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Read the latest articles relevant to your clinical practice, including exclusive insights from Healthed surveys and polls.

By reading selected clinical articles, you earn CPD in the Educational Activities (EA) category whenever you click the “Claim CPD” button and follow the prompts. 

The dementia ‘tsunami’ is coming – but two potential medications offer hope
Dr Linda Calabresi
  • Clinical Articles

Predicting and Preventing Dementia

Adolescent boys who struggle to understand how basic machines work and young girls who have difficulty remembering words are at increased risk of developing dementia when they’re older, new research has found. According to the longitudinal study published in The Journal of the American Medical Association, lower mechanical reasoning in adolescence in boys was associated with a 17% higher risk of having dementia when they were 70. With girls it was a lower memory for words in adolescence that increased the odds of developing the degenerative disease. It has been known for some time that the smarter you are throughout life, even as a child the less likely it is that you will develop dementia. Not a guarantee of protection – just a general trend. It has to do with cognitive reserve, the US researchers explain. “Based on the cognitive reserve hypothesis, high levels of cognitive functioning and reserve accumulated throughout the life course may protect against brain pathology and clinical manifestations of dementia,” they wrote. This theory has been supported by a number of studies such as the Scottish Mental Health Survey that showed that lower mental ability at age 11 increased the risk of dementia down the track. But what had been less well-defined was whether there were any particular aspects of intelligence in young people that were better predictors (or protectors) of dementia than others. This study goes some way to addressing this. Researchers were able to link sociobehavioural data collected from high school children back in 1960 with Medicare claims data over 50 years later that identified those people who had been diagnosed with Alzheimer's disease and related disorders. Interestingly, poor adolescent performance in other areas of intelligence such as mathematics and visualisation were also associated with dementia but not nearly to the extent of mechanical reasoning and word memory. So why is this so? The study authors say there are a few possible explanations. Maybe the poor performance in adolescence reflected poor brain development earlier in life, a risk factor for dementia. Or maybe these adolescents are more susceptible to neuropathology as they get older? Or maybe they are the adolescents who adopt poor health behaviours such as smoking and little exercise? “Regardless of mechanism, our findings emphasise that early-life risk stretches across the life course,” they said. And what can be done about it? That’s the million-dollar question. The researchers say the hope is if we know the at-risk group we can get aggressive with preventive management early. “Efforts to promote cognitive reserve-building experiences and positive health behaviours throughout the life course may prevent or delay clinical symptoms of Alzheimer's disease and related disorder.” An accompanying editorial takes this concept a little further. Dr Tom Russ, a Scottish psychiatrist says interventional research has identified a number of factors that can potentially influence cognitive reserve. These include modifiable health factors, education, social support, positive affect, stimulating activities and/or novel experiences, and cognitive training. As Dr Russ says, you can’t necessarily change all of these risk factors, and even the ones you can change may become less modifiable later in life. But as this study demonstrates, you may be able to work on a person’s cognitive reserve at different stages throughout their life to ultimately lower their risk of dementia.   Reference
  1. Huang AR, Strombotne KL, Horner EM, Lapham SJ, Adolescent Cognitive Aptitudes and Later-in-Life Alzheimer Disease and Related Disorders. JAMA Network Open [Internet]. 2018 Sep; 1(5): e181726. Available from: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2701735 doi:10.1001/jamanetworkopen.2018.1726.
  2. Russ TC, Intelligence, Cognitive Reserve, and Dementia: Time for Intervention? JAMA Network Open [Internet]. 2018 Sep; 1(5): e181724. Available from: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2701735 doi:10.1001/jamanetworkopen.2018.1724.

By Dr Linda Calabresi
vcacinations in pregnancy
Dr James Harraway
  • Clinical Articles

Fetal Fraction – The Essential Factor in Non-Invasive Prenatal Testing

Non-Invasive Prenatal Testing (NIPT), the cell-free DNA-based blood test that screens for fetal chromosomal abnormalities, is fast becoming a routine part of obstetric care. NIPT at a glance During pregnancy, maternal plasma contains fragments of DNA from the mother and from the placenta (fetal DNA). The proportion of DNA fragments from particular chromosomes is usually very stable throughout pregnancy. If there is an excess of fetal fragments from one chromosome, the proportion of fragments from that chromosome will be changed. Inconclusive tests A key reason that NIPTs should precisely measures the amount of fetal DNA in the sample – the fetal fraction – is if there is insufficient fetal DNA, the result may merely reflect the genetic status of the mother. NIPT assays should report a result only if there is sufficient fetal DNA to be confident of accuracy. Rarely, a test for trisomy 21,18 and 13 cannot be reported. This occurs in 3% of women tested by Sonic Genetics and is usually because there is insufficient fetal DNA compared with maternal DNA in the mother’s plasma. This low fetal fraction can be due to a relative excess of maternal DNA and this can vary over time. It is more common in women with increased body weight, and more likely in the presence of infection and inflammation, or after exercise. It also occurs if the mother or fetus has some subtle benign variations in chromosome structure (copy number variants) that make estimating the proportion of fragments from a chromosome unreliable. In some instances, the DNA in the sample has degraded during collection and shipping to the laboratory, and the quality is insufficient for a reliable result. These factors interfere with quality control of the test. Two thirds of women will get a result on re-testing. However, if the second test is inconclusive, it should not be repeated. This occurs in 1% of pregnant women screened. It is also not worth using another form of non-invasive prenatal test. Other tests do not estimate the fetal fraction accurately and may provide false reassurance. A decision about other test modalities (combined first trimester screen, second trimester serum screen, detailed ultrasonography or invasive genetic testing such as CVS/amniocentesis) should be based on assessment of all identified risk factors and may require specialist consultation. More rarely (in 0.5 –1% of women) the test reports a result for trisomy 21, 18 and 13 but not for fetal gender and sex chromosome abnormalities. It is unlikely that a repeat test will provide a result. A decision about using fetal ultrasound or invasive genetic testing to document fetal gender should be based on assessment of need and any identified risk factors.   General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

By Dr James Harraway, Sullivan Nicolaides Pathology
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Dr Linda Calabresi
  • Clinical Articles

New Medicare-Funded BRCA Testing – Use With Caution

GPs may have to correct some patients’ misunderstanding following reports in the general media suggesting that testing for high risk cancer genes was now available to everyone free of charge. Writing in the latest issue of the MJA, Australian genetics experts say that testing for specific high- risk genetic mutations, especially BRCA1 and BRCA2 has been available to appropriate patients free of charge (but not Medicare-rebated) by genetic specialists in public clinics for over 20 years. What’s new is that these tests now attract a Medicare rebate and you don’t have to be a genetic specialist to order them, but they are still only available to selected patients. “Testing is appropriate when there is at least a 10% chance of identifying a gene mutation responsible for the personal or family history of cancer,” the authors of the article wrote. There are a number of algorithms available to help clinicians calculate whether the likelihood of having one of these cancer-causing genetic mutations is at least 10%. Usually testing is initially considered for patients who have been diagnosed with either breast or ovarian cancer, and because of their young age and/or their strong family history are considered at high possibility of having a genetic mutation that explains their condition. The new item numbers (73295,73296 and 73297) cover testing for heritable germline mutations in seven genes including BRCA1 and BRCA2. If such a mutation is found, then at risk adult relatives will be justified in also accessing testing. However, as the article authors point out there are limitations with this type of genetic testing. Firstly most breast and ovarian cancers occur in people without an identifiable underlying genetic variant. “Only 5% of female breast cancers, 15% of invasive epithelial ovarian cancers and up to 14% of male breast cancers are related to BRCA1 or BRCA2 mutations, thus, most patients with breast cancer do not need, nor will they benefit from, a genetic test,” they said. That’s not to say the absence of BRCA1 or BRCA2, or one of the other rarer high-risk mutations currently tested for, excludes the possibility that the patient has inherited a predisposition to the cancer. Families that appear to have a high prevalence of these types of cancer may indeed have an inherited genetic mutation, it is just that because of limitations of technology and knowledge it is yet to be isolated. What’s more, the sensitivity of the current testing methods, means that a number of incidental genetic mutations may be noted, but the significance of these is as yet unknown. It is critical that when testing is requested for a relative of an affected patient, the laboratory is informed of the exact genetic variation found in the original affected patient, to ensure pathologists distinguish between the disease-causing mutation and variants of undetermined significance. The authors also suggest confining testing to only the most likely variant/s rather than requesting testing for mutations in multiple genes. “[T]he testing of multiple genes may uncover unclassified variants, variants outside the usual clinical context, variants unrelated to the current cancer, or unexpected important variants for which the patient has not been well prepared,” they said. They also suggest education and counselling be given to patients considering this genetic testing, and written consent obtained. The new Medicare item numbers represent a major step forward in terms of genetic and genomic testing becoming mainstream, but, as the current incorrect media headlines demonstrate, this transition is going to require information and education. Clinicians who order these tests are likely to benefit from establishing close ties with genetic services and specialists to ensure best and appropriate practice in this ever-expanding area of medicine. Ref: Med J Aust 2018; 209 (5): 193-196. || doi: 10.5694/mja17.01124

By Dr Linda Calabresi
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Healthed
  • Clinical Articles

Health Check: How Long are You Contagious with Gastro?

There’s no way you’d want to go to work when you’ve got the telltale signs of gastro: nausea, abdominal cramps, vomiting and diarrhoea. But what about when you’re feeling a bit better? When is it safe to be around colleagues, or send your kids to school or daycare? The health department recommends staying home from work or school for a minimum of 24 hours after you last vomited or had diarrhoea. But the question of how long someone is contagious after recovering from gastro is a very different question.   What causes gastro? To better understand how long you can be contagious with gastro, we need to look at the various causes. Viruses are the most common causes of gastro. Rotavirus is the leading cause in infants and young children, whereas norovirus is the leading cause of gastro in adults. There are around 1.8 million cases of norovirus infection in Australia each year. This accounts for almost 40% of the total cases of gastro. Bacterial gastroenteritis is also common and accounts for around 1.6 million cases a year. Of those cases, 1.1 million come from E. coli infections. Other bacteria that commonly cause gastro include salmonella, shigella and campylobacter. These bacteria are often found in raw or undercooked meat, seafood, and unpasteurised milk. Parasites such as giardia lamblia, entamoeba histolytica and cryptosporidium account for around 700,000 cases of gastro per year. Most of the time people recover from parasitic gastroenteritis without incident, but it can cause problems for people with weaker immune systems. Read more: Health Check: I feel a bit sick, should I stay home or go to work?   Identifying the bug Most cases of diarrhoea are mild, and resolve themselves with no need for medical attention. But some warrant further investigation, particularly among returned travellers, people who have had diarrhoea for four or five days (or more than one day with a fever), patients with bloody stools, those who have recently used antibiotics, and patients whose immune systems are compromised. The most common test is the stool culture which is used to identify microbes grown from loose or unformed stools. The bacterial yield of stool cultures is generally low. But if it does come back with a positive result, it can be potentially important for the patient. Some organisms that are isolated in stool cultures are notifiable to public health authorities. This is because of their potential to cause serious harm in vulnerable groups such as the elderly, young children, pregnant women and those with weakened immune systems. The health department must be notified of gastro cases caused by campylobacter, cryptosporidium, listeria, salmonella, shigella and certain types of E.coli infection. This can help pinpoint outbreaks when they arise and allow for appropriate control measures.   You might feel better but your poo isn’t Gastro bugs are spread via the the faecal-oral route, which means faeces needs to come into contact with the mouth for transmission to occur. Sometimes this can happen if contaminated faecal material gets into drinking water, or during food preparation. But more commonly, tiny particles of poo might remain on the hands after going to the toilet. Using toilet paper to wipe when you go to the toilet doesn’t completely prevent the contamination of hands, and even more so when the person has diarrhoea. The particles then make their way to another person’s mouth during food preparation or touching a variety of contaminated surfaces and then putting your fingers in your mouth. After completely recovering from the symptoms of gastro, infectious organisms can still be shed into stools. Faecal shedding of campylobacter, the E. coli O157 strain, salmonella, shigella, cryptosporidium, entamoeba, and giardia can last for many days to weeks. In fact, some people who have recovered from salmonella have shed the bacteria into their stools 102 days later. Parasites can remain alive in the bowel for a long period of time after diarrhoea finishes. Infectious cryptosporidium oocysts can be shed into stools for up to 50 days. Giardia oocysts can take even longer to be excreted.   So, how long should you stay away? Much of the current advice on when people can return to work, school or child care after gastro is based on the most common viral gastroenteritis, norovirus, even though few patients will discover the cause of their bug. For norovirus, the highest rate of viral shedding into stools occurs 24 to 48 hours after all symptoms have stopped. The viral shedding rate then starts to quickly decrease. So people can return to work 48 hours after symptoms have stopped. Yes, viral shedding into stools can occur for longer than 48 hours. But because norovirus infection is so common and recovery is rapid, it’s not considered practical to demand patients’ stools be clear of the virus before returning to work. While 24 hours may be appropriate for many people, a specific 48-hour exclusion rule is considered necessary for those in a higher-risk category for spreading gastro to others. These include food handlers, health care workers and children under the age of five at child care or play group. If you have a positive stool culture for a notifiable organism, that may change the situation. Food handlers, childcare workers and health-care workers affected by verotoxin E.coli, for example, are not permitted to work until symptoms have stopped and two consecutive faecal specimens taken at least 24 hours apart have tested negative for verotoxin E. coli. This may lead to a lengthy exclusion period from work, possibly several days.   How to stop the spread Diligently washing your hands often with soap and water is the most effective way to stop the spread of these gastro bugs to others. Consider this: when 10,000 giardia cysts were placed in the palm of a hand, handwashing with soap eliminated 99% of them. To prevent others from becoming sick, disinfect contaminated surfaces thoroughly immediately after someone vomits or has diarrhoea. While wearing disposable gloves, wash surfaces with hot water and a neutral detergent, then use household bleach containing 0.1% hypochlorite solution as a disinfectant.

By Healthed
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Dr Linda Calabresi
  • Clinical Articles

Inpatient Rehab After Knee Surgery – a Rort?

Why are Australians having rehabilitation as an inpatient after their total knee replacements rather than as an outpatient at a rate higher than any other country in the world? And why are our rates of inpatient rehabilitation as opposed to community or home-based rehab increasing? That’s what researchers were investigating in a study just published in the MJA. Could it be inpatient rehab was associated with better health outcomes for the patient than the other options? Or were patients too complex, lived too far away or needed greater supervision to allow them to have their rehab off-site? As it turns out, the reason inpatient rehabilitation rates are increasing has much more to do with private hospitals being able to access funding than any patient factors. According to the study authors, more than 50,000 total knee replacement operations were performed in Australia in 2016, about 70% of which took place in a private hospital. In that year, 2016, 45% of patients underwent inpatient rehabilitation following surgery. This represents a substantial increase from the 31% who had the same inpatient service back in 2009. This bucks an international trend. “Inpatient rehabilitation rates in the United States decreased from a peak of 35% in 2003 to 11% in 2009, with a mean rate during 2009-2014 of 15%,” the researchers said. Randomised controlled trials have failed to show the functional improvements achieved through inpatient rehabilitation are superior to those achieved with home- or community-based rehabilitation. However, the cost was significantly more. A recent analysis including almost 260 privately insured patients at 12 Australian hospitals put the cost differential at an average of $9500. And even though the mean age for patients undergoing inpatient rehab was slightly higher than for those who did not (71.0 vs 67.3 years), and they were more likely to have comorbidities and live alone, the study authors said the differences didn’t explain the wide variation in admission rates from hospital to hospital. “Patients in hospitals with high rates of inpatient rehabilitation were similar to those in hospitals with low rates, eliminating patient complexity as the reason,” they said. It seems the greatest determinant of whether a person had inpatient rehabilitation was the hospital in which the total knee replacement took place. “This factor was substantially more important than the clinical profile of the patient,” the study authors said. They suggested some private hospitals were encouraging inpatient rehabilitation because they were able to access funding on a per day basis for the rehab, in addition to the payment received for the knee surgery. The study authors concede it is an attractive business model, but while these hospitals may be offering excellent rehab in terms of services and facilities, it all comes at a cost ‘that, for many patients, is not justified by better outcomes.’ They suggest the proportion of patients receiving inpatient rehabilitation after a total knee replacement could be reduced, improving health care efficiency without harming health outcomes. “Reducing low value care will require system-level changes to guidelines and incentives for hospitals, as hospital-related factors are the major driver of variation in inpatient rehabilitation practices,” they concluded.   Reference: Schilling C, Keating C, Barker A, Wilson SF, Petrie D,  Predictors of inpatient rehabilitation after total knee replacement: an analysis of private hospital claims data. Med J Aust. 2018 August 27. 209(5): 222-7. Available from: https://www.mja.com.au/journal/2018/209/5/predictors-inpatient-rehabilitation-after-total-knee-replacement-analysis doi:10.5694/mja17.01231  

By Dr Linda Calabresi
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Dr Jenny Robson
  • Clinical Articles

Detecting and treating Mycoplasma genitalium

Mycoplasma genitalium (M. genitalium), is thought to affect up to 400,000 Australians. It causes urethritis in men, and in women it can lead to pelvic inflammatory disease, cervicitis and preterm labour. It is also a recognised cause of anorectal proctitis along with other infections including Chlamydia trachomatis (including the LGV strains), gonorrhoea, syphilis, HSV and shigellosis. Asymptomatic infection is also common. Who to test Only test those with symptoms and their contacts. Screening asymptomatic people for M. genitalium is not currently recommended. Diagnosis Females: PCR on endocervical or vaginal swab, first pass urine (FPU), ThinPrep -collected by cervical brush/swab. Males: PCR on urethral swab (in preference to FPU), anorectal swabs. Throat swabs are not recommended as pharyngeal infection is uncommon. Transport: Ambient temperature; if there is any delay from collection to transport to the laboratory, the sample must be refrigerated Current treatment recommendations Preliminary data from the patient populations suggests resistance rates to macrolides may be as high as 64 per cent. The highest rates are likely to be in the men who have sex with men (MSM) population. Although information regarding fluoroquinolone resistance (moxifloxacin) is not available with this test, some studies suggest resistance to fluoroquinolones is present in 10–15% of infections. Doxycycline alone is ineffective in two-thirds of infections but will lower bacterial load in most cases, increasing the likelihood of cure with a subsequent antibiotic. Pretreating M. genitalium infections with doxycycline for one week and then treating susceptible infections with azithromycin and macrolide-resistant infections with a fluoroquinolone eradicates >90% of infections. Current treatment regimens Macrolide sensitive Doxycycline 100mg bd for seven days followed by azithromycin 1g stat then 500mg daily for three days (total 2.5g) OR Doxycycline 100mg bd for seven days followed by azithromycin 1g single dose. It is not known to what extent the improved outcomes resulting from the use of doxycycline followed by 2.5g azithromycin are due to this dose of azithromycin, rather than simply the pre-treatment with doxycycline. The higher dose of azithromycin requires a private prescription. Macrolide resistant Doxycycline 100mg bd for seven days followed by moxifloxacin 400mg daily for seven days. A longer course of moxifloxacin may be required in women with pelvic inflammatory disease. Moxifloxacin requires a private prescription, cannot be used in pregnancy and is expensive. It is associated with diarrhoea, occasional tendinopathy and rare neurological and cardiac events. Treatment failures following appropriate fluoroquinolone treatment may require specialist advice. Additional actions Advise no sex without condoms until tested for cure (14 days after completion of treatment). Advise no sex with untested previous sexual partners. Test of cure Test of cure by PCR should be done at least two weeks after treatment is completed i.e. four weeks after commencing therapy. Contact tracing In heterosexuals, the risk of PID and reproductive complications suggests a greater need to trace, test and treat infected contacts. The time period for contact tracing is unknown. Asymptomatic infection and macrolide resistance are more common in MSM and there is only limited evidence that this is harmful. As moxifloxacin will probably be required for treatment, contact tracing may be best confined to continuing partners of a symptomatic person.   References: Australian STI Management Guidelines for Use in Primary Care http://www.sti.guidelines.org.au/sexually-transmissible-infections/mycoplasma-genitalium#management Australian Contact Tracing Manual contacttracing.ashm.org.au/conditions/when-contact-tracing-is-recommended/mycoplasma-genitalium   General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

By Dr Jenny Robson
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Dr Linda Calabresi
  • Clinical Articles

Managing the cardiovascular time bomb in patients on antipsychotics

The physical health of mentally ill patients is a "massive problem and we are doing very badly at it,” psychiatrist Dr Matthew Warden told doctors at a recent Healthed evening seminar in Sydney. In particular, the prevalence of high cardiovascular risk among patients with a history of psychosis, means this population was a "ticking time bomb", said Dr Warden, who is the Director of Acute Inpatient Services for Mental Health at St Vincent’s Hospital in Melbourne. Even without antipsychotic medication, a disproportionate number of people with a history of psychosis are overweight or obese, do very little if any physical exercise and smoke. And it is well-known that the metabolic side-effects associated with antipsychotic medications increases this cardiovascular risk enormously. Consequently, there has been growing pressure on psychiatrists to assess, monitor and manage the physical health of their patients with psychosis, but Dr Warden said, realistically this needs to be also done by GPs as they will usually be managing these patients long-term and "they are better at it.” Baseline metabolic measurements need to be taken at first episode of psychosis, including weight, BMI, BP, lipid levels, fasting blood sugar and smoking status. Weight, in particular needs to be monitored carefully following the commencement of antipsychotic medication, as weight gain is extremely common, especially with olanzapine which, Australia-wide is the most commonly prescribed antipsychotic. In answer to a GP’s question following his talk, Dr Ward said it is extremely difficult to avoid or reverse this medication-induced weight gain with diet and exercise alone. In addition, weight loss pharmacotherapy such as phentermine is contraindicated in people with a history of psychosis. Key to managing the weight gain issue was to choose an antipsychotic with the least long-term side effects from the outset. Olanzapine and clozapine are associated with the greatest weight gain while lurasidone and the partial agonists, aripiprazole and ziprasidone have the least effect on weight. Alternatively, for patients who may have been started on olanzapine or similar, swap to a more weight-neutral medication at the first sign they were gaining weight or developing other metabolic side-effects. It is more likely that a person who as gained weight on olanzapine, will lose that weight if switched to another weight-neutral medication early. The longer that patient stays on olanzapine and the weight gain is sustained, the harder it will be to shift even if the medication is changed, Dr Warden said. In addition to managing weight gain in mentally ill patients, Dr Warden also encouraged GPs to offer smoking cessation advice and help. Even though this population were often considered among the most dependent and heaviest smokers, his own research had found a significant number of patients could successfully quit or at the least cut down given the right advice and assistance. While most smoking cessation pharmacotherapy could be used, Dr Warden suggested that varenicline (Champix) was probably best avoided in these patients. At St Vincent’s Hospital in Melbourne, patients receiving antipsychotic therapy have their metabolic markers assessed at admission and at regular intervals after that, including measuring their serum prolactin. “Hyperprolactinaemia is a significant problem and should be monitored every six months if it is elevated or increasing particularly if there are symptoms then either reduce the dose or change antipsychotic or add in low dose aripiprazole which will lower prolactin levels,” Dr Warden explained.   Dr Matthew Warden spoke on the “Management of Metabolic Dysregulation in Patients on Antipsychotics” at the Healthed, Mental Health in General Practice Evening Seminar held in Sydney in June, 2018.

By Dr Linda Calabresi
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Dr Linda Calabresi
  • Clinical Articles

Fewer Caesars with earlier induction

Among low-risk, nulliparous women, inducing a pregnancy at 39 weeks will not only be at least as safe as letting nature run its course but it will reduce the risk of having a Caesarean, according to US research. According to the randomised trial involving over 6000 women, those who were assigned to ‘expectant management’ ended up having a median gestational age of 40 weeks exactly, not a huge difference from the median gestational age of the induction group which was 39.3 weeks. However, the main aim of the study was to determine if induction at 39 weeks resulted in more adverse perinatal outcomes including conditions such as perinatal death, need for respiratory support, Apgars of less than three at five minutes, intracranial haemorrhage and the like. This potential association has been the concern which has dictated what is currently common obstetric practice. “When gestation is between 39 weeks 0 days and 40 weeks 6 days, common practice has been to avoid elective labour induction because of a lack of evidence of perinatal benefit and concern about a higher frequency of Caesarean delivery and other possible adverse maternal outcomes, particularly among nulliparous women”, the study authors said in the new England Journal of Medicine. What they found in their study however, was that these adverse perinatal outcomes occurred in only 4.3% of the babies born in the induction group and in 5.4% of those born to mothers who went into labour naturally. It appears the relative risk was reduced by 20%. And even though the induction group tended to have longer labours they had quicker recovery times and shorter hospital stays. In terms of maternal outcomes, induction at 39 weeks was associated with a significant reduction in the risk of both Caesarean section and hypertensive disorders of pregnancies. The researchers estimated one Caesarean would be avoided for every 28 low-risk, first-time mothers induced at 39 weeks. The study authors suggest that these findings have the capacity to change practice, or at the very least, provide evidence to relook at current obstetric practice policies. “These results suggest that policies aimed at the avoidance of elective labour induction among low-risk nulliparous women at 39 weeks of gestation are unlikely to reduce the rate of Caesarean delivery on a population level”, they concluded. Ref: NEJM 2018; 379:513-23 DOI: 10.1056/NEJMoa1800566

By Dr Linda Calabresi
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Dr Linda Calabresi
  • Clinical Articles

Pass the salt

Salt may have been unfairly targeted as a killer in the healthy heart stakes, according to newly published research. The observational study of over 90000 people in 300 communities across 18 countries, found that sodium consumption was not associated with an increase in health risks unless the average daily consumption was excessive – more than 5g/day or 2.5 teaspoons of salt. And, this average high daily sodium intake was mostly seen in China, with only about 15% of communities outside of China exceeding this 5g a day limit. As part of this ongoing Prospective Urban Rural Epidemiology (PURE) study, participants aged 35-70 were assessed initially at baseline and then followed for an average of 8.1 years, over which time the occurrence of any major cardiovascular events or death was recorded. What the researchers found was that the risk of hypertension and strokes was only increased in communities where the average daily sodium intake was greater than 5g. Perhaps unexpectedly, this higher sodium intake was actually found to be also associated with lower rates of myocardial infarction and total mortality. Furthermore, the research found that very low levels of sodium intake were harmful, being associated with an increased risk of cardiovascular disease and mortality. The findings fly in the face of the current WHO guidelines that recommend, as a global approach we should be aiming for populations to reduce their sodium intake to below 2g/day. However, no communities in the study came close to achieving this target. In fact, no communities in the study had an average sodium intake of less than 3g/day, based on morning fasting urine samples from the participants. “Sodium intake was associated with cardiovascular disease and strokes only in communities where mean intake was greater than 5g/day. A strategy of sodium reduction in these communities and countries but not in others might be appropriate,” the Canadian study authors said. But before we all go and stock up on our Saxa, an accompanying editorial sounds a word of caution. While acknowledging the findings that ‘normal’ salt intake appeared to be at least health-neutral if not beneficial, the editorial authors remind us that the study is observational and has not taken into consideration a number of potential confounders such as diet. Without taking these confounders into account, one can’t assume that just decreasing salt intake in people at high risk of stroke or increasing it in people at risk of a heart attack will work, they said. “Nevertheless the findings are exceedingly interesting and should be tested in a randomised controlled trial,” they concluded, adding that such a trial, to be conducted in a US federal prison population had been proposed.   Ref: Lancet Vol 392 No 10146 pp:496-506 Vol 392 No 10146 pp: 456-458

By Dr Linda Calabresi
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Dr Jenny Robson
  • Clinical Articles

Typhoid in the modern era

The microbiology laboratory has made great strides in introducing clinically useful diagnostics over the past couple of decades, particularly in recent years with the development of molecular assays that ‘narrow the gap’ and provide early diagnoses. While introducing new tests, it has also been important to evaluate and discard old tests that may not contribute greatly to patient outcomes. One such test that has come under the spotlight is the classic Widal agglutination test in the diagnosis of typhoid. The Widal test, developed by George Fernand Widal in 1896, uses a suspension of killed Salmonella typhi as antigen to detect agglutinating antibodies to somatic O antigens and flagellar H antigens present in serum of typhoid patients. There are many reasons for its lack of clinical utility. Antibodies are not present in the acute illness and take time to develop. Significant cross reactivity can occur with other infectious agents that mimic typhoid including malaria, dengue, endocarditis, tuberculosis and chronic liver disease. Other limitations are of a technical nature and include non-standardisation of the antigen preparation used in the assay, interference with serological responses following typhoid vaccination commonly provided to travellers, and prior exposure and antibodies in patients most susceptible to typhoid, especially those from endemic areas visiting friends and relatives (VFRs). Unless multiple antigens are included, it generally does not detect the other causes of enteric fever, S. Paratyphi A, B and C. It is now time to discontinue this simple agglutination test for typhoid in modern medicine and consider more appropriate diagnostic tests. Typhoid fever Typhoid fever is a life-threatening illness caused by the bacterium Salmonella Typhi. Whereas Salmonellae which cause gastroenteritis are zoonoses, humans are the only reservoir for S.Typhi and S. Paratyphi which cause enteric fever. Typhoid fever is still common in the developing world where it affects about 21.5 million people each year but is much less common in the Lucky Country such as ours where good sanitation prevails. About 100 cases are notified each year in Australia. In 2014, 92% of cases were acquired overseas. India continues to be the most common country of acquisition and in 2014 accounted for more than half of cases. Most transmission occurs through contaminated drinking water or food. Large epidemics are most often related to faecal contamination of water supplies or street-vended foods. A chronic carrier state – excretion of the organism for more than one year – occurs in about 5% of infected persons. Where no travel history is present, the likely source of infection is contaminated food or water from a human carrier akin to ‘Typhoid Mary’. Such an outbreak was reported in Auckland, New Zealand, this year where 20 local cases and one death occurred when a carrier from Samoa helped prepare food at a church community gathering. The incubation period is typically eight to 14 days but may be much longer. Without therapy, the illness may last for three to four weeks and death rates range between 12% and 30%. Increasing resistance to available antimicrobial agents, including fluoroquinolones, has occurred in recent years. Resistance to antimicrobials including amoxycillin, and trimethoprim+sulfamethoxazole has limited the options for treatment; reduced susceptibility to quinolones is common in infections acquired on the Indian subcontinent and in Southeast Asia. While awaiting the results of susceptibility testing, azithromycin or ceftriaxone should be used for initial therapy for infections acquired in these regions. Diagnosis of enteric fevers Two sets of blood cultures are the single most useful diagnostic procedure for diagnosis of enteric fever. Other bodily fluids and tissues may yield positive cultures including faeces, urine, and if seeded, bones and joints, liver and gall bladder. Food handlers, healthcare workers, carers of children, and carers of the elderly, and others who are not able to maintain their own personal hygiene, should further be excluded from working with food or caring for people until two consecutive stool specimens – collected at least 48 hours apart and the first specimen collected not sooner than 48 hours post-cessation of antibiotics – are culture negative. Prevention Both an oral live attenuated multi-dose vaccine and a killed vaccine are available. Booster doses after 3-5 years are generally required if continued exposure occurs. Vaccine efficacy is of the order of only 80%. What to order Blood culture x 2 (Salmonella Typhi and Salmonella Paratyphi) Faeces for Bacterial PCR and MCS; Urine MCS Collection Centres: Faeces and urine samples are accepted at all collection centres. Blood cultures are collected only at designated collection centres. Sample Blood (use blood culture bottles), faeces, urine Transportation Ambient Costs Medicare rebate applies Typhoid Mary Mary Mallon, better known as Typhoid Mary, was an Irish immigrant to New York and the first person in the United States identified as an asymptomatic carrier of the pathogen associated with typhoid fever. Over the course of her career as a cook, she was presumed to have infected 51 people, three of whom died. She was twice forcibly isolated by public health authorities and died after a total of nearly three decades in isolation.   General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

By Dr Jenny Robson
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Dr Linda Calabresi
  • Clinical Articles

LDL – The Lower the Better

Low density lipoprotein cholesterol is the well-known culprit in terms of cardiovascular risk. Courtesy of a large meta-analysis of statin trials done in 2010 (the Cholesterol Treatment Trialists Collaboration), we know that for people starting with higher LDL-C levels (approximately 3.4 mmol/L), they can lower their risk of having a major adverse vascular event by 22%, every time they lower their LDL-C level by 1mmol/L. But what happens once your LDL level is lower? Can you continue to increase your protection by lowering your LDL levels further? Or does the beneficial effect plateau at a certain level? Or, worse still can very low LDL levels actually cause harm? A new meta-analysis just published in JAMA Cardiology has gone some way in answering these questions. The researchers analysed data from the 26 statin studies in the CTTC as well as three large trials of non-statin, cholesterol-lowering therapy looking at those patients who had an LDL-C level of 1.8 mmol/L or less at baseline. They found the cardioprotective benefits continued as LDL-C levels declined to even lower levels. “We found consistent clinical benefit from further LDL-C lowering in patient populations starting as low as a median of 1.6 mmol/L and achieving levels as low as a median of 0.5 mmol/L”. What’s more, the incremental benefit was of an almost identical magnitude to that seen when the LDL-C levels were higher - 21% relative risk reduction per 1-mmol/L reduction in LDL-C through this range. “This relative risk reduction is virtually the same as the 22% reduction seen in the overall CTTC analysis in which the starting LDL-C was nearly twice as high,” they said. And even though very low cholesterol levels have been rumoured to be associated with everything from cancer to dementia, across all these studies there were no offsetting safety concerns with LDL-C lowering, even when extremely low levels were recorded, levels that were lower than those seen in newborns. Given the weight of benefit over risk, the study authors suggest the current targets for LDL-C could be lowered further, to even as low as 0.5 mmol/L to reduce cardiovascular risk. This suggestion is supported by an accompanying editorial, in which the author, Dr Antonio Gotto, a New York cardiologist, predicts the findings will be included as part of the revision of the American Heart Association National Cholesterol guidelines which is currently underway. He said the study findings would provide much needed evidence to help clinicians manage patients with these extremely low achieved cholesterol levels, that until recently have been very rare. “Whether one calls it a target or a threshold, practicing physicians need some guidance as they venture into achieved levels of LDL-C levels that are as foreign as travel to outer space. I have confidence that the new guidelines will be closer to a global positioning system map rather than just a compass and the stars”, he concluded. Ref: JAMA Cardiol. Published online August 1, 2018. doi:10.1001/jamacardio.2018.2258

By Dr Linda Calabresi
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Healthed
  • Clinical Articles

Google predicts when people will die ‘with 95% accuracy’

Google has claimed it can predict with 95% accuracy when people will die using new artificial intelligence technology.

In a paper published in the journal Nature, the company’s Medical Brain team detailed how it is using a new type of artificial intelligence algorithm to make predictions about the likelihood of death among patients in two separate hospitals.

For predicting patient mortality, Google’s Medical Brain was 95% accurate in the first hospital and 93% accurate in the second. It works by analysing patient’s data, such as their age, ethnicity and gender. This information is then joined up with hospital information, like prior diagnoses, current vital signs, and any lab results, reports The Sun. But according to Bloomberg, what impressed medical experts most “was Google’s ability to sift through data previously out of reach: notes buried in PDFs or scribbled on old charts. The neural net gobbled up all this unruly information then spat out predictions. And it did it far faster and more accurately than existing techniques.” It is not the first time Google has made inroads into the medical industry. Its DeepMind subsidiary, considered by some experts to lead the way in AI research, “courted controversy” in 2013 after it was revealed it had access to 1.6 million medical records of NHS patients at three hospitals, reports The Independent.   >> Read More Source: The Week UK

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