Menu

Never stop learning

Access over 400 recorded highlight sessions from UEG Week 2014.

UEG E-learning


T  +43 (0) 699 1997 16 39


E  e-learning@remove-this.ueg.eu

 

 

Julia Kasper


T  +43 (0) 699 1997 16 11


E  j.kasper@remove-this.medadvice.co.at

 

 

Irritable Bowel Syndrome

Improve your consultation skills and knowledge of the condition.

2xcdcvsdvv

sdfsdfsdf

Get access to 10 recorded lectures from recent Summer School

This intense clinical-based 4-day course is perfect for trainees and early career medical professionals. Recordings can now conveniently be watched from home. 

NeuroGASTRO Meeting 2015

37 recorded lectures covering advances in neurogastroenterology .

Let’s get physical: Listen to your liver talk! 

Does exercise benefit NAFLD patients?

Summer is just around the corner and I’ve been hitting the gym more often to get ready for the beach (and by more often I mean I actually started going to the gym)! But there are many more important reasons why you should work out and your liver’s health is a major one, particularly concerning non-alcoholic fatty liver disease (NAFLD).

NAFLD consists of a spectrum of histopathological changes that range in severity from simple steatosis to non-alcoholic steatohepatitis (NASH). Although simple steatosis is characterized by a relatively favourable clinical outcome, NASH can progress to cirrhosis and hepatocellular carcinoma, leading to liver-related morbidity and mortality. Largely considered a manifestation of obesity and the metabolic syndrome, NAFLD is becoming the most common cause of chronic liver disease worldwide. Indeed, NAFLD is found in almost 70% of the adult obese population and in more than 90% of morbidly obese individuals.1 NAFLD is also highly prevalent in children and its incidence appears to be increasing in Europe, with 2–12.5% of children and early adolescents presenting with NAFLD, a number that rises to 36–44% in obese children.2 Of note, the risk factors for paediatric NAFLD mirror those for adult NAFLD and further correlate with an increasingly sedentary lifestyle, coupled with unbalanced dietary habits, where changes in macronutrients, increased calorie intake and decreased physical activity negatively influence NAFLD pathogenesis.

There is no current pharmacological treatment for NAFLD, although several clinical trials are ongoing, with promising results reported so far. As a consequence, lifestyle interventions remain the cornerstone of NAFLD treatment; in parallel with healthier and smarter eating choices, the benefit of physical activity for NAFLD patients has recently been expounded. Originally thought to be effective only when combined with the introduction of a healthy diet in obese patients, it is now apparent that different exercise regimens can benefit NAFLD, even without dietary restriction and/or in the absence of significant weight loss. For instance, aerobic exercise alone has been shown to be able to decrease visceral adipose tissue volume and liver fat content in sedentary obese individuals by 12% and 21%, respectively.3 Similarly, Oh and co-workers showed that increased physical exercise with or without dieting significantly reduced hepatic inflammation and associated oxidative stress in obese men.4

More recently, Oh and colleagues have suggested that at least 250 minutes of moderate to vigorous intensity physical exercise per week was required to reduce liver fat in obese men as part of lifestyle management.5 In other words, this is more or less equivalent to 50 minutes of moderate (dancing, gardening, housework/domestic chores, walking domestic animals) to vigorous (walking, running, fast cycling/swimming, aerobics, competitive sports/games) intensity physical activity, 5 times per week. Not bad at all! But it gets even better. In April 2015, Keating et al. showed that inactive and overweight/obese adults placed under different aerobic exercise regimens reduce their liver fat and visceral adipose tissue, irrespective of exercise volume or intensity and in the absence of clinically significant weight loss!6 In my opinion, these findings suggest that regular exercise may also greatly benefit non-obese NAFLD patients, despite there being no expectation that these patients will lose a significant amount of weight (they are lean!).

Although it might be surprising for some to learn that NAFLD is not solely a disease of the obese population, the prevalence of NAFLD in lean individuals is increasing. This increase in prevalence is particularly noticeable in the Asia-Pacific region, due to diverse environmental and genetic factors.7 As such, if you think you have ‘good genes’ because you look lean and healthy despite not working out much and/or eating junk food all the time, you might want to think twice, listen to your liver talk and get physical! If nothing else, individuals who exercise regularly might be, perhaps unknowingly, actively lowering their risk of developing fatty liver or even cardiometabolic disease, as the latter correlates with excess liver fat, even in the absence of NASH. However, the key word here is ‘regularly’; if you are a seasonal gym member like me, I would encourage you (and myself) to find other parallel and fun exercise activities and to stick to them. This might be difficult for some, but the sustainability of any intervention is the key to success. This is why—despite believing that specialized and personalized exercise prescription, in parallel with dietary advice, should continue to represent the main line of treatment for NAFLD patients—I think that the use of pharmacological agents on their own or as adjunctive therapies to lifestyle modification will remain desirable.

When exercising, the old saying, “Feel good on the inside and look good on the outside,” usually crosses my mind. Now, I can also almost picture my liver shouting “I feel good, na na, na na, na na, na…”

 

References: 

  1. Angulo P. Nonalcoholic fatty liver disease. N Engl J Med 2002; 346: 1221–12231.
  2. Durmaz O. Metabolic liver disease in the adolescent. Presentation in the Non-alcoholic fatty liver disease (NAFLD): any news? session at UEG Week 2014.
  3. Johnson NA, et al. Aerobic exercise training reduces hepatic and visceral lipids in obese individuals without weight loss. Hepatology 2009; 50: 1105–1112.
  4. Oh S, et al. Exercise reduces inflammation and oxidative stress in obesity-related liver diseases. Med Sci Sports Exerc 2013; 45: 2214–2222.
  5. Oh S, et al. Moderate to vigorous physical activity volume is an important factor for managing nonalcoholic fatty liver disease: a retrospective study. Hepatology 2015; 61: 1205–1215.
  6. Keating SE, et al. Effect of aerobic exercise training dose on liver fat and visceral adiposity. J Hepatol Epub ahead of print 1 April 2015. DOI: 10.1016/j.jhep.2015.02.022.
  7. Bugianesi E. Non-obese patients with NAFLD. Presentation in the Non-alcoholic fatty liver disease (NAFLD): any news? session at UEG Week 2014.

 

Further UEG Resources:

Bellentani, S. How frequent is NAFLD in Europe and in the world? Presentation in the Update on non-alcoholic fatty liver disease session at UEG Week 2013

Dufour J-F. Impact of lifestyle and diet on disease progression. Presentation in the Non-alcoholic fatty liver  disease (NAFLD): any news? session at UEG Week 2014.

Ratziu, V.  Medical treatment. Presentation in the Non-alcoholic fatty liver disease (NAFLD): any news? session at UEG Week 2014.

Ratziu, V. Treatment modalities for non-alcoholic steatohepatitis. Presentation in the Non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease in 2014 session at UEG Week 2014. 

This was Summer School 2015

164 trainees met for a weekend full of lectures and hands-on training.

9th EDS Postgraduate course

26 surgical lectures from the meeting in Riga are available free of charge. 

Coeliac disease

Based on the ESPGHAN guidelines this course was developed to assist medical professionals with correctly diagnosing the condition.

Wake up Europe—it’s World IBD Day!

World IBD Day is observed on May 19.

World IBD Day (#worldIBDday) is observed on May 19 every year. This is the day for the millions of patients with IBD (inflammatory bowel disease), their supporters and IBD organizations worldwide to raise awareness, advance the understanding of the impact of IBD on human health and highlight the large number of people affected.

Ulcerative colitis and Crohn’s disease, the major types of IBD, are autoimmune diseases, the etiology of which appears multifactorial, involving both genetic and environmental factors. A study in the American Journal of Gastroenterology mapped the risk of acquiring IBD in relatives of patients with IBD.1 The study was based on data in the Danish National Patient Register, which included the 45,857 Danes who were diagnosed with IBD between 1977 and 2011. The team identified that the children, siblings or parents of individuals with IBD had an eightfold increased risk of developing IBD. For grandparents, uncles, aunts, nephews and nieces, the risk was increased by 2.5-fold. Among the younger siblings of patients with Crohn’s disease who were aged 20–25 years, the risk of developing IBD over the following 10 years was as high as 2%. First author on the paper, Frederik Trier Møller, says “Our results can be used in the counselling of relatives of IBD patients and maybe in the long run to identify persons, who could benefit from future available preventive measures.”

Moving on to environmental factors, the intestinal microbiota is thought also to have a key role in the development of IBD. Books, such as ‘An Epidemic of Absence,’2 sum up some of the hypotheses on the etiology of allergic and autoimmune diseases. Intestinal parasites—protists and worms—are eukaryotic symbionts associated with the human intestine that have co-evolved with humans over thousands of years. These symbionts are still almost obligate findings in citizens in some regions of the world where IBD appears to be a very limited problem (e.g. Sub-Saharan Africa). Such organisms tend to establish stable communities in the human gut, but their role in human health and disease remains relatively unexplored. However, there is some evidence that the defaunation of the human gut seen in many countries with a Westernized lifestyle is associated with an increased incidence of immune-mediated and inflammatory diseases.2–5 Hence, while busy ridding ourselves of bugs, maybe particularly so those of our children, we may have inflicted new diseases on ourselves, including IBD. And so, in efforts to ‘dirty up’ our diets again, potential alleviation of IBD using concoctions of microscopic helminth eggs (Trichuris suis) is currently being investigated, the rationale being that helminth therapy will favorably modulate pro-inflammatory cytokine responses associated with intestinal inflammation. Indeed, IBD patients appear much less prone to being hosts of parasites than healthy individuals,6 but until now, only mere associations have been identified, not mechanistic understandings.

Not only parasites—or the lack thereof—but also bacteria may have crucial roles in the etiology of IBD. It’s difficult not to think of peptic ulcers and gastric cancer when the word falls on Helicobacter pylori. Meanwhile, performing a meta-analysis of 33 available studies, comprising 4,400 IBD patients and 4,763 controls, to explore the association between H. pylori infection and IBD, Rokkas and colleagues7 found that 26.5% of IBD patients tested positive for H. pylori infection, compared with 44.7% of individuals in the control group. The significant negative association between H. pylori infection and IBD supports the hypothesis that H. pylori infection protects against the development of IBD. This conclusion is backed up by data in a recent study that was not included in the meta-analysis. Roka et al. found that the occurrence of H. pylori gastritis was less frequent in children with newly diagnosed IBD compared with controls.8 However, the team calls for studies that enable the distinction between a true protective role of H. pylori and a confounding effect due to, for instance, previous use of antibiotics in children with IBD.

The fact that patients with IBD may have a slightly higher risk of developing small bowel cancer and colorectal cancer than individuals without the disease may now be quite well established, but how about the treatment offered to IBD patients? For example, what are the side effects of biologics and how severe are they? A study published in JAMA aimed to investigate whether patients with IBD who were exposed to TNF-α antagonists were at increased risk of developing cancer.9 Exposure to TNF-α antagonists (e.g. infliximab, adalimumab, and certolizumab pegol) among patients with IBD was not associated with an increased risk of cancer over a median follow-up of 3.7 years; an increased risk associated with longer-term accumulated doses and follow-up, however, could not be excluded.

With regard to anti-TNF treatment and beyond, the ‘Therapy update: Best use of biologics in IBD in 2014’ session at UEG Week 2014 is available in the UEG Education Library. In the presentation, Professor Séverine Vermeire uses the ECCO guidelines and her experience to advise on when to use anti-TNF agents.10 Dr Silvio Danese then talks us through emerging therapeutic monoclonal antibodies, such as vedolizumab, golimumab, etrolizumab, tofacitinib, including their mechanisms of action.11 Dr Alessandro Armuzzi reviews the efficacy of drugs used for prevention of postoperative recurrence of Crohn’s disease recurrence, distinguishing between endoscopic and clinical recurrence, and highlights the importance of revisiting strategies to managing postoperative Crohn’s disease.12 In the final presentation from the session, Professor Gils highlights the importance of using pharmacokinetics to guide anti-TNF treatment in clinical practice.13 For more on the same topic, I guide your attention to the ‘How to manage IBD in 2014’ session from UEG Week 2014.

Professor Maria Abreu brings you the best on IBD from Digestive Disease Week 201414 and also provides a strategy for how to make a confident diagnosis of IBD15 in the collection of presentations from the postgraduate course ‘What is important when diagnosing IBD?’ This collection also includes Dr Shomron Ben-Horin asking the question ‘Do characteristics at diagnosis predict disease outcome and complications?’,16 something which is also to some extent taken up by Dr Geert D’Haens in a very ‘good-for-teaching’ talk that aims to answer the question ‘Is differentiating ulcerative colitis from Crohn’s disease important?’17

The IBD material available in the UEG Education Library is vast, and I can only encourage you to mark #worldIBDday2015 by listening to some of these presentations. Also, if you want to know more about the activities related to World IBD Day, you may want to visit the World IBD events page.

Finally, perhaps it is worth suggesting that World IBD Day should receive special attention on the Faroe Islands. This North-Atlantic archipelago has the highest incidence of IBD in the world, going from 8 per 100,000 person years in 1960–1979 to 75 per 100,000 person years in 2010–2014.18 Such a rapid change is most likely linked not only to increased diagnostic awareness but also to so-far-unidentified environmental factors.

 

References

  1. Moller FT, et al. Familial risk of inflammatory bowel disease: a population-based cohort study 1977–2011. Am J Gastroenterol 2015; 110: 564–571.
  2. Velasquez-Manoff M. An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases. New York: Scribner, 2013.
  3. Elliot DE, and Weinstock JV. Where are we on worms? Curr Opin Gastroenterol 2012; 28: 551–556.
  4. Wiria AE, et al. Helminth infection in populations undergoing epidemiological transition: a friend or foe? Semin Immunopathol 2012; 34: 889–901.
  5. Rook GA, et al. Microbial ’Old Friends’, immunoregulation and stress resilience. Evol Med Public Health 2013; 2013: 46–64. 
  6. Petersen AM et al. Active ulcerative colitis associated with low prevalence of Blastocystis and Dientamoeba fragilis infection. Scand J Gastroenterol 2013; 48: 638–639. 
  7. Rokkas T, et al. The association between Helicobacter pylori infection and inflammatory bowel disease based on meta-analysis. United European Gastroenterology Journal Epub ahead of print April 9 2015. DOI:10.1177/2050640615580889. 
  8. Roka K, et al. The prevalence of Helicobacter pylori gastritis in newly diagnosed children with inflammatory bowel disease. Helicobacter 2014; 19: 400–405.
  9. Nyboe Andersen N, et al. Association between tumor necrosis factor-α antagonists and risk of cancer in patients with inflammatory bowel disease. JAMA 2014; 311: 2406–2413.
  10. Vermeire S. When should we start anti-TNF in IBD? Presentation in the “Therapy update: Best use of biologics in IBD in 2014” session at UEG Week 2014. 
  11. Danese S. Looking beyond anti-TNF in IBD: Vedolizumab, tofacitinib, etc. Presentation in the “Therapy update: Best use of biologics in IBD in 2014” session at UEG Week 2014. 
  12. Armuzzi A. Anti-TNF to prevent and treat postoperative recurrence of Crohn’s disease. Presentation in the “Therapy update: Best use of biologics in IBD in 2014” session at UEG Week 2014. 
  13. Gils A. Use of pharmacokinetics to guide anti-TNF treatment in clinical practice. Presentation in the “Therapy update: Best use of biologics in IBD in 2014” session at UEG Week 2014.
  14. Abreu MT. Inflammatory bowel disease. Presentation in the “Best of DDW” session at UEG Week 2014.
  15. Abreu MT. Diagnostic strategy to make a confident diagnosis of IBD. Presentation at UEG Week 2014. Presentation in the Postgraduate Teaching Programme at UEG Week 2014. 
  16. Ben-Horin S. Do characteristics at diagnosis predict disease outcome and complications? Presentation in the Postgraduate Teaching Programme at UEG Week 2014.
  17. d’Haens G. Is differentiating UC from CD important? Presentation in the Postgraduate Teaching Programme at UEG Week 2014.
  18. Hammer T et al. DOP010 Incidence of inflammatory bowel diseases in the Faroe Islands from 1960–2014: a 54-year overview from a population-based cohort. Presentation in “DOP Session 2 – Epidemiology of IBD" at ECCO Congress 2015.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The need for novel GORD diagnostic tools.

The need of noninvasive methods.

Gone are the days when a doctor would diagnose gastroesophageal reflux disease (GORD) simply by asking about symptoms and/or evaluating the response to acid suppression. Though this is still the case in many clinical practices, particularly for patients who have uncomplicated symptoms, a more accurate diagnosis usually involves undertaking invasive and expensive procedures that, nonetheless, are still claimed to have only moderate sensitivity and specificity. As such, more specific, noninvasive and cost-effective methods are needed for the diagnosis of GORD.

GORD is a common and chronic condition that has a significant impact on quality of life and confers a significant economic burden. It generally arises from the reflux of stomach contents into the oesophagus, thus leading to oesophageal injury and associated complications. The most common cause of GORD is the disrupted relaxation of the anti-reflux barrier, which is composed of the lower oesophageal sphincter and the diaphragmatic crura; when failing to respond to swallowing, these transient lower oesophageal relaxations result in reflux of gastric fluid through the oesophagogastric junction. Heartburn and acid regurgitation follow. Ultimately, in some patients acid reflux may damage the oesophageal squamous epithelium and lead to the development of Barrett oesophagus. Left untreated, Barret oesophagus can progress to oesophageal adenocarcinoma.1

The European Association of Endoscopic Surgery (EAES) states that the two main GORD diagnostic tools are upper endoscopy and long-term impedance esophageal pH monitoring. Indeed, the combined information obtained from clinical symptoms, endoscopy and pH testing is usually considered to be sufficient and specific for the diagnosis of GORD.  The EAES also highlight that “…further diagnostic investigations may be needed to verify functional abnormalities and establish the indication for surgery or other invasive therapies.”2 These additional diagnostic tools include high-resolution manometry (HRM), video-radiography and scintigraphy. For patients who have more severe symptoms, such as dysphagia and odynophagia, those who do not respond to acid suppression, or those in whom Barrett oesophagus is suspected, such additional diagnostic tools should be employed.3 Unfortunately, this comes at a sizeable financial cost.

In Germany, the incidence of GORD is high and the associated healthcare costs have been estimated at €4.8 billion.4 In the United States, GORD represents the most common GI-related diagnosis; annually, GORD accounts for 8.9 million patient visits to the clinic and endoscopy exams cost $32.4 billion.5 These budgets emphasize the need for alternative, cheaper diagnostic methods for GORD and, ideally, noninvasive ones. Encouragingly, we might be on the right track with two recently published studies on novel GORD diagnostic tools, namely pepsin detection in saliva and minimally invasive oesophageal mucosal impedance testing.

Several pathological settings may lead to pepsin being found in the laryngeal and paranasal sinus mucosa, saliva, middle ear effusion, tracheal secretions and bronchoalveolar lavage fluid. In their study, Hayat and co-workers sought to determine the value of salivary pepsin for discriminating patients with reflux-related symptoms from those with functional heartburn (FH).6 Pepsin was more likely to be detected in the saliva of patients with GORD and hypersensitive oesophagus (HO) and at higher concentrations than in the saliva of controls or FH patients. As such, the authors propose that salivary pepsin testing may complement GORD diagnosis.6 The fact that salivary pepsin can distinguish between GORD/HO and FH is extremely relevant, as most GORD patients benefit from pharmacological or surgical anti-reflux therapy, whereas FH patients do not. Interestingly, the detection of pepsin in saliva may also help in the diagnosis of laryngopharyngeal reflux (LPR).7 Despite the belief that LPR symptoms primarily result from GORD-related alterations of the laryngeal mucosa by gastric fluids, LPR differs from GORD in symptomatology and treatment modalities. A higher concentration of pepsin and bile acids has also been found in the saliva of patients with early laryngeal cancer than in the saliva of healthy volunteers, suggesting that LPR plays a role in the development of laryngeal carcinoma and might have utility as a disease biomarker.8

The question of how specific pepsin is for the diagnosis of GORD then arises. Indeed, is salivary pepsin diagnosing GORD, LPR or laryngeal carcinoma in development? As it currently stands, the measurement of salivary pepsin seems to represent a quick, cost-effective, noninvasive and simple 'office-based' method for GORD diagnosis, which I believe should be  followed or paralleled with other disease-specific methods. Nonetheless, it holds a great value on its own in pinpointing the next step; for instance, the absence of pepsin could be taken as a sign of null or low frequency reflux events.

Ates and co-workers have developed a minimally invasive device to assess oesophageal mucosal impedance as a marker of chronic reflux in GORD, where impedance is measured close to the squamocolumnar junction.9 They found that the impedance values were significantly lower in patients with GORD, with mucosal impedance patterns being identified in patients with oesophagitis at higher levels of specificity and positive predictive values than wireless pH monitoring.9

Despite being a simple method that’s easy to use and provides immediate results, it is unlikely that mucosal impedance will fully replace current GORD diagnosis tools, as it is unable to distinguish between different GORD symptoms or even GORD-related disorders, which require different therapeutic approaches. Still, it represents an excellent strategy to differentiate between GORD and FH, much like salivary pepsin. Though measurement of mucosal impedance is still invasive, the procedure is quick, which makes it attractive for patients who cannot (or will not) tolerate a transnasal probe that must be in place for 24 hours.  

Salivary pepsin levels and oesophageal mucosal impedance stand as two recent major breakthroughs in GORD diagnosis, but more are needed. I hope to see a lot of new and exciting discoveries on GORD diagnosis and management this October at UEG Week 2015! In the meantime, please feel free to browse the UEG Education Library for more resources.

 

References:

  1. Subramanian CR and Triadafilopoulos G. Refractory gastroesophageal reflux disease. Gastroenterol Rep (Oxf) 2015; 3: 41–53.
  2. Fuchs KH, Babic B, Breithaupt W, et al. EAES recommendations for the management of gastroesophageal reflux disease. Surg Endosc 2014; 28: 1753–1773.
  3. Badillo R and Francis D. Diagnosis and treatment of gastroesophageal reflux disease. World J Gastrointest Pharmacol Ther 2014; 5: 105–112.
  4. UEG White Book Brochure [https://ueg.eu/epaper/WhiteBook.Brochure/index.html].
  5. Medical Economics. Treatment of GERD evolving [May 2013, accessed April 14, 2015].
  6. Hayat JO, Gabieta-Somnez S, Yazaki E, et al. Pepsin in saliva for the diagnosis of gastro-oesophageal reflux disease. Gut 2015; 64: 373–380.
  7. Ocak E, Kubat G and Yorulmaz I. Immunoserologic pepsin detection in the saliva as a non-invasive rapid diagnostic test for laryngopharyngeal reflux. Balkan Med J 2015; 32: 46–50.
  8. Sereg-Bahar M, Jerin A and Hocevar-Boltezar I. Higher levels of total pepsin and bile acids in the saliva as a possible risk factor for early laryngeal cancer. Radiol Oncol 2015; 49: 59–64.
  9. Ates F, Yuksel ES, Higginbotham T, et al. Mucosal impedance discriminates GERD from non-GERD conditions. Gastroenterology 2015; 148: 334–343.

 

Further UEG Resources

“Challenges in GORD” Session at UEG Week 2014.

“Therapy update: GORD” Session at UEG Week 2014.

“New options in gastro-oesophageal reflux disease” Session at UEG Week 2014.

 

 

 

 

 

 

Benign or malignant disease?

The photo shows the findings in a 65 year-old woman.

The photo shows the findings in a 65 year-old woman.

The photograph shows the findings in a 65-year-old woman undergoing investigations for anaemia. Her only medications are ibuprofen for backache and tamoxifen, which was started 7 years previously.

WHAT IS THE MOST LIKELY DIAGNOSIS? 

a) NSAID-induced gastric ulceration

b) CMV gastritis

c) Gastric lymphoma

d) Linitis plastica

e) Gastric metastates

 

 

Is your ward happy?

All health services in Europe are under immense pressure …

I was woken up whilst on call recently by one of the staff nurses on our gastroenterology ward. It had been a busy day and, in addition to five new admissions, one patient—a withdrawing alcoholic—had become encephalopathic and was in the process of using a chair to try to smash through a window on the fifth floor. Earlier in the evening the same nurse had been hit in the mouth when she told another liver patient that he couldn’t go for a cigarette.

The 50 inpatient beds in our ward are always occupied by a mixture of patients who have alcoholic liver disease, inflammatory bowel disease, emergency GI bleeding, infective diarrhoea, GI cancer or eating disorders of such severity that they are unable to maintain their weight let alone their electrolyte balance.

In my opinion, gastroenterology wards are undoubtedly the most challenging in any hospital. No other hospital ward hosts such a wide-ranging mixture of disease, affecting patients of any age and with such severity! In spite of the state-of-the-art care that we provide, we have more deaths on our ward than any other ward in our hospital. This is because our patients are the sickest.

Of course all health services in Europe are under immense pressure. In the UK, the number of patients presenting to GPs and Accident & Emergency departments is increasing, as is the number of patients admitted to hospital.1

As the workload increases, hospital cost cutting has led to a reduction the number of nurses and an increasing pressure to squeeze as much work as possible out of the existing workforce. In the NHS, 12-hour shifts are now the norm. I am sceptical that a 12-hour working day is compatible with the provision of compassionate, expert care to a complex GI patient and would like to see the evidence that this is achievable.

The “Registered Nurse Forecast Study”, published in the Lancet in February 2014, looked at the impact of nursing numbers on patient mortality in 300 hospitals across Norway, Ireland, Netherlands, Finland, Sweden, Switzerland, England, Belgium and Spain.2 The authors found that hospitals in which trained nurses cared for an average of 6 patients had almost 30% lower mortality than in hospitals where nurses cared for an average of 8 patients.

Similarly, a study by Rafferty et al.3 showed that in the UK “Patients and nurses in the quartile of hospitals with the best staffing levels had consistently better outcomes.” Mortality was 31% worse in hospitals where a single nurse cared for 8 patients compared with those hospitals where a single nurse cared for only 4 patients.

Naturally, morale drops as workloads and stress increase. A study by Aiken et al.4 looked at staffing levels at Canadian, American, English and Scottish sites. Higher staffing levels led to higher nurse reported satisfaction with care given, resulting in better nurse retention and reduced burn out.

Similarly a study of the safety and quality of hospital care across 12 European countries and the US concluded that better ratios of patients to nurses were associated with increased care quality and patient satisfaction.5

The UK nursing trade union UNISON conduct an annual survey of workload. In 2014, 51% of nurses said that they did not have sufficient staff numbers to deliver dignified, compassionate care.6 Furthermore, an astonishing 48% of respondents described their organisation as being at risk of a similar situation to "the Staffordshire Hospital".

The Francis report7 into the Staffordshire Hospital scandal concluded that quality of care had become a secondary priority to financial savings. As a result, the Staffordshire Hospital failed in its duty of care to hundreds of patients and families. Patients died needlessly and loved ones were left in the dark without adequate answers or explanations.

There are no European guidelines on minimum nurse staffing levels. In every country, it remains up to each institution to decide how many nurses it should employ. Unfortunately, many hospital managers seem to have no idea of the challenges faced on gastroenterology wards, which have to accommodate the widest range of the most complex conditions in patients aged anywhere between 15 and 115 years old (our oldest ever patient).

Next time you do your ward round, make a note of the patient-to-staff ratio and ask yourself whether it is good enough.

 

References

  1. The King’s Fund. What’s going on in A&E? The key questions answered, http://www.kingsfund.org.uk/projects/urgent-emergency-care/urgent-and-emergency-care-mythbusters (14 January 2015, accessed 7 May 2015)
  2. Aiken LH, et.al. Nurse Staffing and education and hospital mortality in nine European countries; a retrospective observational study. Lancet 2014; 383:1824–1830.
  3. Rafferty AM, et al. Outcomes of variation in hospital nurse staffing in English hospitals: cross-sectional analysis of survey data and discharge records, Int J Nursing Studies 2007; 44: 175–182. 
  4. Aiken LH, Clarke SP and Sloane DM. Hospital staffing, organization, and quality of care: cross-national findings, Int J Quality in Health Care 2002; 14: 5–13. 
  5. Aiken LH, et al. Patient safety, satisfaction, and quality of hospital care: cross sectional surveys of nurses and patients in 12 countries in Europe and the United States. BMJ 2012;344:e1717. 
  6. UNISON. Running on Empty—NHS staff stretched to the limit: UNISON’s staffing levels survey 2014, https://www.unison.org.uk/upload/sharepoint/On%20line%20Catalogue/22245.pdf (14 May 2014, accessed 7 May 2015).
  7. Francis R. Report of the Mid Staffordshire NHS Foundation Trust Public Inquiry Executive Summary, http://www.midstaffspublicinquiry.com/sites/default/files/report/Executive%20summary.pdf (6 February 2013, accessed 7 May 2015).

 

 

 

 

 

 

A 30-year-old diagnosis.

An elderly patient being investigated for iron deficiency anaemia.

The photograph shows what was found in an elderly patient who was being investigated for iron deficiency anaemia.

WHAT IS THE MOST LIKELY DIAGNOSIS?

a) Gastritis associated with Helicobacter pylori infection

b) Gastric cytomegalovirus infection

c) Cameron ulceration

d) NSAID-induced ulceration

e) Ulceration from a diffusely infiltrating gastric cancer

Back to Top