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Miller, Vivienne

Dr Vivienne Miller

GP and Medical Editor
I have special expertise in psychology and psychiatry, obstetrics and gynaecology and paediatrics, as well as having a great interest in general medicine.

More from this expert

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Assessing stroke risk – easier than saying “CHA2DS2-VA Score”!

General Practitioner Dr Vivienne Miller takes a look at what’s changed in the recently updated CHA2DS2-VASC Score for the determination of stroke risk factors from atrial fibrillation. The CHA2DS2-VA Score was updated from the CHA2DS2-VASC Score last year to exclude female sex (represented by Sc) in the determination of stroke risk factors from atrial fibrillation. The two scores are identical, apart from the exclusion of female sex, which is no longer considered an outright risk factor in stroke from atrial fibrillation, but more of a ‘risk modifier’ of this complication.1General Practitioner Dr Vivienne Miller takes a look at what’s changed in the recently updated CHA2DS2-VASC Score for the determination of stroke risk factors from atrial fibrillation. The CHA2DS2-VA Score was updated from the CHA2DS2-VASC Score last year to exclude female sex (represented by Sc) in the determination of stroke risk factors from atrial fibrillation. The two scores are identical, apart from the exclusion of female sex, which is no longer considered an outright risk factor in stroke from atrial fibrillation, but more of a ‘risk modifier’ of this complication.

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Managing Heavy Menstrual Bleeding in General Practice

Based on an interview with Associate Professor Kirsten Black and Clinical Associate Professor Deborah Bateson conducted at the Annual Women’s and Children’s Health Update, Sydney in February 2018. "Heavy menstrual bleeding" is the new term for menorrhagia. This under-treated condition is easy to screen for in general practice. And screening for it is important as, apart from the discomfort, inconvenience, disturbed sleep, embarrassment and expense heavy menstrual bleeding causes, it is a major cause of iron deficiency in women. Common causes of heavy menstrual bleeding include hormonal variations relating to menarche and menopause, polycystic ovarian syndrome, polyps, fibroids and coagulation disorders. Identifying heavy menstrual bleeding initially involves discussing menstrual patterns with patients, as the diagnosis relies on the subjective experience of the woman as it affects her physical, emotional, social and/or material quality of life. Women may be unsure whether their periods are abnormally heavy compared with other women.  Questions that may assist in the diagnosis of  heavy menstrual bleeding include asking whether a woman needs to wear both a pad and a tampon simultaneously to prevent leakage, whether she has to use super pads and/or tampons and needs to change them every three hours or less, , whether she is concerned about flooding or staining during the day and avoids social activities as a result, whether she regularly takes time off work at the time of her period, whether she has to get up several times overnight to change her pad or tampon, whether she frequently passes clots (often this is associated with significant period pain), and finally, how the issue is affecting her quality of life. It is also important to inquire about associated symptoms such as pain, bloating and feelings of pressure on the bladder or bowel.Investigations usually include iron studies, a full blood count and a pelvic ultrasound. Ideally the ultrasound should be transvaginal as well as transabdominal. Also, ideally the ultrasound should be conducted between days five to 10 of the menstrual cycle, as this is when the uterine lining is less echogenic and scanning at this time reduces the chance of missing lesions such as polyps, within the uterine cavity. It should be noted that heavy menstrual bleeding may be a symptom of malignancy, especially in women over the age of 45 years. Other more specialised tests may also be indicated, such as coagulation studies, if there is suggestion of a bleeding diathesis. Once malignancy has been excluded as a cause of the bleeding, management usually includes hormonal control of the ovulation cycle, such as with the combined oral contraceptives. These reduce bleeding by 30%. An excellent alternative is the hormonal intrauterine system (Mirena®). If the woman prefers not to use such methods and is not at risk of pregnancy, tranexamic acid or norethisterone, 5mg three times daily, from days five to 26 of the menstrual cycle, can be used. NSAIDS such as mefenamic acid are most effective if commenced just prior to the onset of bleeding and continued into the first few days. Surgical management of heavy menstrual bleeding is usually indicated for women who have completed their families. The less invasive options include endometrial ablation and embolisation of fibroids. Hysterectomy is generally reserved for women in whom less invasive treatments have been unsuccessful, where there is a particular indication (such as large fibroids causing pressure symptoms) or less commonly, at the woman’s request.

1 in 3 young adults is lonely – and it affects their mental health
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Managing Hyperhidrosis

Based on an interview with Sydney dermatologist, Dr Rob Rosen conducted at the Annual Women’s and Children’s Health Update, Sydney in February 2018. Hyperhidrosis is a very distressing condition that equally affects both men and women, across all ethnicities.  It occurs in approximately 3% of the general population and the onset is in childhood or adolescence. However, only about one third of people affected seek medical advice. In addition to the physical effects, the psychological impact on affected individuals is significant. Embarrassment, anxiety and depression are very commonly associated with this condition. In primary hyperhidrosis, the sweat glands are normal but there is an apparently exaggerated sympathetic response. The sweat glands most susceptible to these sympathetic cholinergic effects are the eccrine glands found in the palms, soles and axillae. Primary, focal hyperhidrosis tends to be bilateral and symmetrical, occurring at least once a week. It usually commences before a person reaches their mid-twenties and is often familial.  In its typical form, and if there is nothing to suggest a secondary cause, it requires no investigations. Secondary hyperhidrosis is typically generalised, affecting the entire surface of the skin. By definition, it has an underlying cause, such as infection, endocrine disturbance, neuropathy, malignancy, menopause, drug withdrawal or the side-effect of medications.  A full history, examination and targeted investigations are required before this condition can be called idiopathic. “It is important to make the distinction between “generalised” and “focal” hyperhidrosis at the outset,” says Sydney dermatologist, Dr Rob Rosen The management of hyperhidrosis begins conservatively. By the time they present to a doctor they usually have already tried a range of antiperspirants.  Aluminium hydroxide 20%, topically, daily for four weeks should be trialled before further treatment is considered. Many patients develop localised irritation to this treatment, as it obstructs the eccrine ducts, causing their atrophy. The most effective management is Botulinum A toxin injections. This drug blocks the release of acetylcholine from presynaptic nerve terminals, thus inhibiting the stimulation of the eccrine sweat gland. The injections are done intradermally and retreatment is needed approximately every six months. Over time, this duration between treatments may become longer. Side effects include discomfort at the injection site and, less commonly, weakness of local muscles (especially relating to small muscles in the hand, for example, in palmer hyperhidrosis). In the research done by Dr Rosen t al, over 90% of patients were happy with this therapy.1 Oral anticholinergics such as oxybutynin (5mg to 15mg daily) or glycopyrrolate (1mg to 4mg daily) may be used and are most effective in refractory cases of generalised sweating. The anticholinergic side effects (urinary retention, dry mouth, constipation) tend to be a limiting factor in their use. Other treatments for hyperhidrosis tend to be either less effective or more invasive. For patients over 12 years old, there is a Medicare rebate for Botulinum A injection therapy for severe primary axillary hyperhidrosis, if aluminium hydroxide has failed and if it is administered by a dermatologist, neurologist or paediatrician. Some cosmetic clinics treat patients without a rebate and this is often a more expensive option.
  1. Rosen R, Stewart T. Results of a 10-year follow-up study of botulinum toxin A therapy for primary axillary hyperhidrosis in Australia. Intern Med J; 48;343-347.

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What Now with Vaginal Mesh for Prolapse?

Based on an interview with Melbourne urologist, Dr Caroline Dowling conducted in March, 2018 Australia was the first country to ban vaginal mesh products used surgically via transvaginal implantation for the treatment of pelvic organ prolapse. Australia was also a leader in evaluating the complications of these implant, through large scale research.1 On November 28th 2017, the Therapeutic Goods Administration withdrew implants for use in prolapse, stating it “was of the belief that the benefits of using transvaginal mesh products in the treatment of pelvic organ prolapse do not outweigh the risks these products pose to patients”. There are unique risks related to mesh use. These include mesh erosion (up to 14% of cases)1, vaginal and groin pain (up to 3% to 4%)1 and mesh exposure. These complications may be more common and more severe (requiring surgery) if the mesh is used for prolapse repair, as opposed to the treatment of stress incontinence. Reports of complications associated with transvaginal mesh products began over a decade, with the Food and Drug Administration issuing an alert about their use back in 2008. Repeated warnings were then given. In 2013, legal action began in Australia with 300 women registering for a national class action against Johnson & Johnson Medical Australia. So what do GPs tell their patients who have a vaginal mesh in situ, and what alternative managements are there for vaginal prolapse and stress incontinence? Patients who feel they have complications should be reviewed by the surgeon who operated on them, but it worth noting that most women have had no problems with these products and so, in the absence of symptoms may be reassured that they need no further management. “Women who have no problems from their transvaginal mesh implants should be reassured that they do not require them to be removed,” says Melbourne urologist Dr Caroline Dowling There is not an inherent risk with mesh as an implant, it is used widely in general surgery for inguinal hernia and abdominal wound repair. Nonetheless, it would be wise to explain the possible side-effects of the vaginal mesh in case these occur in the future. Alternatives to the vaginal mesh implant are the traditional vaginal prolapse repair using native tissue, and these are effective procedures for most women seeking surgical treatment of their prolapse. There are several alternatives to mesh for the treatment of stress incontinence that has failed conservative therapy, including an autologous fascial sling, bulking agents and Burch colposuspension. In 2015, the Cochrane Incontinence Group concluded that mid-urethral slings were highly effective in the short-term and medium-term and had a good safety profile. The mid-urethral sling remains available in its retropubic and transobturator form, but patients can no longer access mini-slings or single incision slings outside trial settings. This may change once the results of longer term studies become available. Single incisions may have a more favourable side-effect profile than full-length slings. More conservative management includes pelvic floor exercises and silicon pessaries inserted for prolapse and stress incontinence treatment. Pelvic floor exercises may be difficult to do effectively and repeatedly for many women, especially over time. They may also be less effective in cases of significant cystocoele. Silicon pessaries are particularly useful in women who are symptomatic but wish to have further pregnancies, in women who do not want surgery, in the elderly and for those in poor health.3 Patients may need help with the insertion and correct placement, but pessaries work well and may be an underutilised option.
  1. A/Prof. Christopher Maher, Explaining the Vaginal Mesh Controversy. Royal Brisbane and Women's and Wesley Hospitals Brisbane, The University of Queensland. June 17th
https://medicine.uq.edu.au/article/2017/06/explaining-vaginal-mesh-controversy
  1. Ford et al. Mid-urethral sling operations for stress urinary incontinence in women. Cochrane Incontinence Group, July 2015.
http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD006375.pub3/abstract
  1. Jones, K. Harmanli, O. Pessary Use in Pelvic Organ Prolapse and Urinary Incontinence. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876320

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Managing Sexual Dysfunction in Depression

Based on an interview with Dr Jon-Paul Khoo, psychiatrist, co-owner and director at the Toowong Specialist Clinic, Brisbane held at the Annual Women and Children’s Health Update, Melbourne, March 2018 Modern antidepressant medication is efficacious and effective for sufferers of major depressive disorder. However, residual symptoms, even in those who appear to be in remission, are common and can contribute to ongoing distress. Sexual dysfunction is one particularly relevant example. Up to a quarter of the general population report this, and the rate increases to about half of those who are depressed but not on treatment. Sexual dysfunction may affect up to 80% of treated depressed people and is affected by their background, the depression itself and the treatment. Even when mood recovery occurs, sexual dysfunction can persist. As GPs are the main prescribers of antidepressants in Australia, before choosing a medication, they need to feel informed and comfortable when discussing the impact of depression and its treatment on all aspects of functioning, specifically sexual functioning. Following a complete assessment, the GP may feel that antidepressant medication is indicated. This would be an opportune time to ask about current sexual function. It is likely to be a more comfortable discussion if the patient and doctor are already acquainted, but even if this is not the case, it a straight-forward approach with some advance warning about the need for personal questions often helps. “We have to introduce the topic of sexual dysfunction as very few patients will spontaneously bring up this topic”, says psychiatrist Dr Jon-Paul Khoo. Sexual behaviour in humans is complex, individual and highly personal. Nothing should be assumed about the patient’s sexual habits. It may be necessary to discuss relationship problems, at-risk behaviour, sociocultural issues and medical conditions affecting sexual function. It should also be discussed with patients that many people in the general population who are not depressed have sexual dysfunction. Given this, the usual sexual dysfunction associated with antidepressant use in women is lack of desire and difficulty achieving orgasm. The usual sexual dysfunction associated with antidepressant use in men is lack of desire, erectile dysfunction and delayed or absent ejaculation. The impact of these side-effects may be more severe for men than for women (although sexual side-effects occur more commonly in women). People who have less supportive relationships, those in the older age groups, those with medical conditions and those with sexual problems prior to the depression, or because of it, are most likely to be adversely affected sexually by antidepressant medication. On the positive side, antidepressants may be beneficial in patients who have premature ejaculation. Furthermore, judicious decision-making about antidepressant type may allow those with pre-existing impotence, pain disorders and sexual dysfunction due to other causes to undertake effective treatment without a worsening of sexual dysfunction We are familiar with efficacy data and the overall clinical utility of antidepressant medications, but we are less well-educated regarding the adverse sexual effects of treatment. Although there are minimal efficacy differences between antidepressant therapies in the treatment of major depressive disorder, there are distinct tolerability differences. The propensity for causing sexual dysfunction varies both between and within antidepressant subtypes. A brief summary of antidepressant-induced sexual dysfunction is that approximately 80% of people taking (most types of) selective serotonin reuptake inhibitors (SSRI) or venlafaxine, a serotonin noradrenaline reuptake inhibitor (SNRI), will report some sort of adverse sexual effect. A more moderate risk of sexual dysfunction occurs with imipramine, as well as escitalopram and fluvoxamine (both SSRIs) and duloxetine (an SNRI). The lowest rates of sexual dysfunction (placebo-equivalent rates) in controlled studies are reported with agomelatine, moclobemide, mirtazapine (though sedation may affect desire) and vortioxitine (on pooled analysis). In comparison, atypical antipsychotics have a higher rates of sexual dysfunction than antidepressant therapies, probably related to their propensity to elevate prolactin. It is wise to exclude or manage drug and alcohol issues, and to discuss with the patient the adverse effect of these regarding both the remission of depression and adequate sexual functioning. Patients at high risk of, or who already have, pre-existing sexual dysfunction should be commenced on a low-risk antidepressant when clinically reasonable. If a higher risk medication is working well for mood stability, the patient may decide not to change treatments. Commonly cited strategies of waiting for sexual dysfunction to improve with time, or scheduling sexual activity against dosing, have limited benefit for the majority of patients. Similarly, dose reduction and ‘drug holidays’ are not generally effective. The most gain in arresting sexual dysfunction occurs with changing the antidepressant to a lower risk alternative. Augmenting the antidepressant therapy with an intervention that might improve any induced sexual dysfunction is probably the next best option. For women, this might include exercise 30 minutes prior to sexual activity, as may increasing the frequency of sexual activity. For men, the best augmentation strategy appears to be prostaglandin E inhibitors. There are data for both sildenafil and tadalafil, both of which are indicated in men who have sexual dysfunction. Finally, it is also suggested that involving the partner, where appropriate, may help reduce stigma and increase support and understanding for patients affected by sexual dysfunction.

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Can My Genes Be Making Me Overweight?

Based on an interview with endocrinologist and obesity expert, Professor Joseph Proietto at the Annual Women and Children’s Health Update, Melbourne, March 2018 There are many reasons proposed for our society becoming more overweight than ever before. The commonest explanation is that people are overeating because they have more refined, energy dense foods easily available and requiring little physical effort to access. The other consideration is that people are not moving and exercising as much, due to increased sedentary employment and entertainments that are clearly less effort. Once people become overweight, they feel less like exercising and so the situation worsens. Unfortunately, in our society, food (including alcohol), socialising and entertainment are all strongly associated. Food is easily obtained and is abundant in variety and quantity. Previous generations ate less because of cost, availability and the fact that food generally plainer and perhaps less tasty. This was especially true for the poorer in society, who also tended to have more physically demanding jobs, with less time and money to spend on eating during the day. On a scientific level, genetics and epigenetics are now known to play an important role in the development of obesity. In particular, there are many genes currently being researched in relation to appetite and obesity including leptin (a hormone made mostly by adipose cells that inhibits hunger) and its receptor, and the melanocortin 4 receptor. "For obvious evolutionary reasons, there are no genes (yet) identified that reduce metabolic rate," said Professor Joseph Proietto. So far, all genes that have been found to be associated with obesity have been linked to increased hunger. There are no genes known that reduce metabolism. It is interesting that force-feeding increases energy expenditure while weight loss reduces energy expenditure and, in both cases, it is spontaneous activity that changes, with only minor alteration in basal metabolic rate. This has been demonstrated in overfeeding experiments. Some causes of obesity may be epigenetic. For example, some women who gain excess weight during pregnancy find it more difficult to lose after the pregnancy. This is likely to be due to epigenetic change in the expression of genes connected with obesity. Unfortunately, the offspring of mothers who become overweight before or during pregnancy are likely to inherit these genes, and hence themselves have trouble with weight gain. Certain medical conditions (hypothyroidism, Cushing's syndrome) may induce modest weight gain, but the extreme numbers of people in our society with serious weight problems mean that endocrinological causes are very much in the minority. Hence, we need to look for other causes for obesity in the modern age. One of the biggest problems with healthy lifestyle programmes and extensive community information about diet, weight and exercise in our society is that genetics trump willpower in many cases, especially over the long-term. Following weight loss there are hormonal changes that lead to increased hunger (leptin levels fall and ghrelin levels increase) and in 2011 these changes were shown to be long lasting, so the weight-reduced individual has to fight increased hunger. Given the prolific amount of available food, temptation adds to the problem. In effect, one is then fighting nature.

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An Update in Heart Failure

How easy is it to say HFpEF and HFrEF?   The answer is… not very easy! However, heart failure has a new classification based on ejection fraction that doctors will need to know about. HFpEF stands for “heart failure with preserved ejection fraction.” This preserved ejection fraction is defined as greater than or equal to 50%. HFrEF stands for “heart failure with reduced ejection fraction.” This is the “classic” form of heart failure that doctors are familiar with. The ejection fraction in HRrEF is defined as less than or equal to 50%. Patients who have clinical signs of heart failure and a normal ejection fraction used to be diagnosed with diastolic heart failure.  They are now said, under the new classification, to have HFpEF. It should be noted that a patient may have diastolic dysfunction typically reported on echo, however if they do not have any clinical signs of heart failure they do NOT have HFpEF. In this situation, the diastolic dysfunction refers to the cardiac echo finding of impaired diastolic relaxation. This may be an age-related change or due to left ventricular hypertrophy, both of which may occur without necessarily causing symptoms and signs of heart failure. There is an additional group that some researchers refer to, and that is HFmEF, which stands for “heart failure with mid-range ejection fraction”. HFmEF is defined as an ejection fraction of between 40% and 50%. There is debate about the utility of the additional sub-classification of HFmEF. Most clinicians would consider HFmEF as simply mild HFrEF. Most agree that HFmEF simply identifies as subgroup of HFrEF for which there are fewer clinical trials or evidence for effective therapy, and so this highlights areas for future investigation and research. The utility of this new classification, particularly HFrEF versus HFpEF, is mainly to distinguish different pathophysiological processes, cardiac mechanics and treatment options. Presently, it is only HFrEF for which there exists medications that reduce mortality and improve survival. Additionally, device therapies such as implantable cardioverter defibrillators and biventricular pacemakers (now more commonly referred to as “cardiac resynchronisation therapies”) have only demonstrated benefit in HFrEF. For HFpEF, there are no medications or devices that have been shown to reduce mortality and improve survival. Typically, symptoms are managed with diuretic therapy. There is evidence to support a benefit from spironolactone, however the most recent trial (TOPCAT)1 failed to demonstrate a mortality benefit and it was plagued with disparities regarding the nature of recruitment in one of the large regions participating. Certainly, from a treatment viewpoint, the underlying causes contributing to HFpEF can often be managed. These typically include hypertension, diabetes, obesity and coronary artery disease. Not surprisingly, there are studies to show that patients with HFpEF do benefit from exercise, and from maintaining a healthy weight. But how best do we explain these definitions to the patient sitting in front of us? 'It can be very helpful to clarify the term [heart failure] and to explain that their heart has neither “failed”, nor has it “stopped working”, but that “it is just not working as well as normal”, said cardiologist, Dr Hendrik Zimmet. HFrEF can be explained as “the heart muscle not pumping as well as usual”. HFpEF can be explained as “the heart muscle being stiffer than usual, and not relaxing as well”. But no matter how the problem is explained to the patient, it is important to stress, as positively as possible, what can be done to help.
  1. Pfeffer, Marc et al. Regional Variation in Patients and Outcomes in the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) Trial
Circulation. 2014; CIRCULATIONAHA.114.013255 Originally published November 18, 2014 https://doi.org/10.1161/CIRCULATIONAHA.114.013255 Based on an interview with cardiologist, Dr Hendrik Zimmet at the Annual Women and Children’s Health Update, Melbourne, March 2018

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There is no perfect contraception…

Let us imagine that there has been a significant side-effect from a contraceptive choice occurs and a patient suffers harm. It is a known but very rare side-effect. How much legal and ethical responsibility lies with the doctor who prescribes the contraceptive, how much lies with the medical experts advocating this form of contraception as reasonable and safe, and how much lies with the pharmaceutical company who researched this product? Should this contraceptive be withdrawn from use, and if so, why would it be still available and advised for use in other countries around the world? A reasonable response to this question would include an assessment of the incidence of this particular complication among all users of this contraceptive, the incidence of any other significant complications, and the outcome for the patients of these complications. However, let us imagine the media finds this story and runs with it, giving widespread coverage of this single case and highlighting the contraceptive as the cause. This is the situation at present with the progestogen IUD, Mirena® in the United States. It is also the case with oral contraceptive pills that contain cyproterone acetate (such as Diane-35®) in Australia. Contraceptive pills like Diane-35® are more oestrogenic in their balance and this could potentially increase their risk of venous-thromboembolism (VTE), although this still remains somewhat controversial. It was temporarily banned in France because of this in 2013. However, the risks need to be put in perspective. Even if the worst case-scenario is accepted, the actual increased risk of VTE for these newer pills over older types is an extra four to six VTEs per 10,000 Pill users per year.1 “The risk of death from a VTE induced by a combined oral contraceptive is approximately one in 100,000, significantly less than the risk during pregnancy,” said Dr Foran. It is known that oral contraceptive pills containing 35ug ethinyl oestradiol and cyproterone acetate are being prescribed in Australia for indications beyond contraception, namely androgenising signs in women.  It is also known, that for some women these pills provide the best control of their symptoms. In Europe, the regulatory authorities decided that the benefits outweighed the rare risks for properly selected patients and this OCP was quickly reintroduced to the market after only six months. However, in Australia there have recently been calls for the banning or restriction of this product in Australia following the diagnosis of a VTE in a young woman. How reasonable is it in our society to allow the traumatic stories of individuals to override medical opinion and determine regulation? The public needs to be made to realise that not only are these products very safe for the overwhelming majority of women, when prescribed appropriately, but they are also so much safer for women than an unplanned pregnancy would be. It might be valid to argue that there are other combined oral contraceptives that are ‘safer’ than those containing 35ug ethinyl oestradiol and cyproterone acetate, or that cyproterone acetate is available separately for use. However, what happens when one of these other oral contraceptive choices causes a major medical event in a different woman? In the UK, doctors have been advised to warn patients that there is an increased risk of VTE with Femodene®, Marvelon® and Yasmin® named as some examples. The Daily Mail UK1 had a massive heading to this effect: “Deadly risk of pill used by one million women: Every GP in Britain told to warn about threat from popular contraceptive” If media and legal pressure is allowed to result in the withdrawal of these medications, at some stage, there will be no oral contraceptive choices left. The seriousness of the situation is highlighted in the case of the Mirena® IUD, since there is no similar alternative to this product in Australia. In the United States, this contraceptive device has been under a cloud of bad publicity since 2009, due to US Food and Drug Administration warnings relating to migration and perforation. Since then, the Mirena® IUD has been scrutinised by patients with side-effects and, of course, lawyers. “The real question here is whether hysterectomy or endometrial ablation is a safer option than the Mirena® IUD for women with heavy menstrual bleeding.” Dr Foran. The maintenance of a range of choices is important and women should have the right to make these decisions for themselves in consultation with their doctors. The Mirena IUD is also a safe form of contraception, especially for women who have thrombophilias and for older premenopausal women, most of whose other choices are less safe. Is it still enough for doctors to fully inform women of the side-effects and complications of their contraceptive options and to let them decide, or is modern contraception becoming a very personal, public and legal battlefield, the main casualties of this being expert medical advice and a woman’s choice?  …and in the end, who is left holding the baby?  
  1. Bitzer J et al. Statement on combined hormonal contraceptives containing third- or fourth-generation progestogens or cyproterone acetate and the associated risk of thromboembolism. J Fam Plann Reprod Health Care. doi: 10. 1136/ jfprhc-2013-100624 http://srh.bmj.com/content/familyplanning/early/2013/04/10/jfprhc-2013-100624.full.pdf
  2. Daily Mail, UK, 22nd Feb 2018 http://www.dailymail.co.uk/news/article-2550216/Deadly-risk-pill-used-1m-women-Every-GP-Britain-told-warn-threat-popular-contraceptive.html
  This article is based on an interview with Dr Terri Foran, Sexual Health Physician, Lecturer with the UNSW’s School of Women’s and Children’s Health and Director of Master Women’s Health Medicine on Saturday 17th February 2018 at the Annual Women’s and Children’s Health Update, Sydney

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New privacy laws affect all GPs

From February this year, changes to privacy laws have been put in place that are likely to significantly affect doctors and their practice. Many doctors will not be aware of their new obligations leaving them vulnerable to inadvertently breaching the Privacy Amendment Act, 2017. “Ignorance is no excuse as a legal argument,” Dr Peter Walker, GP and senior risk manager at Avant explained. This latest amendment to the privacy laws demands that doctors must have an updated protocol on how breaches of a patient’s privacy should be handled. Both the patient and the relevant authority must be notified if a breach occurs that is thought to potentially cause the patient harm. If something goes wrong and the patient’s privacy is breached, doctors must now conduct a risk assessment, including an assessment of the risk of harm resulting from the breach. If harm is possible (physical, emotional, psychological, financial, or harm to reputation), the doctor is then obliged to alert the patient/s concerned and write a statement for the Office of the Australian Information Commission via their online form. Fines may be incurred if the action to reduce the risk of possible breaches has not been made, or if it is insufficient, especially if serious harm results. Fines are also possible for doctors who fail to comply with the amended Privacy Act (for example, if they do not notify the Australian Information Commission of a breach or if they do not have an updated privacy plan). The obligation to notify a patient of a privacy breach does enable that patient to take further action if they perceive they have been harmed. They may then escalate the issue themselves, perhaps in Court. In serious circumstances, the Commission will also refer to other entities, such as the Australian Health Practitioner Regulation Agency or if the matter is criminal, to the Police. If no harm is likely to result, doctors do not have to notify the patient or the Commission, but this is likely to be difficult for a clinician to assess without legal advice. “Prevention really is better than cure, but many doctors are unaware of this new legislation.” Dr Walker said. The following examples are given to illustrate to GPs considerations about privacy in the light of the amended Act. “Sorry, Mr B, I need your consent before I fax that referral letter to the specialist for you because this is not a form of communication that is absolutely safe regarding your privacy. For example, a wrong number may be typed in by accident or the specialist may not receive the fax. For your interest, the fax has a hard drive that will store information and so for this reason we remove this before we dispose of the fax machine. If any of this is of concern to you regarding your privacy you can pass the letter over yourself on the day of your consultation…” “Sorry, Mr B, we don’t email information either to you or the specialist, as email may be hacked; this is less likely to happen to medical email systems, but it is still possible and our practice policy has decided not to use email…” “Mr B, I can text the information from the referral letter to the specialist’s mobile phone with your permission to do so. However, please understand that someone who is holding his phone for him may see the message. This is quite possible, as he is operating now…” “Sorry, Mr B, I understand your concern about needing an urgent appointment, and that the post is slow and the referral may not get to the specialist in time, but this is considered to be a legally safe way of sending correspondence if you don’t take the referral with you now. I know the specialist wants to see the referral before offering you an urgent appointment …” Other possible scenarios in which privacy breaches may occur include the theft of documents (e.g. laptop, briefcase), conversations about a patient’s condition being overheard where the patient can be identified, the incorrect disposal of paperwork that identifies a patient, and discussions about a patient with a third party (who is not part of the health team managing them) without that patient’s consent. The Privacy Amendment Act 2017 builds upon the Privacy Act, amended in March 2014, that instructed all medical practices to have a Privacy Policy. The Australian Information Commission is able to audit any medical practice regarding this to see if that practice complies. This legislation is aimed at promoting the security of a patient’s personal details in all communications between themselves and health professionals, and among health professionals generally. To this end, doctors will need to look carefully for any potential breaches of these new privacy laws resulting from their current means of communication with colleagues and the patients themselves. Reference Office of the Australian Information Commissioner. Notifiable Data Breaches. Available at: oaic.gov.au/engage-with-us/consultations/notifiable-data-breaches This article is based on Dr Peter Walker’s video interview conducted at the Sydney Women’s and Children’s Health Update on Saturday February 17th 2018.

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New privacy laws affect all GPs

From February this year, changes to privacy laws have been put in place that are likely to significantly affect doctors and their practice. Many doctors will not be aware of their new obligations leaving them vulnerable to inadvertently breaching the Privacy Amendment Act, 2017. “Ignorance is no excuse as a legal argument,” Dr Peter Walker, GP and senior risk manager at Avant explained. This latest amendment to the privacy laws demands that doctors must have an updated protocol on how breaches of a patient’s privacy should be handled. Both the patient and the relevant authority must be notified if a breach occurs that is thought to potentially cause the patient harm. If something goes wrong and the patient’s privacy is breached, doctors must now conduct a risk assessment, including an assessment of the risk of harm resulting from the breach. If harm is possible (physical, emotional, psychological, financial, or harm to reputation), the doctor is then obliged to alert the patient/s concerned and write a statement for the Office of the Australian Information Commission via their online form. Fines may be incurred if the action to reduce the risk of possible breaches has not been made, or if it is insufficient, especially if serious harm results. Fines are also possible for doctors who fail to comply with the amended Privacy Act (for example, if they do not notify the Australian Information Commission of a breach or if they do not have an updated privacy plan). The obligation to notify a patient of a privacy breach does enable that patient to take further action if they perceive they have been harmed. They may then escalate the issue themselves, perhaps in Court. In serious circumstances, the Commission will also refer to other entities, such as the Australian Health Practitioner Regulation Agency or if the matter is criminal, to the Police. If no harm is likely to result, doctors do not have to notify the patient or the Commission, but this is likely to be difficult for a clinician to assess without legal advice. “Prevention really is better than cure, but many doctors are unaware of this new legislation.” Dr Walker said. The following examples are given to illustrate to GPs considerations about privacy in the light of the amended Act. “Sorry, Mr B, I need your consent before I fax that referral letter to the specialist for you because this is not a form of communication that is absolutely safe regarding your privacy. For example, a wrong number may be typed in by accident or the specialist may not receive the fax. For your interest, the fax has a hard drive that will store information and so for this reason we remove this before we dispose of the fax machine. If any of this is of concern to you regarding your privacy you can pass the letter over yourself on the day of your consultation…” “Sorry, Mr B, we don’t email information either to you or the specialist, as email may be hacked; this is less likely to happen to medical email systems, but it is still possible and our practice policy has decided not to use email…” “Mr B, I can text the information from the referral letter to the specialist’s mobile phone with your permission to do so. However, please understand that someone who is holding his phone for him may see the message. This is quite possible, as he is operating now…” “Sorry, Mr B, I understand your concern about needing an urgent appointment, and that the post is slow and the referral may not get to the specialist in time, but this is considered to be a legally safe way of sending correspondence if you don’t take the referral with you now. I know the specialist wants to see the referral before offering you an urgent appointment …” Other possible scenarios in which privacy breaches may occur include the theft of documents (e.g. laptop, briefcase), conversations about a patient’s condition being overheard where the patient can be identified, the incorrect disposal of paperwork that identifies a patient, and discussions about a patient with a third party (who is not part of the health team managing them) without that patient’s consent. The Privacy Amendment Act 2017 builds upon the Privacy Act, amended in March 2014, that instructed all medical practices to have a Privacy Policy. The Australian Information Commission is able to audit any medical practice regarding this to see if that practice complies. This legislation is aimed at promoting the security of a patient’s personal details in all communications between themselves and health professionals, and among health professionals generally. To this end, doctors will need to look carefully for any potential breaches of these new privacy laws resulting from their current means of communication with colleagues and the patients themselves. Reference Office of the Australian Information Commissioner. Notifiable Data Breaches. Available at: oaic.gov.au/engage-with-us/consultations/notifiable-data-breaches This article is based on Dr Peter Walker’s video interview conducted at the Sydney Women’s and Children’s Health Update on Saturday February 17th 2018.

By Dr Vivienne Miller
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There is no perfect contraception…

Let us imagine that there has been a significant side-effect from a contraceptive choice occurs and a patient suffers harm. It is a known but very rare side-effect. How much legal and ethical responsibility lies with the doctor who prescribes the contraceptive, how much lies with the medical experts advocating this form of contraception as reasonable and safe, and how much lies with the pharmaceutical company who researched this product? Should this contraceptive be withdrawn from use, and if so, why would it be still available and advised for use in other countries around the world? A reasonable response to this question would include an assessment of the incidence of this particular complication among all users of this contraceptive, the incidence of any other significant complications, and the outcome for the patients of these complications. However, let us imagine the media finds this story and runs with it, giving widespread coverage of this single case and highlighting the contraceptive as the cause. This is the situation at present with the progestogen IUD, Mirena® in the United States. It is also the case with oral contraceptive pills that contain cyproterone acetate (such as Diane-35®) in Australia. Contraceptive pills like Diane-35® are more oestrogenic in their balance and this could potentially increase their risk of venous-thromboembolism (VTE), although this still remains somewhat controversial. It was temporarily banned in France because of this in 2013. However, the risks need to be put in perspective. Even if the worst case-scenario is accepted, the actual increased risk of VTE for these newer pills over older types is an extra four to six VTEs per 10,000 Pill users per year.1 “The risk of death from a VTE induced by a combined oral contraceptive is approximately one in 100,000, significantly less than the risk during pregnancy,” said Dr Foran. It is known that oral contraceptive pills containing 35ug ethinyl oestradiol and cyproterone acetate are being prescribed in Australia for indications beyond contraception, namely androgenising signs in women.  It is also known, that for some women these pills provide the best control of their symptoms. In Europe, the regulatory authorities decided that the benefits outweighed the rare risks for properly selected patients and this OCP was quickly reintroduced to the market after only six months. However, in Australia there have recently been calls for the banning or restriction of this product in Australia following the diagnosis of a VTE in a young woman. How reasonable is it in our society to allow the traumatic stories of individuals to override medical opinion and determine regulation? The public needs to be made to realise that not only are these products very safe for the overwhelming majority of women, when prescribed appropriately, but they are also so much safer for women than an unplanned pregnancy would be. It might be valid to argue that there are other combined oral contraceptives that are ‘safer’ than those containing 35ug ethinyl oestradiol and cyproterone acetate, or that cyproterone acetate is available separately for use. However, what happens when one of these other oral contraceptive choices causes a major medical event in a different woman? In the UK, doctors have been advised to warn patients that there is an increased risk of VTE with Femodene®, Marvelon® and Yasmin® named as some examples. The Daily Mail UK1 had a massive heading to this effect: “Deadly risk of pill used by one million women: Every GP in Britain told to warn about threat from popular contraceptive” If media and legal pressure is allowed to result in the withdrawal of these medications, at some stage, there will be no oral contraceptive choices left. The seriousness of the situation is highlighted in the case of the Mirena® IUD, since there is no similar alternative to this product in Australia. In the United States, this contraceptive device has been under a cloud of bad publicity since 2009, due to US Food and Drug Administration warnings relating to migration and perforation. Since then, the Mirena® IUD has been scrutinised by patients with side-effects and, of course, lawyers. “The real question here is whether hysterectomy or endometrial ablation is a safer option than the Mirena® IUD for women with heavy menstrual bleeding.” Dr Foran. The maintenance of a range of choices is important and women should have the right to make these decisions for themselves in consultation with their doctors. The Mirena IUD is also a safe form of contraception, especially for women who have thrombophilias and for older premenopausal women, most of whose other choices are less safe. Is it still enough for doctors to fully inform women of the side-effects and complications of their contraceptive options and to let them decide, or is modern contraception becoming a very personal, public and legal battlefield, the main casualties of this being expert medical advice and a woman’s choice?  …and in the end, who is left holding the baby?  
  1. Bitzer J et al. Statement on combined hormonal contraceptives containing third- or fourth-generation progestogens or cyproterone acetate and the associated risk of thromboembolism. J Fam Plann Reprod Health Care. doi: 10. 1136/ jfprhc-2013-100624 http://srh.bmj.com/content/familyplanning/early/2013/04/10/jfprhc-2013-100624.full.pdf
  2. Daily Mail, UK, 22nd Feb 2018 http://www.dailymail.co.uk/news/article-2550216/Deadly-risk-pill-used-1m-women-Every-GP-Britain-told-warn-threat-popular-contraceptive.html
  This article is based on an interview with Dr Terri Foran, Sexual Health Physician, Lecturer with the UNSW’s School of Women’s and Children’s Health and Director of Master Women’s Health Medicine on Saturday 17th February 2018 at the Annual Women’s and Children’s Health Update, Sydney

By Dr Vivienne Miller
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An Update in Heart Failure

How easy is it to say HFpEF and HFrEF?   The answer is… not very easy! However, heart failure has a new classification based on ejection fraction that doctors will need to know about. HFpEF stands for “heart failure with preserved ejection fraction.” This preserved ejection fraction is defined as greater than or equal to 50%. HFrEF stands for “heart failure with reduced ejection fraction.” This is the “classic” form of heart failure that doctors are familiar with. The ejection fraction in HRrEF is defined as less than or equal to 50%. Patients who have clinical signs of heart failure and a normal ejection fraction used to be diagnosed with diastolic heart failure.  They are now said, under the new classification, to have HFpEF. It should be noted that a patient may have diastolic dysfunction typically reported on echo, however if they do not have any clinical signs of heart failure they do NOT have HFpEF. In this situation, the diastolic dysfunction refers to the cardiac echo finding of impaired diastolic relaxation. This may be an age-related change or due to left ventricular hypertrophy, both of which may occur without necessarily causing symptoms and signs of heart failure. There is an additional group that some researchers refer to, and that is HFmEF, which stands for “heart failure with mid-range ejection fraction”. HFmEF is defined as an ejection fraction of between 40% and 50%. There is debate about the utility of the additional sub-classification of HFmEF. Most clinicians would consider HFmEF as simply mild HFrEF. Most agree that HFmEF simply identifies as subgroup of HFrEF for which there are fewer clinical trials or evidence for effective therapy, and so this highlights areas for future investigation and research. The utility of this new classification, particularly HFrEF versus HFpEF, is mainly to distinguish different pathophysiological processes, cardiac mechanics and treatment options. Presently, it is only HFrEF for which there exists medications that reduce mortality and improve survival. Additionally, device therapies such as implantable cardioverter defibrillators and biventricular pacemakers (now more commonly referred to as “cardiac resynchronisation therapies”) have only demonstrated benefit in HFrEF. For HFpEF, there are no medications or devices that have been shown to reduce mortality and improve survival. Typically, symptoms are managed with diuretic therapy. There is evidence to support a benefit from spironolactone, however the most recent trial (TOPCAT)1 failed to demonstrate a mortality benefit and it was plagued with disparities regarding the nature of recruitment in one of the large regions participating. Certainly, from a treatment viewpoint, the underlying causes contributing to HFpEF can often be managed. These typically include hypertension, diabetes, obesity and coronary artery disease. Not surprisingly, there are studies to show that patients with HFpEF do benefit from exercise, and from maintaining a healthy weight. But how best do we explain these definitions to the patient sitting in front of us? 'It can be very helpful to clarify the term [heart failure] and to explain that their heart has neither “failed”, nor has it “stopped working”, but that “it is just not working as well as normal”, said cardiologist, Dr Hendrik Zimmet. HFrEF can be explained as “the heart muscle not pumping as well as usual”. HFpEF can be explained as “the heart muscle being stiffer than usual, and not relaxing as well”. But no matter how the problem is explained to the patient, it is important to stress, as positively as possible, what can be done to help.
  1. Pfeffer, Marc et al. Regional Variation in Patients and Outcomes in the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) Trial
Circulation. 2014; CIRCULATIONAHA.114.013255 Originally published November 18, 2014 https://doi.org/10.1161/CIRCULATIONAHA.114.013255 Based on an interview with cardiologist, Dr Hendrik Zimmet at the Annual Women and Children’s Health Update, Melbourne, March 2018

By Dr Vivienne Miller
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Can My Genes Be Making Me Overweight?

Based on an interview with endocrinologist and obesity expert, Professor Joseph Proietto at the Annual Women and Children’s Health Update, Melbourne, March 2018 There are many reasons proposed for our society becoming more overweight than ever before. The commonest explanation is that people are overeating because they have more refined, energy dense foods easily available and requiring little physical effort to access. The other consideration is that people are not moving and exercising as much, due to increased sedentary employment and entertainments that are clearly less effort. Once people become overweight, they feel less like exercising and so the situation worsens. Unfortunately, in our society, food (including alcohol), socialising and entertainment are all strongly associated. Food is easily obtained and is abundant in variety and quantity. Previous generations ate less because of cost, availability and the fact that food generally plainer and perhaps less tasty. This was especially true for the poorer in society, who also tended to have more physically demanding jobs, with less time and money to spend on eating during the day. On a scientific level, genetics and epigenetics are now known to play an important role in the development of obesity. In particular, there are many genes currently being researched in relation to appetite and obesity including leptin (a hormone made mostly by adipose cells that inhibits hunger) and its receptor, and the melanocortin 4 receptor. "For obvious evolutionary reasons, there are no genes (yet) identified that reduce metabolic rate," said Professor Joseph Proietto. So far, all genes that have been found to be associated with obesity have been linked to increased hunger. There are no genes known that reduce metabolism. It is interesting that force-feeding increases energy expenditure while weight loss reduces energy expenditure and, in both cases, it is spontaneous activity that changes, with only minor alteration in basal metabolic rate. This has been demonstrated in overfeeding experiments. Some causes of obesity may be epigenetic. For example, some women who gain excess weight during pregnancy find it more difficult to lose after the pregnancy. This is likely to be due to epigenetic change in the expression of genes connected with obesity. Unfortunately, the offspring of mothers who become overweight before or during pregnancy are likely to inherit these genes, and hence themselves have trouble with weight gain. Certain medical conditions (hypothyroidism, Cushing's syndrome) may induce modest weight gain, but the extreme numbers of people in our society with serious weight problems mean that endocrinological causes are very much in the minority. Hence, we need to look for other causes for obesity in the modern age. One of the biggest problems with healthy lifestyle programmes and extensive community information about diet, weight and exercise in our society is that genetics trump willpower in many cases, especially over the long-term. Following weight loss there are hormonal changes that lead to increased hunger (leptin levels fall and ghrelin levels increase) and in 2011 these changes were shown to be long lasting, so the weight-reduced individual has to fight increased hunger. Given the prolific amount of available food, temptation adds to the problem. In effect, one is then fighting nature.

By Dr Vivienne Miller
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Managing Sexual Dysfunction in Depression

Based on an interview with Dr Jon-Paul Khoo, psychiatrist, co-owner and director at the Toowong Specialist Clinic, Brisbane held at the Annual Women and Children’s Health Update, Melbourne, March 2018 Modern antidepressant medication is efficacious and effective for sufferers of major depressive disorder. However, residual symptoms, even in those who appear to be in remission, are common and can contribute to ongoing distress. Sexual dysfunction is one particularly relevant example. Up to a quarter of the general population report this, and the rate increases to about half of those who are depressed but not on treatment. Sexual dysfunction may affect up to 80% of treated depressed people and is affected by their background, the depression itself and the treatment. Even when mood recovery occurs, sexual dysfunction can persist. As GPs are the main prescribers of antidepressants in Australia, before choosing a medication, they need to feel informed and comfortable when discussing the impact of depression and its treatment on all aspects of functioning, specifically sexual functioning. Following a complete assessment, the GP may feel that antidepressant medication is indicated. This would be an opportune time to ask about current sexual function. It is likely to be a more comfortable discussion if the patient and doctor are already acquainted, but even if this is not the case, it a straight-forward approach with some advance warning about the need for personal questions often helps. “We have to introduce the topic of sexual dysfunction as very few patients will spontaneously bring up this topic”, says psychiatrist Dr Jon-Paul Khoo. Sexual behaviour in humans is complex, individual and highly personal. Nothing should be assumed about the patient’s sexual habits. It may be necessary to discuss relationship problems, at-risk behaviour, sociocultural issues and medical conditions affecting sexual function. It should also be discussed with patients that many people in the general population who are not depressed have sexual dysfunction. Given this, the usual sexual dysfunction associated with antidepressant use in women is lack of desire and difficulty achieving orgasm. The usual sexual dysfunction associated with antidepressant use in men is lack of desire, erectile dysfunction and delayed or absent ejaculation. The impact of these side-effects may be more severe for men than for women (although sexual side-effects occur more commonly in women). People who have less supportive relationships, those in the older age groups, those with medical conditions and those with sexual problems prior to the depression, or because of it, are most likely to be adversely affected sexually by antidepressant medication. On the positive side, antidepressants may be beneficial in patients who have premature ejaculation. Furthermore, judicious decision-making about antidepressant type may allow those with pre-existing impotence, pain disorders and sexual dysfunction due to other causes to undertake effective treatment without a worsening of sexual dysfunction We are familiar with efficacy data and the overall clinical utility of antidepressant medications, but we are less well-educated regarding the adverse sexual effects of treatment. Although there are minimal efficacy differences between antidepressant therapies in the treatment of major depressive disorder, there are distinct tolerability differences. The propensity for causing sexual dysfunction varies both between and within antidepressant subtypes. A brief summary of antidepressant-induced sexual dysfunction is that approximately 80% of people taking (most types of) selective serotonin reuptake inhibitors (SSRI) or venlafaxine, a serotonin noradrenaline reuptake inhibitor (SNRI), will report some sort of adverse sexual effect. A more moderate risk of sexual dysfunction occurs with imipramine, as well as escitalopram and fluvoxamine (both SSRIs) and duloxetine (an SNRI). The lowest rates of sexual dysfunction (placebo-equivalent rates) in controlled studies are reported with agomelatine, moclobemide, mirtazapine (though sedation may affect desire) and vortioxitine (on pooled analysis). In comparison, atypical antipsychotics have a higher rates of sexual dysfunction than antidepressant therapies, probably related to their propensity to elevate prolactin. It is wise to exclude or manage drug and alcohol issues, and to discuss with the patient the adverse effect of these regarding both the remission of depression and adequate sexual functioning. Patients at high risk of, or who already have, pre-existing sexual dysfunction should be commenced on a low-risk antidepressant when clinically reasonable. If a higher risk medication is working well for mood stability, the patient may decide not to change treatments. Commonly cited strategies of waiting for sexual dysfunction to improve with time, or scheduling sexual activity against dosing, have limited benefit for the majority of patients. Similarly, dose reduction and ‘drug holidays’ are not generally effective. The most gain in arresting sexual dysfunction occurs with changing the antidepressant to a lower risk alternative. Augmenting the antidepressant therapy with an intervention that might improve any induced sexual dysfunction is probably the next best option. For women, this might include exercise 30 minutes prior to sexual activity, as may increasing the frequency of sexual activity. For men, the best augmentation strategy appears to be prostaglandin E inhibitors. There are data for both sildenafil and tadalafil, both of which are indicated in men who have sexual dysfunction. Finally, it is also suggested that involving the partner, where appropriate, may help reduce stigma and increase support and understanding for patients affected by sexual dysfunction.

By Dr Vivienne Miller
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What Now with Vaginal Mesh for Prolapse?

Based on an interview with Melbourne urologist, Dr Caroline Dowling conducted in March, 2018 Australia was the first country to ban vaginal mesh products used surgically via transvaginal implantation for the treatment of pelvic organ prolapse. Australia was also a leader in evaluating the complications of these implant, through large scale research.1 On November 28th 2017, the Therapeutic Goods Administration withdrew implants for use in prolapse, stating it “was of the belief that the benefits of using transvaginal mesh products in the treatment of pelvic organ prolapse do not outweigh the risks these products pose to patients”. There are unique risks related to mesh use. These include mesh erosion (up to 14% of cases)1, vaginal and groin pain (up to 3% to 4%)1 and mesh exposure. These complications may be more common and more severe (requiring surgery) if the mesh is used for prolapse repair, as opposed to the treatment of stress incontinence. Reports of complications associated with transvaginal mesh products began over a decade, with the Food and Drug Administration issuing an alert about their use back in 2008. Repeated warnings were then given. In 2013, legal action began in Australia with 300 women registering for a national class action against Johnson & Johnson Medical Australia. So what do GPs tell their patients who have a vaginal mesh in situ, and what alternative managements are there for vaginal prolapse and stress incontinence? Patients who feel they have complications should be reviewed by the surgeon who operated on them, but it worth noting that most women have had no problems with these products and so, in the absence of symptoms may be reassured that they need no further management. “Women who have no problems from their transvaginal mesh implants should be reassured that they do not require them to be removed,” says Melbourne urologist Dr Caroline Dowling There is not an inherent risk with mesh as an implant, it is used widely in general surgery for inguinal hernia and abdominal wound repair. Nonetheless, it would be wise to explain the possible side-effects of the vaginal mesh in case these occur in the future. Alternatives to the vaginal mesh implant are the traditional vaginal prolapse repair using native tissue, and these are effective procedures for most women seeking surgical treatment of their prolapse. There are several alternatives to mesh for the treatment of stress incontinence that has failed conservative therapy, including an autologous fascial sling, bulking agents and Burch colposuspension. In 2015, the Cochrane Incontinence Group concluded that mid-urethral slings were highly effective in the short-term and medium-term and had a good safety profile. The mid-urethral sling remains available in its retropubic and transobturator form, but patients can no longer access mini-slings or single incision slings outside trial settings. This may change once the results of longer term studies become available. Single incisions may have a more favourable side-effect profile than full-length slings. More conservative management includes pelvic floor exercises and silicon pessaries inserted for prolapse and stress incontinence treatment. Pelvic floor exercises may be difficult to do effectively and repeatedly for many women, especially over time. They may also be less effective in cases of significant cystocoele. Silicon pessaries are particularly useful in women who are symptomatic but wish to have further pregnancies, in women who do not want surgery, in the elderly and for those in poor health.3 Patients may need help with the insertion and correct placement, but pessaries work well and may be an underutilised option.
  1. A/Prof. Christopher Maher, Explaining the Vaginal Mesh Controversy. Royal Brisbane and Women's and Wesley Hospitals Brisbane, The University of Queensland. June 17th
https://medicine.uq.edu.au/article/2017/06/explaining-vaginal-mesh-controversy
  1. Ford et al. Mid-urethral sling operations for stress urinary incontinence in women. Cochrane Incontinence Group, July 2015.
http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD006375.pub3/abstract
  1. Jones, K. Harmanli, O. Pessary Use in Pelvic Organ Prolapse and Urinary Incontinence. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876320

By Dr Vivienne Miller
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1 in 3 young adults is lonely – and it affects their mental health

Managing Hyperhidrosis

Based on an interview with Sydney dermatologist, Dr Rob Rosen conducted at the Annual Women’s and Children’s Health Update, Sydney in February 2018. Hyperhidrosis is a very distressing condition that equally affects both men and women, across all ethnicities.  It occurs in approximately 3% of the general population and the onset is in childhood or adolescence. However, only about one third of people affected seek medical advice. In addition to the physical effects, the psychological impact on affected individuals is significant. Embarrassment, anxiety and depression are very commonly associated with this condition. In primary hyperhidrosis, the sweat glands are normal but there is an apparently exaggerated sympathetic response. The sweat glands most susceptible to these sympathetic cholinergic effects are the eccrine glands found in the palms, soles and axillae. Primary, focal hyperhidrosis tends to be bilateral and symmetrical, occurring at least once a week. It usually commences before a person reaches their mid-twenties and is often familial.  In its typical form, and if there is nothing to suggest a secondary cause, it requires no investigations. Secondary hyperhidrosis is typically generalised, affecting the entire surface of the skin. By definition, it has an underlying cause, such as infection, endocrine disturbance, neuropathy, malignancy, menopause, drug withdrawal or the side-effect of medications.  A full history, examination and targeted investigations are required before this condition can be called idiopathic. “It is important to make the distinction between “generalised” and “focal” hyperhidrosis at the outset,” says Sydney dermatologist, Dr Rob Rosen The management of hyperhidrosis begins conservatively. By the time they present to a doctor they usually have already tried a range of antiperspirants.  Aluminium hydroxide 20%, topically, daily for four weeks should be trialled before further treatment is considered. Many patients develop localised irritation to this treatment, as it obstructs the eccrine ducts, causing their atrophy. The most effective management is Botulinum A toxin injections. This drug blocks the release of acetylcholine from presynaptic nerve terminals, thus inhibiting the stimulation of the eccrine sweat gland. The injections are done intradermally and retreatment is needed approximately every six months. Over time, this duration between treatments may become longer. Side effects include discomfort at the injection site and, less commonly, weakness of local muscles (especially relating to small muscles in the hand, for example, in palmer hyperhidrosis). In the research done by Dr Rosen t al, over 90% of patients were happy with this therapy.1 Oral anticholinergics such as oxybutynin (5mg to 15mg daily) or glycopyrrolate (1mg to 4mg daily) may be used and are most effective in refractory cases of generalised sweating. The anticholinergic side effects (urinary retention, dry mouth, constipation) tend to be a limiting factor in their use. Other treatments for hyperhidrosis tend to be either less effective or more invasive. For patients over 12 years old, there is a Medicare rebate for Botulinum A injection therapy for severe primary axillary hyperhidrosis, if aluminium hydroxide has failed and if it is administered by a dermatologist, neurologist or paediatrician. Some cosmetic clinics treat patients without a rebate and this is often a more expensive option.
  1. Rosen R, Stewart T. Results of a 10-year follow-up study of botulinum toxin A therapy for primary axillary hyperhidrosis in Australia. Intern Med J; 48;343-347.

By Dr Vivienne Miller
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Managing Heavy Menstrual Bleeding in General Practice

Based on an interview with Associate Professor Kirsten Black and Clinical Associate Professor Deborah Bateson conducted at the Annual Women’s and Children’s Health Update, Sydney in February 2018. "Heavy menstrual bleeding" is the new term for menorrhagia. This under-treated condition is easy to screen for in general practice. And screening for it is important as, apart from the discomfort, inconvenience, disturbed sleep, embarrassment and expense heavy menstrual bleeding causes, it is a major cause of iron deficiency in women. Common causes of heavy menstrual bleeding include hormonal variations relating to menarche and menopause, polycystic ovarian syndrome, polyps, fibroids and coagulation disorders. Identifying heavy menstrual bleeding initially involves discussing menstrual patterns with patients, as the diagnosis relies on the subjective experience of the woman as it affects her physical, emotional, social and/or material quality of life. Women may be unsure whether their periods are abnormally heavy compared with other women.  Questions that may assist in the diagnosis of  heavy menstrual bleeding include asking whether a woman needs to wear both a pad and a tampon simultaneously to prevent leakage, whether she has to use super pads and/or tampons and needs to change them every three hours or less, , whether she is concerned about flooding or staining during the day and avoids social activities as a result, whether she regularly takes time off work at the time of her period, whether she has to get up several times overnight to change her pad or tampon, whether she frequently passes clots (often this is associated with significant period pain), and finally, how the issue is affecting her quality of life. It is also important to inquire about associated symptoms such as pain, bloating and feelings of pressure on the bladder or bowel.Investigations usually include iron studies, a full blood count and a pelvic ultrasound. Ideally the ultrasound should be transvaginal as well as transabdominal. Also, ideally the ultrasound should be conducted between days five to 10 of the menstrual cycle, as this is when the uterine lining is less echogenic and scanning at this time reduces the chance of missing lesions such as polyps, within the uterine cavity. It should be noted that heavy menstrual bleeding may be a symptom of malignancy, especially in women over the age of 45 years. Other more specialised tests may also be indicated, such as coagulation studies, if there is suggestion of a bleeding diathesis. Once malignancy has been excluded as a cause of the bleeding, management usually includes hormonal control of the ovulation cycle, such as with the combined oral contraceptives. These reduce bleeding by 30%. An excellent alternative is the hormonal intrauterine system (Mirena®). If the woman prefers not to use such methods and is not at risk of pregnancy, tranexamic acid or norethisterone, 5mg three times daily, from days five to 26 of the menstrual cycle, can be used. NSAIDS such as mefenamic acid are most effective if commenced just prior to the onset of bleeding and continued into the first few days. Surgical management of heavy menstrual bleeding is usually indicated for women who have completed their families. The less invasive options include endometrial ablation and embolisation of fibroids. Hysterectomy is generally reserved for women in whom less invasive treatments have been unsuccessful, where there is a particular indication (such as large fibroids causing pressure symptoms) or less commonly, at the woman’s request.

By Dr Vivienne Miller
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Assessing stroke risk – easier than saying “CHA2DS2-VA Score”!

General Practitioner Dr Vivienne Miller takes a look at what’s changed in the recently updated CHA2DS2-VASC Score for the determination of stroke risk factors from atrial fibrillation. The CHA2DS2-VA Score was updated from the CHA2DS2-VASC Score last year to exclude female sex (represented by Sc) in the determination of stroke risk factors from atrial fibrillation. The two scores are identical, apart from the exclusion of female sex, which is no longer considered an outright risk factor in stroke from atrial fibrillation, but more of a ‘risk modifier’ of this complication.1General Practitioner Dr Vivienne Miller takes a look at what’s changed in the recently updated CHA2DS2-VASC Score for the determination of stroke risk factors from atrial fibrillation. The CHA2DS2-VA Score was updated from the CHA2DS2-VASC Score last year to exclude female sex (represented by Sc) in the determination of stroke risk factors from atrial fibrillation. The two scores are identical, apart from the exclusion of female sex, which is no longer considered an outright risk factor in stroke from atrial fibrillation, but more of a ‘risk modifier’ of this complication.

By Dr Vivienne Miller
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