Displacement of nasogastric (NG) feeding tubes can have serious implications if undetected. Incorrectly positioned tubes leave patients vulnerable to the risks of regurgitation and respiratory aspiration. It is crucial to differentiate between gastric and respiratory placement on initial insertion to prevent potentially fatal pulmonary complications. Insertion and care of an NG tube should therefore only be carried out by a registered doctor or nurse who has undergone theoretical and practical training and is deemed competent or is supervised by someone competent. Assistant practitioners and other unregistered staff must never insert NG tubes or be involved in the initial confirmation of safe NG tube position.

Staff must ensure that if they take any part in the transfusion process, their competency assessment is updated every three years. All staff are responsible for ensuring that they attend the mandatory training identified for their roles. Relevant training courses are clearly identified in Appendix 1 of the Mandatory Training Matrix.

Our guidelines state that ‘at least a level 2 medication review will occur’, i.e. the minimum standard is a treatment review of medicines with the full notes but not necessarily with the patient present. However, the guidelines go on to say that ‘all patients should have the chance to raise questions and highlight problems about their medicines’ and that ‘any changes resulting from the review are agreed with the patient’.

It also states that GP practices are expected to

• minimise waste in prescribing and avoid ineffective treatments.
• engage effectively in the prevention of ill health.
• avoid the need for costly treatments by proactively managing patients to recovery through the whole care pathway

In August, an alert was issued on the safe use of opioids in hospitals. This reported the incidence of respiratory depression among post-surgical patients to an average 0.5% – thus for every 5,000 surgical patients, 25 will experience respiratory depression. Failure to recognise respiratory depression and institute timely intervention can lead to cardiopulmonary arrest, resulting in brain injury or death. A retrospective multi-centre study of 14,720 cardiopulmonary arrest cases showed that 44% were respiratory related and more than 35% occurred on the general care floor. It is therefore recommended that post-operative patients now have continuous monitoring, instead of spot checks, of both oxygenation and ventilation.

Text 1: Sleep deprivation

Millions of people who suffer sleep problems also suffer myriad health burdens. In addition to emotional distress and cognitive impairments, these can include high blood pressure, obesity, and metabolic syndrome. ‘In the studies we’ve done, almost every variable we measured was affected. There’s not a system in the body that’s not affected by sleep,’ says University of Chicago sleep researcher Eve Van Cauter. ‘Every time we sleep deprive ourselves, things go wrong.’

A common refrain among sleep scientists about two decades ago was that sleep was performed by the brain in the interest of the brain. That wasn’t a fully elaborated theory, but it wasn’t wrong. Numerous recent studies have hinted at the purpose of sleep by confirming that neurological function and cognition are messed up during sleep loss, with the patient’s reaction time, mood, and judgement all suffering if they are kept awake too long.

In 1997, Bob McCarley and colleagues at Harvard Medical School found that when they kept cats awake by playing with them, a compound known as adenosine increased in the basal forebrain as the sleepy felines stayed up longer, and slowly returned to normal levels when they were later allowed to sleep. McCarley’s team also found that administering adenosine to the basal forebrain acted as a sedative, putting animals to sleep. It should come as no surprise then that caffeine, which blocks adenosine’s receptor, keeps us awake. Teaming up with Basheer and others, McCarley later discovered that, as adenosine levels rise during sleep deprivation, so do concentrations of adenosine receptors, magnifying the molecule’s sleep-inducing effect. ‘The brain has cleverly designed a two-stage defence against the consequences of sleep loss,’ McCarley says. Adenosine may underlie some of the cognitive deficits that result from sleep loss. McCarley and colleagues found that infusing adenosine into rats’ basal forebrain impaired their performance on an attention test, similar to that seen in sleep-deprived humans. But adenosine levels are by no means the be-all and end-all of sleep deprivation’s effects on the brain or the body.

Over a century of sleep research has revealed numerous undesirable outcomes from staying awake too long. In 1999, Van Cauter and colleagues had eleven men sleep in the university lab. For three nights, they spent eight hours in bed, then for six nights they were allowed only four hours (accruing what Van Cauter calls a sleep debt), and then for six nights they could sleep for up to twelve hours (sleep recovery). During sleep debt and recovery, researchers gave the participants a glucose tolerance test and found striking differences. While sleep deprived, the men’s glucose metabolism resembled a pre-diabetic state. ‘We knew it would be affected,’ says Van Cauter. ‘The big surprise was the effect being much greater than we thought.’

Subsequent studies also found insulin resistance increased during bouts of sleep restriction, and in 2012, Van Cauter’s team observed impairments in insulin signalling in subjects’ fat cells. Another recent study showed that sleep-restricted people will add 300 calories to their daily diet. Echoing Van Cauter’s results, Basheer has found evidence that enforced lack of sleep sends the brain into a catabolic, or energy-consuming, state. This is because it degrades the energy molecule adenosine triphosphate (ATP) to produce adenosine monophosphate and this results in the activation of AMP kinase, an enzyme that boosts fatty acid synthesis and glucose utilization. ‘The system sends a message that there’s a need for more energy,’ Basheer says. Whether this is indeed the mechanism underlying late-night binge-eating is still speculative.

Within the brain, scientists have glimpsed signs of physical damage from sleep loss, and the time-line for recovery, if any occurs, is unknown. Chiara Cirelli’s team at the Madison School of Medicine in the USA found structural changes in the cortical neurons of mice when the animals are kept awake for long periods. Specifically, Cirelli and colleagues saw signs of mitochondrial activation – which makes sense, as ‘neurons need more energy to stay awake,’ she says – as well as unexpected changes, such as undigested cellular debris, signs of cellular aging that are unusual in the neurons of young, healthy mice. ‘The number [of debris granules] was small, but it’s worrisome because it’s only four to five days’ of sleep deprivation,’ says Cirelli. After thirty-six hours of sleep recovery, a period during which she expected normalcy to resume, those changes remained.

Further insights could be drawn from the study of shift workers and insomniacs, who serve as natural experiments on how the human body reacts to losing out on such a basic life need for chronic periods. But with so much of our physiology affected, an effective therapy − other than sleep itself – is hard to imagine. ‘People like to define a clear pathway of action for health conditions,’ says Van Cauter. ‘With sleep deprivation, everything you measure is affected and interacts synergistically to produce the effect.’

Text 2: ADHD

The American Psychiatric Association (APA) recognised Attention Deficit Hyperactivity Disorder (ADHD) as a childhood disorder in the 1960s, but it wasn’t until 1978 that the condition was formally recognised as afflicting adults. In recent years, the USA has seen a 40% rise in diagnoses of ADHD in children. It could be that the disorder is becoming more prevalent, or, as seems more plausible, doctors are making the diagnosis more frequently. The issue is complicated by the lack of any recognised neurological markers for ADHD. The APA relies instead on a set of behavioural patterns for diagnosis. It specifies that patients under 17 must display at least six symptoms of inattention and/or hyperactivity; adults need only display five.

ADHD can be a controversial condition. Dr Russell Barkley, Professor of Psychiatry at the University of Massachusetts insists; ‘the science is overwhelming: it’s a real disorder, which can be managed, in many cases, by using stimulant medication in combination with other treatments’. Dr Richard Saul, a behavioural neurologist with five decades of experience, disagrees; ‘Many of us have difficulty with organization or details, a tendency to lose things, or to be forgetful or distracted. Under such subjective criteria, the entire population could potentially qualify. Although some patients might need stimulants to function well in daily life, the lumping together of many vague and subjective symptoms could be causing a national phenomenon of misdiagnosis and over-prescription of stimulants.’

A recent study found children in foster care three times more likely than others to be diagnosed with ADHD. Researchers also found that children with ADHD in foster care were more likely to have another disorder, such as depression or anxiety. This finding certainly reveals the need for medical and behavioural services for these children, but it could also prove the non-specific nature of the symptoms of ADHD: anxiety and depression, or an altered state, can easily be mistaken for manifestations of ADHD.

ADHD, the thinking goes, begins in childhood. In fact, in order to be diagnosed with it as an adult, a patient must demonstrate that they had traits of the condition in childhood. However, studies from the UK and Brazil, published in JAMA Psychiatry, are fuelling questions about the origins and trajectory of ADHD, suggesting not only that it can begin in adulthood, but that there may be two distinct syndromes: adult-onset ADHD and childhood ADHD. They echo earlier research from New Zealand. However, an editorial by Dr Stephen Faraone in JAMA Psychiatry highlights potential flaws in the findings. Among them, underestimating the persistence of ADHD into adulthood and overestimating the prevalence of adult-onset ADHD. In Dr Faraone’s words, ‘the researchers found a group of people who had sub-threshold ADHD in their youth. There may have been signs that things weren’t right, but not enough to go to a doctor. Perhaps these were smart kids with particularly supportive parents or teachers who helped them cope with attention problems. Such intellectual and social scaffolding would help in early life, but when the scaffolding is removed, full ADHD could develop’.

Until this century, adult ADHD was a seldom-diagnosed disorder. Nowadays however, it’s common in mainstream medicine in the USA, a paradigm shift apparently driven by two factors: reworked – many say less stringent – diagnostic criteria, introduced by the APA in 2013, and marketing by manufacturers of ADHD medications. Some have suggested that this new, broader definition of ADHD was fuelled, at least in part, to broaden the market for medication. In many instances, the evidence proffered to expand the definitions came from studies funded in whole or part by manufacturers. And as the criteria for the condition loosened, reports emerged about clinicians involved in diagnosing ADHD receiving money from drug-makers.

This brings us to the issue of the addictive nature of ADHD medication. As Dr Saul asserts, ‘addiction to stimulant medication isn’t rare; it’s common. Just observe the many patients periodically seeking an increased dosage as their powers of concentration diminish. This is because the body stops producing the appropriate levels of neurotransmitters that ADHD drugs replace − a trademark of addictive substances.’ Much has been written about the staggering increase in opioid overdoses and abuse of prescription painkillers in the USA, but the abuse of drugs used to treat ADHD is no less a threat. While opioids are more lethal than prescription stimulants, there are parallels between the opioid epidemic and the increase in problems tied to stimulants. In the former, users switch from prescription narcotics to heroin and illicit fentanyl. With ADHD drugs, patients are switching from legally prescribed stimulants to illicit ones such as methamphetamine and cocaine. The medication is particularly prone to abuse because people feel it improves their lives. These drugs are antidepressants, aid weight-loss and improve confidence, and can be abused by students seeking to improve their focus or academic performance. So, more work needs to be done before we can settle the questions surrounding the diagnosis and treatment of ADHD.