A new commentary by infectious disease experts published in Annals of Internal Medicine says that, for patient safety, masking should continue in health care settings. This message, from authors at George Washington University School of Medicine and the National Institutes of Health (NIH), conflicts with a recent commentary from authors from 8 US institutions suggesting that the time for universal masking is over.
Masking has been a controversial mitigation strategy during the COVID pandemic because high-quality evidence of efficacy is lacking and because the topic has become highly politicised. Regardless, real-world experience demonstrates the effectiveness of mask-wearing in clinical settings where data shows that transmission from patient-to-staff and staff-to-patent, when both are masked, is uncommon. Since health care personnel report being driven to show up for work even when they are ill themselves, the argument in support of mask-wearing becomes even more compelling.
Those without symptoms may also transmit respiratory viruses, particularly SARS-CoV-2. While the Omicron strain has been milder, infection could still cause severe or life-threatening disease or prolonged illness if transmitted to at-risk patients, such as the elderly or immunocompromised. With the still-looming risks, now does not seem the time to take off masks in the health care setting. Instead, the authors advocate strongly for continued mask use for infection prevention.
A new study led by Yale School of Medicine scientists and published inBMChas pinpointed why some adults – by some estimates, at least 50% of the population after 75 years of age – develop hearing problems.
While congenital hearing impairment – usually presenting in childhood – result from rare mutations, hearing problems in adults are likely due to the cumulative effect of polygenic risk and environmental factors.
Recent genome-wide association studies have uncovered several risk genes that are implicated in hearing problems in adults, however some factors still have not adequately been investigated by large-scale genetic studies.
For instance, there is limited information about why hearing problems among older adults are more common, more severe, and with earlier onset in men than in women. It is uncertain how hearing-related polygenic risk translates among people of diverse ancestral backgrounds.
While environmental risk factors such as noise exposure and tobacco smoking are known to increase the risk of hearing problems, the molecular mechanisms underlying these associations are unclear.
Researchers sampled nearly 750 000 adults and identified 54 risk variants – including 12 novel variants – that could contribute to hearing problems. They also highlighted how hormonal regulation may play a role in the differences between hearing problems in men and women.
Analysing multiple ancestry groups, the researchers demonstrated that polygenic risk in hearing problems is shared across human populations. They also determined genes involved in brain development interact with sex, noise pollution, and tobacco smoking in relation to their associations with hearing problems.
“Our results support that large-scale genetic studies are useful instruments to understand the biology and the epidemiology of hearing problems in adults,” said Renato Polimanti, PhD, associate professor of psychiatry at Yale School of Medicine and senior author of the study.
Overall, the findings contribute to identifying possible molecular targets for drug development and define novel strategies to identify older adults at risk of losing their hearing.
The study could lead to changes in how older adults with hearing problems are assessed and treated. Hearing loss can impair communications, and that can result in social isolation with major health, psychosocial, and economic consequences, reducing the quality of life of those affected.
In the US, drug approval needs “substantial evidence” of effectiveness – but an investigation by The BMJ into the recent approval of the antibiotic Recarbrio from Merck suggests that these standards are being bypassed.
Recarbrio is a combination therapy made up of a new beta-lactamase inhibitor (relebactam) and a decades old Merck antibiotic (imipenem-cilastatin) to treat complicated infections. It costs $4000–$15 000 for a course, compared with a couple of hundred dollars for the generic version of Merck’s old antibiotic.
Peter Doshi, senior editor at The BMJ, describes how US Food and Drug Administration (FDA) scientists had serious doubts about its highly expensive Recarbrio but the agency approved it anyway.
Did the FDA break its own rules in approving this antibiotic, and what does this case tell us about problems within the agency, he asks?
In its FDA application, Merck submitted results from two clinical trials comparing Recarbrio with imipenem in adults with complicated urinary tract infections and in patients with complex intra-abdominal infections.
But FDA reviewers noted that Merck had studied the wrong patient population to evaluate the added benefits of the new drug, and said the trial for urinary tract infections showed that Recarbrio was as much as 21% less effective than the older, cheaper imipenem.
The FDA concluded that “these studies are not considered adequate and well-controlled.” And of a third clinical study, the FDA called it a “very small,” “difficult to interpret” “descriptive trial with no pre-specified plans for hypothesis testing.”
Yet despite all three clinical studies not providing substantial evidence of effectiveness, FDA approved Recarbrio.
“Instead of basing its decision on the clinical trials in Merck’s application, FDA’s determination of Recarbrio’s efficacy was justified on past evidence that imipenem was effective, plus – to justify the new relebactam component – in vitro (lab) studies and animal models of infection rather than evidence from human trials as required by law,” writes Doshi.
Others are concerned that Recarbrio’s approval essentially amounts to a return to a way of regulating medicines that the FDA abandoned a half century ago prior to the agency’s “substantial evidence” standard.
Doshi explains that, under specific circumstances, the Director of the Center for Drug Evaluation and Research (CDER) can waive in whole or in part the FDA’s “adequate and well-controlled studies” approval criteria. But the FDA told The BMJ ”there was no center director memo in the file” for Recarbrio.
And when The BMJ contacted Janet Woodcock, CDER Director at the time, and now the FDA’s Principal Deputy Commissioner, she said she was not aware that clinical studies showed Recarbrio did not provide substantial evidence of effectiveness.
Woodcock was also unable to confirm that approvals of new drugs require at least one clinical study of the drug itself that demonstrates substantial evidence – evidence lacking in the case of Recarbrio.
A spokesperson for CDER told The BMJ that FDA “applied regulatory flexibility” in approving Recarbrio.
It is unclear whether this regulatory flexibility enabled FDA to conclude Recarbrio had met the legal “substantial evidence” standard without “adequate and well-controlled investigations” of Recarbrio, says Doshi. FDA declined to answer the question, saying “We have no additional information to provide.”
The decline of science at the FDA has become unmanageable, argues David Ross, associate clinical professor of medicine at George Washington University, School of Medicine and Health Sciences, and former FDA medical reviewer, in a linked commentary.
He describes Recarbrio’s approval as “shocking” and says while much of the blame must go to the FDA’s reliance on industry paid user fees for around two-thirds of its annual drugs budget, “the corruption of the FDA’s scientific culture remains the primary culprit driving the deterioration of safety and effectiveness standards.”
To address this “dismal situation” he suggests tapering the FDA’s dependence on user fees and improving public access to the information received by the FDA, its reasoning, and its decisions.
“The Recarbrio approval is a sentinel event, warning of a return to an era when drug effectiveness was an afterthought,” argues Ross. “Although the FDA crowed about this approval, it would have been better advised to remember that “for a successful technology, reality must take precedence over public relations, for nature cannot be fooled,” he concludes.
With the administration of the first COVID vaccines two years ago, public health officials found an increase in cases of myocarditis, particularly among young males who had been vaccinated with mRNA vaccines. The underlying cause of these reactions remained a mystery.
Now Yale scientists have identified the immune signature of these heart inflammation cases. Published in the journal Science Immunology, their findings eliminate some of the theorised causes of the heart inflammation and point to the consequences of a slightly over-stimulated immune system.
Myocarditis is a generally mild inflammation of heart tissue which can cause scarring but is usually resolved within days. The increased incidence of myocarditis during vaccination was seen primarily in males in their teens or early 20s, who had been vaccinated with mRNA vaccines, which are designed to elicit immune responses specifically to the SARS-CoV-2 virus.
According to the Centers for Disease Control and Prevention (CDC), among males aged 12 to 17, about 22 to 36 per 100 000 experienced myocarditis within 21 days after receiving a second vaccine dose. The incidence of myocarditis was 50.1 to 64.9 cases per 100 000 after infection with the COVID virus among males in this age group.
For the new study, the Yale research team conducted a detailed analysis of immune system responses in those rare cases of myocarditis among vaccinated individuals. They found that the heart inflammation was not caused by antibodies created by the vaccine, but rather by a more generalised response involving immune cells and inflammation.
“The immune systems of these individuals get a little too revved up and over-produce cytokine and cellular responses,” said team leader Carrie Lucas, associate professor of immunobiology.
Earlier research had suggested that increasing the time between vaccination shots from four to eight weeks may reduce risk of developing myocarditis.
Lucas noted that, according to CDC findings, the risk of myocarditis is significantly greater in unvaccinated individuals who contract COVID than in the vaccinated. She emphasised that vaccination offers the best protection from COVID-related disease.
“I hope this new knowledge will enable further optimising mRNA vaccines, which, in addition to offering clear health benefits during the pandemic, have a tremendous potential to save lives across numerous future applications,” said Anis Barmada, an MD/PhD student at Yale School of Medicine, who is a co-first author of the paper with Jon Klein, also a Yale MD/PhD student.
Postmenopausal women with atherosclerosis are at higher risk of heart attacks than men of similar age, according to research presented at EACVI 2023, a scientific congress of the European Society of Cardiology (ESC), and published in European Heart Journal – Cardiovascular Imaging. Researchers used imaging techniques to examine the arteries of nearly 25 000 patients and followed them for heart attacks and death.
“The study suggests that a given burden of atherosclerosis is riskier in postmenopausal women than it is in men of that age,” said study author Dr Sophie van Rosendael of Leiden University Medical Centre. “Since atherosclerotic plaque burden is emerging as a target to decide the intensity of therapy to prevent heart attacks, the findings may impact treatment. Our results indicate that after menopause, women may need a higher dose of statins or the addition of another lipid-lowering drug. More studies are needed to confirm these findings.”
While young women do have heart attacks, in general, women develop atherosclerosis (narrowing of arteries due to plaque buildup) later in life than men and have heart attacks at an older age than men, in part because of the protective effect of oestrogen. This study examined whether the prognostic importance of atherosclerotic plaques are the same for women and men at different ages as this could be important for selecting treatments to prevent heart attacks.
The study included 24 950 patients referred for coronary computed tomography angiography (CCTA) and enrolled in the CONFIRM registry, which was conducted in six countries in North America, Europe, and Asia. CCTA is used to obtain 3D images of the arteries in the heart.
Total atherosclerotic burden was rated using the Leiden CCTA score, which incorporates the following items for each coronary segment: plaque presence (yes/no), composition (calcified, noncalcified or mixed), location, and severity of narrowing, for a final value of 0 to 42. Patients were divided into three categories previously found to predict the risk myocardial infarction: low atherosclerotic burden (0 to 5), medium (6 to 20) and high (over 20). In addition, obstructive coronary artery disease was defined as 50% narrowing or more.
The primary outcome was the difference in Leiden CCTA score between women and men of similar age. The investigators also analysed sex differences in the rates of major adverse cardiovascular events (MACE), which included all-cause death and myocardial infarction, after adjusting for age and cardiovascular risk factors (hypertension, high cholesterol, diabetes, current smoking and family history of coronary artery disease).
A total of 11 678 women (average age 58.5 years) and 13 272 men (average age 55.6 years) were followed for 3.7 years. Regarding the primary outcome, the study showed an approximately 12 year delay in the onset of coronary atherosclerosis in women: the median Leiden CCTA risk score was above zero at age 64 to 68 years in women versus 52 to 56 years in men (p<0.001). In addition, the overall plaque burden as quantified by the Leiden CCTA score was significantly lower in women, who had more non-obstructive disease.
Dr. van Rosendael said: “The results confirm the previously reported delay in the start of atherosclerosis in women. We also found that women are more likely to have non-obstructive disease. It was formerly thought that only obstructive atherosclerosis caused myocardial infarction but we now know that non-obstructive disease is also risky.”
The burden of atherosclerosis was equally predictive of MACE in premenopausal women (aged under 55 years) and men of the same age group. However, in postmenopausal women (age 55 years and older), the risk of MACE was higher than men for a given score. In postmenopausal women, compared to those with a low burden, those with a medium and high burden had 2.21-fold and 6.11-fold higher risks of MACE. While in men aged 55 years and older, compared to those with a low burden, those with a medium and high burden had 1.57-fold and 2.25-fold greater risks of MACE.
Dr van Rosendael said: “In this study, the elevated risk for women versus men was especially observed in postmenopausal women with the highest Leiden CCTA score. This could be partly because the inner diameter of coronary arteries is smaller in women, meaning that the same amount of plaque could have a larger impact on blood flow. Our findings link the known acceleration of atherosclerosis development after menopause with a significant increase in relative risk for women compared to men, despite a similar burden of atherosclerotic disease. This may have implications for the intensity of medical treatment.”
New research in the Annals of Internal Medicine reports that the drug solriamfetol is the most effective treatment for excessive daytime sleepiness (EDS) for people with obstructive sleep apnoea (OSA).
The standard treatment for OSA is a positive airway pressure (PAP) mask that uses compressed air to support lung airways during sleep. However, some people with OSA still experience EDS and may benefit from anti-fatigue medication.
“The most important thing that people with OSA should do is use their PAP machine, but if they are still sleepy there are options in the form of medications that can reduce their tiredness,” said first author Tyler Pitre, a resident physician in internal medicine at McMaster University and incoming respirology fellow at the University of Toronto.
“Fifteen to 30 per cent of people in North America have a diagnosis of OSA and the prevalence could be much higher as many others are undiagnosed. Many people have symptoms as the condition is highly associated with obesity, which affects a large and increasing number of people in Canada, the United States and other high-income countries,” he said.
“Among those patients, many will have EDS, which affects their quality of life, making them less productive and also puts them at risk of other psychological issues. Improving this situation is of paramount importance to physicians.”
Pitre said that OSA affects nearly one billion people globally, leaving many of them at risk of EDS.
Zeraatkar and Pitre made their findings by conducting a systematic review of 14 clinical trials of anti-fatigue medications involving 3085 people, as well as analysing data from MEDLINE, CENTRAL, EMBASE and ClinicalTrials.gov in a specific network meta-analysis. They conducted their research from October 2022 to January 2023.
Senior author Zeraatkar said that while solriamfetol is likely the best medication for EDS, the drugs armodafinil-modafinil and pitolisant are also effective in combatting fatigue.
Solriamfetol can also raise blood pressure, especially risky for people with OSA, as many of them also have cardiovascular issues.
“It would be interesting to see how effective these anti-fatigue medications will be for treating related illnesses such as chronic fatigue syndrome and long COVID, now that we know they work for a similar condition,” said Zeraatkar, an assistant professor of the Department of Anesthesia.
Using new genetic tools to study statins in human cells and mice, researchers have uncovered how these drugs protect the cells that line blood vessels. Published in Nature Cardiovascular Research, the findings provide new insight into statins’ curiously wide-ranging benefits, for conditions ranging from arteriosclerosis to diabetes, that have long been observed in the clinic.
“The study gives us an understanding, at a very deep mechanistic level, of why statins have such a positive effect outside of reducing LDL [low-density lipoprotein],” said professor of medicine Joseph Wu, MD, PhD, the study’s senior author. “Given how many people take statins, I think the implications are pretty profound.”
Developed in the 1980s from compounds found in mould and fungi, statins target an enzyme that regulates cholesterol production in the liver. But clinical trials have shown that they also seem to safeguard against cardiovascular disease beyond their ability to lower cholesterol.
Heart failure patients who take statins, for example, are less likely to suffer a second heart attack. They have also been shown to prevent the clogging of arteries, reduce inflammation and even lower cancer risk. Yet these underlying mechanisms are poorly understood.
“Statins were invented to lower cholesterol by targeting the liver. But we didn’t know the targets or the pathways in the cardiovascular system,” said Chun Liu, PhD, an instructor at the Stanford Cardiovascular Institute and co-lead author.
Mesenchymal cells are poor substitutes
To take a closer look at statins’ effect on blood vessels, Liu and colleagues tested a common statin, simvastatin, on lab-grown human endothelial cells derived from induced pluripotent stem cells. Endothelial cells make up the lining of blood vessels, but in many diseases they transform into a different cell type, known as mesenchymal cells, which are poor substitutes.
“Mesenchymal cells are less functional and make tissues stiffer so they cannot relax or contract correctly,” Liu said.
The researchers suspected that statins could reduce this harmful transition. Indeed, endothelial cells treated with simvastatin in a dish formed more capillary-like tubes, a sign of their enhanced ability to grow into new blood vessels.
RNA sequencing of the treated cells offered few clues. The researchers saw some changes in gene expression, but they “didn’t find anything interesting,” Liu said.
It was not until they employed a newer technique called ATAC-seq that the role of statins became apparent. ATAC-seq reveals what happens at the epigenetic level, meaning the changes to gene expression that do not involve changes to the genetic sequence.
They found that the changes in gene expression stemmed from the way strings of DNA are packaged inside the cell nucleus. DNA exists in our cells not as loose strands but as a series of tight spools around proteins, together known as chromatin. Whether particular DNA sequences are exposed or hidden in these spools determines how much they are expressed.
“When we adopted the ATAC-seq technology, we were quite surprised to find a really robust epigenetic change of the chromatin,” Liu said.
ATAC-seq revealed that simvastatin-treated cells had closed chromatin structures that reduced the expression of genes that cause the endothelial-to-mesenchymal transition. Working backward, the researchers found that simvastatin prevents a protein known as YAP from entering the nucleus and opening chromatin.
The YAP protein is known to play important roles in development, such as regulating the size of our organs, but also has been implicated in the abnormal cell growth seen in cancer.
A look at diabetes
To see the drug in context, the researchers tested simvastatin on diabetic mice. Diabetes causes subtle changes to blood vessels that mimic the damage commonly seen in people who are prescribed statins — older patients who do not have a cardiovascular condition, Liu said.
They found that after eight weeks on simvastatin, the diabetic mice had significantly improved vascular function, with arteries that more easily relaxed and contracted.
“If we can understand the mechanism, we can fine-tune this drug to be more specific to rescuing vascular function,” Liu said.
The findings also provide a more detailed picture of the vascular disease process, which could help doctors identify and treat early signs of vascular damage.
A population-based study of 22 million people in the UK estimates that around one in ten individuals in the UK now live with an autoimmune disorder. The findings, published in The Lancet, also highlight important socioeconomic, seasonal and regional differences for several autoimmune disorders, providing new clues as to what factors may be involved in these conditions.
There are more than 80 known autoimmune diseases, including conditions like rheumatoid arthritis, type 1 diabetes and multiple sclerosis, some of which have been increasing in the last few decades.
This has raised the question whether overall incidence of autoimmune disorders is on the rise and what factors are involved, such as environmental factors or behavioural changes in society. The exact causes of autoimmune diseases remain largely unknown, including how much can be attributed to a genetic predisposition to disease and how much is down to exposure to environmental factors.
The study used anonymised electronic health data from 22 million individuals in the UK to investigate 19 of the most common autoimmune diseases. The authors examined whether incidence of autoimmune diseases is rising over time, who is most affected by these conditions and how different autoimmune diseases may co-exist with each other.
They found that the 19 autoimmune diseases studied affect around 10% of the population. This is higher than previous estimates, which ranged from 3–9% and often relied on smaller sample sizes and included fewer autoimmune conditions. The analysis also highlighted a higher incidence in women (13%) than men (7%).
The research discovered evidence of socioeconomic, seasonal and regional disparities for several autoimmune disorders, suggesting that these conditions are unlikely to be caused by genetic differences alone. This observation may point to the involvement of potentially modifiable risk factors such as smoking, obesity or stress. It was also found that in some cases a person with one autoimmune disease is more likely to develop a second, compared to someone without an autoimmune disease.
Dr Nathalie Conrad at the University of Oxford said: “We observed that some autoimmune diseases tended to co-occur with one another more commonly than would be expected by chance or increased surveillance alone. This could mean that some autoimmune diseases share common risk factors, such as genetic predispositions or environmental triggers. This was particularly visible among rheumatic diseases and among endocrine diseases. But this phenomenon was not generalised across all autoimmune diseases. Multiple sclerosis, for example, stood out as having low rates of co-occurrence with other autoimmune diseases, suggesting a distinct pathophysiology.”
These findings reveal novel patterns that will inform the design of further research into the possible common causes of different autoimmune diseases.
Professor Geraldine Cambridge at UCL Medicine said: “Our study highlights the considerable burden that autoimmune diseases place upon individuals and the wider population. Disentangling the commonalities and differences within this large and varied set of conditions is a complex task. There is a crucial need, therefore, to increase research efforts aimed at understanding the underlying causes of these conditions, which will support the development of targeted interventions to reduce the contribution of environmental and social risk factors.”
It has been believed speed of information transmitted among regions of the brain stabilised during early adolescence. A study in Nature Neuroscience has instead found that transmission speeds continue to increase into early adulthood, which may explain the emergence of mental health problems over this period. In fact, transmission speeds increase until around age 40, reaching a speed twice that of a 4-year old child.
As mental health problems such as anxiety, depression and bipolar disorders can emerge in late adolescence and early adulthood, a better understanding of brain development may lead to new treatments.
“A fundamental understanding of the developmental trajectory of brain circuitry may help identify sensitive periods of development when doctors could offer therapies to their patients,” says senior author Dora Hermes, PhD, a biomedical engineer at Mayo Clinic.
Called the human connectome, the structural system of neural pathways in the brain or nervous system develops as people age. But how structural changes affect the speed of neuronal signalling has not been well described.
“Just as transit time for a truck would depend on the structure of the road, so does the transmission speed of signals among brain areas depend on the structure of neural pathways,” Dr Hermes explains. “The human connectome matures during development and aging, and can be affected by disease. All these processes may affect the speed of information flow in the brain.” In the study, Dr Hermes and colleagues stimulated pairs of electrodes with a brief electrical pulse to measure the time it took signals to travel among brain regions in 74 research participants between the ages of 4 and 51. The intracranial measurements were done in a small population of patients who had electrodes implanted for epilepsy monitoring at University Medical Center Utrecht, Netherlands.
The response delays in connected brain regions showed that transmission speeds in the human brain increase throughout childhood and even into early adulthood. They plateau around 30 to 40 years of age.
The team’s data indicate that adult transmission speeds were about two times faster compared to those typically found in children. Transmission speeds also were typically faster in 30- or 40-year-old subjects compared to teenagers.
Brain transmission speed is measured in milliseconds, a unit of time equal to one-thousandth of a second. For example, the researchers measured the neuronal speed of a 4-year-old patient at 45 milliseconds for a signal to travel from the frontal to parietal regions of the brain. In a 38-year-old patient, the same pathway was measured at 20 milliseconds. For comparison, the blink of an eye takes about 100 to 400 milliseconds.
The researchers are working to characterise electrical stimulation-driven connectivity in the human brain. One of the next steps is to better understand how transmission speeds change with neurological diseases. They are collaborating with paediatric neurosurgeons and neurologists to understand how diseases change transmission speeds compared to what would be considered within the normal range for a certain age group.
Today we celebrate Nurses as we do every year on 12 May. The International Council of Nurses proclaimed this year’s slogan as ‘Our Nurses, Our Future’, but what is the future of nurses in South Africa?
During the height of the COVID pandemic, we saw a huge campaign launched by the World Health Organization, uplifting the stature of nurses and midwives and showcasing them as the backbone of health systems at a global level. In the South African context, the story goes that they will also be central to the health system once National Health Insurance is implemented yet there are many red flags raised as we continue the planning discussions in preparation for this change with little to no answers about that future.
“I will never be a nurse”
By the time my mother had to decide on a career, nursing was one of those professions that provided stability and security to black and coloured women during Apartheid. You had two choices – become a nurse or a teacher. That’s how my mother began her nursing journey, but she was so passionate about it so that it would probably have been her choice, regardless.
Her passion was not what spurred me on to become a nurse, though. I looked at her long hours and tireless devotion to her community and the mental health fraternity and literally uttered the words, “I will never be a nurse”. Then I met a young staff nurse during a youth weekend away. She was so proud of her profession. She just oozed pride, and at that moment, I went from a potential engineering student to a nursing student.
My father was livid. He could not comprehend why his only daughter would observe the work hours of her mother and still choose to become a nurse. But in many ways, I believe nursing chose me. Once I made the decision, I never looked back. I remember being mocked and berated for my choice in social circles, but feeling a deep connection to this calling.
I have not entered it blindly though. I was aware of my privilege and the weight of caring for people at their most vulnerable. The experiences I have made while holding the hand of someone taking their last breath, supporting a mother delivering a stillborn baby, to engaging with my first person living with HIV, or watching someone slip away after a huge battle with cancer have been deeply embedded in my consciousness. I do not believe these experiences to be without life-altering potential and believe it has shaped me into the healthcare worker I am today.
Threats to nurse autonomy
It is often believed that nurses are the handmaiden to the doctor and we should not think but do. Those sayings were so wrong, but even today, the inferiority of the quality of nurse training, lack of supervision, and only very limited mentoring all threaten the autonomy of the nurse.
Nurses, despite having a day and even a week dedicated to celebrating them, are still, for the most part, underpaid, overworked, and professionally stunted. By stunted I am referring to the lack of mandatory continuous professional development and upskilling. Somehow, as the backbone of primary healthcare, they are often unable to take time out for much-needed training.
One often hears of nurses being rude and impatient. Though some may very well display these horrible traits, for the most part, people have entered this profession to improve healthcare services to individuals, families, and communities at large. In my 21 years of experience, the issue is hugely exacerbated by the healthcare system, which does not support nurses. The hours are long and gruelling – exacerbated by staff shortages in facilities. The environment is hostile, the workload unequal, and the pay shoddy. Many nurses find themselves moonlighting to make ends meet.
Advocate for us
Though not an excuse for unprofessional behaviour, I do want activists and health advocates to fight for better working conditions, upskilling opportunities, and a larger health workforce in our public health sector.
The mental health of our clients and communities appears topical at the moment, but what about the nurse? The trauma of loss, observation of patient suffering, and abuse by many of the actors in the health space can take its toll on the mental health and well-being of our nurses, too. When we plan for the public, we must remember to include the healthcare workers and their health and well-being.
This is even more critical now as we embark on establishing the National Health Insurance (NHI) system.
As NHI looms, the threat that nurses will be ill-equipped to render quality healthcare services is a glaring reality. The South African Nursing Council (SANC) notes that 47% of the nurses on its database are older than 50 years of age. This narrative of aging nursing personnel started years ago and if we had a proactive plan to address this, South Africa may in fact have had some fighting chance to implement NHI smoothly.
In a damning article published in February, the Democratic Nursing Organisation of South Africa (DENOSA) highlighted that the South African public health sector has a deficit of 27 000 nurses and yet there are 5 000 nurses currently unemployed. How can this be acceptable? It further noted that the South African government has placed certain nursing specialities on a scarce skills list in the hope of recruiting from other countries instead of planning to upskill and uplift domestically.
Part of me wants to speak about accountability, collaboration, and change management, but the other part bleeds for nurses as the workload and responsibilities increase and the work environment becomes more hostile. All this makes it hard to see the silver lining.
I do, however, believe that if the South African Nursing Council and National Department of Health actually engage the people on the ground, those at the coal face, those with expertise, and review their current implementation plans, they will see the same glaring gaps that we see every day.
There must be a call to action for all nursing leadership, nursing activists, nurses, and nursing education establishments to collectively take a stand and demand that we revise our current approach to the nursing curriculum and work on making nursing more appealing to the youth. This could be one step in the right direction.
When I qualified as a nurse, it was a four-year course. The nursing degree I completed included Community Nursing, Psychiatric Nursing, General Nursing, and Midwifery, and although I might not practise it all, I am able to fall back on that knowledge during client or patient engagements. Now it is a five-year course with one qualification with the nurse trained as a generalist. The fear is how does that serve our communities? We need midwifery, for example, to do NIMART (initiate people on HIV treatment) and you need community nurses to be working in primary healthcare, If you come out with one general qualification – how exactly will this pan out?
We need a rethink of how we train nurses and how we can strengthen the curriculum so that we can get nurses who can address HIV and all issues in primary healthcare. In my programme – HIV testing, for example, nurses don’t get trained on HIV testing. It is just monkey see, monkey do and unfortunately, that doesn’t translate into quality service.
Very often nursing practice is see one, do one, and then you’re the expert. I’m arguing that these things must be part of the curriculum. For example, why must a nurse come out of nursing school and then only learn IMCI (Integrated Management of Childhood Illness) Why is IMCI not being done practically in the facility and the theory in class, as part of the curriculum?
Nurses, today, are expected to know everything, which is impossible but we are not upskilling them and making sure the curriculum is so robust that it addresses all disease profiles and our communities’ healthcare needs. We are talking about integrative and holistic healthcare so we cannot be only training nurses in one way. There is a malalignment of what our communities need and what nursing schools are churning out.
We must fix that.
We need an urgent change in the curriculum of nurses to ensure we can support the needs of the health system and communities, build great leadership for the future, and ensure quality health services for all.
* Sparks is a nurse, health equity advocate, and Tekano and Aspen New Voices Fellow with 21 years’ experience working across South Africa with a focus on ensuring equitable and just access to quality healthcare for all.She is also a Quote This Women + Voice of the Year Award Winner.
