategy can be significant especially in developing countries. In Brazil, most drug candidates discovered in research institutes hardly go beyond the publication of papers, and Brazilian pharmaceutical companies only produce drugs derived from plants (used as analgesic or anti-aging agents), me-too compounds (e.g., to treat erectile dysfunction) or generic medicines, rarely addressing the public health needs [13,14].

As part of my doctoral research, I have followed 26 molecules presented over the past 15 years in international scientific journals and in Brazilian newspapers and general magazines as promising medicines. The molecules represented new hope against cancer, tuberculosis, pain, inflammation, arterial hypertension, Alzheimer’s disease, arthritis, epilepsy, mycosis, and ulcers, as well as typically tropical health problems such as Chagas disease and schistosomiasis. The scientists responsible for the research have stated, through the media, that these molecules would be evaluated in humans or be available as medicine in a few years. For various reasons, until 2010 none of the molecules has reached the promised goals.

Figure 2. P-Mapa purified: a medicine in the pipeline (Credit: Courtesy Farmabrasilis)

An unusual story

P-Mapa has had an unusual story. Initially, the physician Odilon da Silva Nunes worked for almost 40 years in a private laboratory, away from formal science research centers, to develop a molecule that could block tumors, according to his own hypothesis about the origin of cancer. The research advanced through collective work by other physicians and both non-academic and academic researchers who evaluated the compound’s properties according to drug development guidelines. In the 1990s, Farmabrasilis teams, led by Dr. Iseu Nunes as CEO and Prof. Nelson Duran as scientific director, scaled up the production and tested the compound on a group of HIV-positive people. Next, unable to forge alliances with pharmaceutical companies in Brazil, the research group reorganized, grew internationally and focused the research on infectious diseases, especially the most common in poor countries, such as AIDS and tuberculosis.

As a science writer and later as a PhD candidate, I have followed the P-Mapa story since 1991. I was privileged to visit the laboratories where P-Mapa was produced and talk to the scientists involved in this research. Their motivation to work voluntarily was “to satisfy idealism or curiosity, seek new challenges, hone skills, build a reputation or enhance careers”, as in other open source researches [15].

In 2007, as a Reuters Institute for the Study of Journalism Fellow at Oxford University, I examined how penicillin emerged in London and was later developed at Oxford. After comparing the course of the English and the Brazilian compounds, I concluded that their development is similar. Briefly, both started in the hands of physicians, moved ahead through a multidisciplinary task force and required overseas aid to be concluded [16]. However, the P-Mapa effect is broader, due to its ability to deter tumours, viruses and bacteria. Unlike penicillin, P-Mapa is a medicine in the pipeline.

References

1. Nunes I et al. United States Patent Application: US20060093628. “Protein aggregate magnesium-ammonium phospholinoleate-palmitoleate anhydride immunomodulator, its production process and formulation”.

2. Justo GZ, Durán N, Queiroz MLS. Myelopoietic response in tumor-bearing mice by an aggregated polymer isolated from Aspergillus orizae. Eur. J. Phamacol. 1999, 388: 219–226.

3. Farmabrasilis. P-MAPA toxicity and safety. Available from: www.farmabrasilis.org.br/todos conteudos interna.php?idioma=eng&id=217. [Accessed: 22th June 2010]

4. Farmabrasilis. P-MAPA clinical trial phase I. Available from: www.farmabrasilis.org.br/interna relatorios clinicos.php?idioma=eng&id=180 [Accessed: 22th June 2010]

5. Melo A, Justo GZ, Queiroz MLS. Stimulation of myelopoiesis in Listeria monocytogenes-infected mice by an aggregated polymer isolated from Aspergillus oryzae. Human Exp. Toxicol. 2001, 20: 38–45.

6. Justo GZ, Durán N, Queiroz MLS. Natural killer cell activity, lymphocyte proliferation and cytokines profile in tupour-bearing mice treated with MAPA, a magnesium aggregated polymer from Aspergillus orizae. Immunopharmacol. Immunotoxicol. 2003, 25: 305–319.

7. Farmabrasilis. P-Mapa Product Monograph. Available from: http://www.farmabrasilis.org.br/todos_conteudos_interna.php?idioma=eng&id=110 [Accessed: 22th June 2010]

8. Durán N, Gowene BB et al. A biotechnological product and its potential as a new immunomodulator for treatment of animal phlebovirus infection: Punta Toro virus. Antiviral Res. 2009, 83: 143–147.

9. Farmabrasilis. Assessment of the efficacy of the immunomodulator P-MAPA against M. tuberculosis in a standard mouse model. Available from: http://www.farmabrasilis.org.br/todos_conteudos_interna.php?idioma=eng&id=276 [Accessed: 22th June 2010]

10. Farmabrasilis. Infectious diseases proposal. Available from: http://www.farmabrasilis.org.br/pesquisa_desenvolvimento_interna.php?idioma=eng&id=255 [Accessed: 22th June 2010]

11 Rawlins MD. Cutting the cost of drug development? Nat. Rev. Drug Discov. 2004, 3: 360-364

12 Bhan A, Singh JA et al. Grand Challenges in Global Health: Engaging Civil Society Organizations in Biomedical Research in Developing Countries. PLoS Med. 2007, 4(9): e272.

13. Rezaie R, Frew S et al. Brazilian health biotech—fostering crosstalk between public and private sectors. Nat. Biotechnol. 2008, 26: 627-644.

14. Vidotti CC, de Castro LL, Calil SS. New drugs in Brazil: Do they meet Brazilian public health needs? Rev Panam Salud Publica. 2008, 24(1):36-45.

15. Munos B. Can open-source R&D reinvigorate drug research? Nat. Rev. Drug Discov. 2006, 5, 723-729.

16. Fioravanti C. New perspectives on drug development in developing countries: A case study of the Brazilian compound P-Mapa. Reuters Institute for the Study of Journalism 2007. Available from: http://reutersinstitute.politics.ox.ac.uk/fileadmin/documents/Publications/fellows__papers/2006-2007/NEW_PERSPECTIVES_ON_DRUG_DEVELOPMENT_IN_DEVELOPING_COUNTRIES.pdf [Accessed: 22th June 2010]

Katie Ball, a medical student, has accepted this week’s TLS challenge to complete the 10-point medical school questionnaire. Read on to find out more, and don’t forget to look here for more information on how YOU can take up the 10 question challenge.

Here are her answers:

1. Why did you decide to study medicine?

I considered studying medicine from an early age but decided against it as I felt unable to commit to 5 or 6 years at university and a lifetime of learning. Instead, I did a degree in Biochemistry. After my degree I became a health care assistant due to my persistent interest in medicine. My enthusiasm for care of the elderly and a desire to help vulnerable people confirmed that medicine was the only route for me.

2. Can you share some things that you wish that someone had told you before you applied to study medicine?

I wish someone had emphasised the importance of researching different types of medicine courses available. I am currently doing a problem-based learning (PBL) course and although I like it and think it has a place in medical learning today, I feel that in hindsight, I personally would have suited a course that combined a traditional and PBL approach. Hearing opinions from current student on different courses, or having a ‘taster day’ might have helped me make a more educated decision.

3. What profession would you be in if you weren’t in medicine?

I considered applying for a PhD to lead into a career in research.

4. What is your biggest motivation?

I am very conscientious and this makes me motivated. I like people and so caring for vulnerable people motivates me.

5. What are you most interested in so far and why?

I believe that too much emphasis is placed upon specialities and too often patients get shifted from one specialist consultant to the next. In my paediatric rotation however, I noticed that there was a much more holistic approach to medicine which I found fantastic. In paediatrics, the doctor is not only treating the child, they are interacting and helping the whole family. I think that this is a real skill of communication and a great challenge.

6. What has been your most difficult module so far and why?

Although I enjoyed psychiatry and neurology, I was overwhelmed by the amount we had to learn in such a short amount of time. I really struggled with remembering the relevant information for psychiatry and found neuroanatomy incredibly difficult. The brain is incredible but how on earth can people understand it!

7. What is the most memorable positive moment in your medical studies so far?

It sounds pretty pathetic but, a doctor telling me that I would make a nice GP during a teaching session is one of my most memorable moments from my studies so far. It was just before my exams and their confidence in me gave me the boost that I needed.

8 ) What is the worst horror story in your medical studies to date?

Watching a lady in labour horrified me! The midwives said it was a good labour. I found it thoroughly traumatizing! I’ve been really fortunate and not had a truly horrendous experience…yet.

9) Where do you see yourself in 10 years time?

a) The wishful thinking version: A paediatrician trusted and respected by colleagues and patients. My only real aim is to be personally requested by my patients – a sign of a really good doctor!

b) Perhaps slightly more realistic version: I hope (a) is true. If it isn’t I think I’ll quit! To be honest, I will probably end up being a GP with a special interest in Paediatrics.

10) Can you share some tips/advice for others

a) Wanting to study medicine: If you believe medicine to be the only way for you, get lots of work experience. Work hard and go for it!

The reason I didn’t do medicine originally was because my parents, who are also in health care, highlighted the fact that medicine is not only a job, it is a career and lifestyle choice. If you do not feel ready to commit to studying for the next 5 or 6 years, take a break. Do something first and postpone the decision. I wouldn’t have done it any other way.

b) Already studying medicine: Support your friends. You’ll need them too at some point. Don’t compare yourself too much to others- there will always be people better and worse than you.

Not only do patients want a doctor with great clinical ability, but also one who is approachable and who listens to them. Good communication skills are a necessity, that need to be practiced.