Mistakes in CT for the acute abdomen and how to avoid them
There are many pitfalls to be aware of when requesting/interpreting abdominal CT scans
Abdominal CT (computed tomography) is among the most common imaging tests performed for the investigation of acute abdominal pathology. There are many pitfalls that clinicians and radiologists should be aware of when requesting these studies and interpreting the findings.This article covers ten mistakes frequently made with abdominal CT, focusing on gastrointestinal tract and hepatobiliary pathology. These mistakes and their discussions are based on the available literature where possible and thereafter on our clinical experience.
Mistakes in the use of PPIs and how to avoid them
PPIs are frequently prescribed—being knowledgeable about them is fundamental.
Proton pump inhibitors (PPIs) inhibit gastric acid secretion by blocking the gastric hydrogen potassium ATPase (H-K-ATPase). When omeprazole, the first PPI, became available in 1988, it soon appeared to be more effective than H2 antagonists, and PPIs rapidly became one of the most prescribed drug classes worldwide.1PPIs have proven highly efficient for the management of gastro-oesophageal reflux disease (GORD), gastroduodenal ulcers and in the treatment of Helicobacter pylori infections. PPIs are, however, also commonly prescribed for chronic complaints of dyspepsia and upper abdominal discomfort, for which there is no proof that gastric acid is an underlying pathophysiological factor. Lately, the safety of long-term PPI use has been the subject of debate, because chronic use of PPIs has been linked to several complications, such as vitamin and mineral malabsorption, pneumonia, gastrointestinal infections and dementia.2 For anyone working in gastroenterology, having knowledge of one of the most prescribed drugs in this field is fundamental. As such, we address nine frequently made mistakes when it comes to the use of PPIs, and also hope to disprove some of the misconceptions about PPI use.
Mistakes in alcoholic liver disease and how to avoid them
ALD is multifaceted—its management poses many difficulties and pitfalls.
Alcohol consumption is the most prevalent aetiology for liver cirrhosis in Europe and the third leading risk factor for overall mortality.1,2 In fact, alcoholic liver cirrhosis accounts for almost half a million deaths a year worldwide, corresponding to 50% of all cases of cirrhosis, according to the World Health Organization (WHO).3 Alcoholic liver disease (ALD) is multifaceted, with several cofactors influencing its progression. Patients abusing alcohol can simultaneously have viral hepatitis B or C, or a genetic disease, such as alpha-1 antitrypsin deficiency or haemochromatosis.Alcohol consumption is usually assessed in pure grams per day and has a direct relationship with liver damage. Daily alcohol consumption of >30 g for men and >20 g for women is considered the cut-off volume at which there is a risk of developing alcohol-related liver disease.4 Besides volume, the pattern of consumption is also a significant factor, with heavy episodic drinking (HED) defined as an intake of 60 g or more of pure alcohol on at least one occasion in the past 30 days. Regarding HED, there is scarce information on the threshold to be applied to this pattern of drinking.5 Although the relationship between alcohol consumption and ALD is well defined, it must be acknowledged that severe disease only develops in a fraction of those who consume excessive amounts of alcohol. Nonetheless, the disease course is very much influenced by the pattern of drinking, with periods of abstinence or heavy drinking clearly altering its progression.5 ALD can present in different stages, ranging from steatosis to more severe disease, such as the clinical syndrome of alcoholic hepatitis, or decompensated liver cirrhosis, which is sometimes complicated by liver cancer. In the setting of alcoholic hepatitis, several scores, such as the Maddrey discriminant function, Glasgow alcoholic hepatitis score (GASH) and ABIC, may be used to evaluate disease severity, predict short-term survival, and decide on the need for specific treatment. Later on, the Lille score, which includes the reduction in serum bilirubin levels at day 7, evaluates the response to prednisolone after one week, in order to decide whether to continue or stop treatment.5 Despite being a frequent disease, the different aspects of ALD mean that its management still poses many difficulties and pitfalls. In this article we discuss frequent mistakes in ALD, based on the current guidelines and some paradigmatic real-life cases.
Mistakes in EoE and how to avoid them
EoE is the second-most frequent cause of chronic oesophagitis.
Eosinophilic oesophagitis (EoE) is a chronic immune-mediated inflammatory condition that is confined to the oesophagus. Clinically, EoE is characterized by symptoms of oesophageal dysfunction; histologically, by eosinophil-predominant inflammation.1,2 At present, EoE is the second-most frequent cause of chronic oesophagitis (gastro-oesophageal reflux disease [GORD] is the primary cause) and the foremost cause of dysphagia and food impaction in young adults and children.The first descriptions of EoE date back to the early 1990s,3,4 but at that time the condition was largely underappreciated and treated as GORD. Recognition of EoE grew with the rapid increase of paediatric and adult patients diagnosed since 2003, but so did confusion surrounding diagnostic criteria and treatment. The first consensus guidelines for the diagnosis and management of EoE were published in 2007 and were instrumental in bringing EoE to light as a distinct new condition.5 Since 2007, the diagnostic criteria for EoE have constantly and rapidly changed. New evidence for therapeutic agents has mounted, especially during the past 5 years. Here, we discuss the critical pitfalls that frequently occur in daily practice when dealing with EoE patients. The discussion is evidence based and in line with the recommendations included in the updated guidelines for diagnosis and management of EoE in children and adults.6
Mistakes in liver function test abnormalities and how to avoid them
Liver function tests (LFTs) are routinely used to screen for liver disease, but the assessment of LFTs can be challenging. The LFT itself must be clearly understood and the results interpreted in light of the specific clinical setting.
Liver function tests (LFTs) are routinely used to screen for liver disease. A correct interpretation of LFT abnormalities may suggest the cause, severity, and prognosis of an underlying disease. Once the diagnosis has been established, sequential LFT assessment can be used to assess treatment efficacy.Abnormal LFTs are frequently encountered in clinical practice, since elevation of at least one LFT occurs in more than 20% of the population.1 Many patients with abnormal LFTs, however, do not suffer from structural liver disease, since these tests can be influenced by factors unrelated to significant liver damage or liver function loss. During normal pregnancy, for example, serum albumin levels fall due to plasma volume expansion, and alkaline phosphatase (ALP) levels rise due to placental influx. Patients who have elevated transaminase levels may not suffer from liver disease, but rather from cardiac or skeletal muscle damage. Conversely, patients who suffer from advanced liver disease, such as chronic hepatitis or compensated liver cirrhosis, may have normal LFTs.
In short, the assessment of LFTs can represent a challenge for physicians. The observations above demonstrate the need for a firm understanding of the individual LFT, and the ability to interpret the results in the light of a specific clinical setting. Such an understanding is not merely a goal on its own, but may serve as a template to avoid mistakes in interpreting LFT abnormalities. In the following sections, we discuss several mistakes frequently made in the interpretation of LFTs and how to avoid them. Most of the discussion is evidence based, but where evidence is lacking the discussion is based on extensive clinical experience.
Mistakes in managing perianal disease and how to avoid them
Perianal disease is very common and can impair quality of life significantly. It is crucial to identify the serious causes of these symptoms, but also to reduce the burden of the less dangerous conditions that nevertheless can be debilitating and interfere with an individual’s work and life.
Perianal disease takes many forms, is very common and can impair quality of life significantly. The symptoms of perianal disease, including pain, bleeding, discharge and pruritus, are common to several conditions that are sometimes difficult to disentangle.
It is crucial to identify the serious causes of perianal symptoms, but also to reduce the burden of the less dangerous conditions that nevertheless can be debilitating and interfere with an individual’s work, social or intimate life. Below we discuss some of the frequent and important mistakes made in the management of perianal disease based, where possible, on evidence, and where not, on clinical experience.
Mistakes in endoscopy and how to avoid them
Diagnostic and therapeutic mistakes discussed in the context of evidence and endoscopic experience.
Upper and lower gastrointestinal endoscopy examinations are performed daily as routine diagnostic procedures in a large number of patients with nonspecific indications, such as heartburn, pain, anaemia, bleeding, workup of portal hypertension and so on.Most of the examinations will point to a classic diagnosis (e.g. peptic disease, cancer, variceal management), but sometimes we see patients who've had multiple diagnostic endoscopic procedures in the previous few months with nonconclusive findings. The diagnostic mistakes discussed here are those that sprang to mind based on our endoscopic experience and they are discussed in an evidence-based approach. For therapeutic endoscopic procedures (e.g. ERCP and resections), we present the most important mistakes that are often seen in our practice and have major consequences for the patient. We propose, from our experience, a simple approach to avoid these mistakes.
Mistakes in paediatric functional constipation diagnosis and treatment and how to avoid them
Have a look at the major mistakes that are made when diagnosing and treating children with functional constipation.
Constipation is a bothersome problem for many children. It may present as one or more of the following: infrequent bowel movements with faecal incontinence, hard and often large stools, painful defecation and abdominal pain. No organic cause of the constipation can be found in approximately 95% of children—these children suffer from functional constipation. The prevalence of functional constipation ranges between 0.7% and 29.6% and it occurs in girls more often than in boys (ratio 2.1:1).1The diagnosis of functional constipation is based on the paediatric diagnostic Rome criteria for functional gastrointestinal disorders.2,3 Additional investigations are indicated only if the diagnosis is not clear or in order to rule out an underlying organic disease, such as Hirschsprung disease.4 Education, demystification of constipation, following a reward-based toilet program and keeping a daily bowel diary form part of the nonpharmacological management process.4 Disimpaction, maintenance treatment and weaning of medication are all elements of pharmacological treatment.4 Polyethylene glycol (PEG) is the first-choice laxative for both disimpaction and maintenance treatment; however, if PEG is not available or is poorly tolerated, lactulose is recommended. Other laxatives are available as a second-line or additional treatment if treatment with PEG is insufficient. Here we discuss the major mistakes that are made when diagnosing and treating children with functional constipation. The discussion that follows is evidence based in the majority of cases, but where evidence is lacking the discussion is based on the lead author’s clinical experience of more than 20 years in the field as a paediatric gastroenterologist.
Mistakes in irritable bowel syndrome and how to avoid them
Learn more about the mistakes that can be made when diagnosing and managing IBS!
Around 11% of the worldwide population experience irritable bowel syndrome (IBS), making it one of the most frequent gastroenterological diagnoses.1 The symptoms of IBS include abdominal pain associated with unpredictable bowel habits and variable changes in the form and frequency of stool.2While all patients with IBS suffer from recurrent bouts of abdominal pain, their bowel habits are varied: around one-third suffer predominantly with diarrhoea (IBS-D), one-fifth experience predominantly constipation (IBS-C) and half have an erratic mixed pattern of both diarrhoea and constipation (IBS-M).3 This very heterogeneous condition undoubtedly has multiple causes and an individualized approach to management and treatment is required. Here I discuss the mistakes most frequently made when diagnosing and managing IBS. The mistakes and discussion that follow are based, where possible, on published data and failing that on many years of my own clinical experience.
Mistakes in the management of acute pancreatitis and how to avoid them
Critical decision-making points & pitfalls
Acute pancreatitis is a common inflammatory disorder of the pancreas and its incidence is increasing among hospitalized patients worldwide.
The main symptoms include severe upper abdominal pain (often sudden onset), nausea, vomiting, bloating and the development of ileus. In many cases jaundice will also be present. The diagnosis, as agreed by international consensus, can be established by fulfilling two of the following three criteria: upper abdominal pain of sudden onset, elevation of either serum lipase or amylase activity to greater than three times the upper limit of normal, and imaging findings consistent with inflammation of the pancreas.4–6
By far the most common risk factors for the development of acute pancreatitis are excessive alcohol consumption and gallstone disease. Several mutations have been identified that, in combination with nongenetic factors or alone, can lead to pancreatitis. Certain drugs are known to be associated with the development of pancreatitis and smoking might also increase the probability of it developing. 80–85% of patients diagnosed with the disease will have mild disease and make an uneventful recovery with little more than adequate fluid therapy and analgesia needed to support them. The remaining patients, however, will suffer from moderately severe to severe acute pancreatitis, with the development of pancreatic necrosis, severe sepsis or abdominal compartment syndrome. These patients are at immediate danger of multiorgan failure and death and require multidisciplinary intensive care, organ support and often pancreatic interventions conducted by experienced investigators. Since it is difficult to predict outcomes and complications develop during the disease course, treatment in specialized centres that have a high case load is recommended.4
Here, we discuss critical decision-making points and pitfalls frequently occurring when managing patients with acute pancreatitis. The discussion is based on the medical literature and many years of clinical experience.
In 2009, it was the most frequent diagnosis in patients discharged from GI services in the US and the fifth leading cause of in-hospital mortality.1 Because of this high disease burden, acute pancreatitis is also a substantial contributor to healthcare spending, accounting for an estimated annual spend of US$4–7 million per million inhabitants in western countries.2,3
Mistakes in endoscopic retrograde cholangiopancreatography and how to avoid them
Endoscopic retrograde cholangiopancreatography (ERCP) is a widespread technique used for the treatment of different diseases of the bile and pancreatic ducts.
Endoscopic retrograde cholangiopancreatography (ERCP) is a widespread technique used for the treatment of different diseases of the bile and pancreatic ducts. The technique is, however, associated with rare but potentially severe morbidity.Some of the adverse events associated with ERCP are directly linked to commonly made mistakes and can, therefore, be prevented. Here, we discuss 10 common and/or high-impact mistakes that are made during ERCP and how they can be avoided.
Mistakes in IBD and reproduction and how to avoid them
Find out more about the major mistakes and misperceptions!
Inflammatory bowel disease (IBD) is a chronic relapsing gastrointestinal disease, often affecting young people during their fertile years. The chronic character of IBD means that lifelong medical treatment is often required. As such, it is not surprising that questions often arise about fertility and pregnancy in patients with IBD.The most important risk factor for adverse pregnancy outcomes in IBD patients is the presence of disease activity during pregnancy. Indeed, negative pregnancy outcomes (e.g. spontaneous abortion, preterm delivery and low birth weight) are associated with disease activity at the time of conception and during pregnancy.1–4 The majority of pregnancies in women with quiescent IBD are uncomplicated. This demonstrates the importance of maintaining remission by continuing medication during pregnancy. Counselling patients before pregnancy on the effects of IBD drugs and disease activity on the child in utero is, therefore, of utmost importance. Although much is known about reproduction and IBD, misbeliefs regarding pregnancy and IBD still persist. Here, we present 10 major mistakes and misperceptions that are made when treating IBD patients who wish to reproduce. The list and discussion are evidence based and integrated in our clinical practice.
Mistakes in upper gastrointestinal bleeding and how to avoid them
Discover more about the most frequent mistakes!
Mistakes in mouse models of IBD and how to avoid them
Learn how to get the most from experimental colitis models!
In general, mouse models of colitis are used to study its pathophysiology and for the development of new treatment modalities for inflammatory bowel disease (IBD). For the latter it is essential to select a mouse model that has many overlapping features with human IBD.More than 50 experimental colitis models have been developed and they have provided us with very useful insights into IBD physiology, as reviewed by Bouma and Strober1 and others,2–4 but they have limited use in predicting the clinical relevance of therapeutic targets in IBD.5 Experimental colitis models broadly fit into four different groups. First is spontaneous colitis, resulting from a naturally occurring genetic abnormality. Second is induced colitis occurring as a consequence of a targeted mutation or the introduction of a transgene. Third is induced colitis resulting from administration of different exogenous causative agents. Fourth is induction of colitis by manipulation of the immune system. We have learned a great deal from these models about the involvement of genetics, the microbiota and the role of different cells and the mucus layer in the development of IBD. Here we discuss the major mistakes that are made using experimental colitis models, based on our own experience and the scientific literature. Recently increased awareness has developed for the necessity to improve the methodological quality of animal studies.
Mistakes in colorectal cancer and how to avoid them
Specialist tips on diagnosis, prevention and treatment!
Colorectal cancer (CRC) is one of the most common malignancies and the second leading cause of cancer death in both sexes in developed countries. Over the past 30 years, a great advance in the understanding of this disease has occurred, from colorectal carcinogenesis to diagnosis, prevention and treatment.Although the majority of CRCs are related to environmental factors, up to 25% of cases have a familial component and potential genetic basis, and highly penetrant monogenic germline mutations account for up to 5% of all CRC cases1. Identification and characterization of these hereditary disorders have allowed modification of their natural history, with a substantial decrease in morbidity and mortality among high-risk patients1. Nonetheless, the majority of patients who are at high risk of CRC remain undiagnosed due to lack of suspicion. On the other hand, studies from the past two decades have suggested that besides adenomas, serrated polyps are also precursors of CRC, responsible for up to 15–30% of all malignancies.2 Several studies have demonstrated that serrated polyps are common precursors of colonoscopy interval cancers (cancers diagnosed within the surveillance interval after a complete colonoscopy), mainly due to their challenging clinical management.2 Finally, strategies for CRC prevention have shown efficacy in reducing CRC incidence and mortality, and colonoscopy is an integral part of CRC screening strategies. The main objective of screening colonoscopy is the detection and removal of premalignant lesions or early CRC.3 However, colonoscopy is not perfect, and some lesions may be missed. Colonoscopy quality is an emerging concept, and some quality indicators have been demonstrated to be directly related to the development of interval CRC.3 Here we discuss the major mistakes that are made when gastroenterologists deal with CRC diagnosis, prevention and treatment, and how to avoid them. The list of mistakes and the discussion that follows is evidence based and integrated with our longstanding clinical experience.
Mistakes in dyspepsia and how to avoid them
Expert knowledge at your fingertips!
Dyspepsia refers to upper abdominal discomfort that is thought to arise from the upper gastrointestinal tract. Symptoms include epigastric pain or discomfort, bloating, early satiety and/or fullness after meals, repeated belching or regurgitation (often rumination), nausea and heartburn.1 The symptoms of dyspepsia are nonspecific, but most commonly result from one of four underlying disorders: functional (nonulcer) dyspepsia, gastro-oesophageal reflux disease (GORD; 10–20% erosive esophagitis), peptic ulcer disease (5–15%) and malignancy (~1%).2 Dyspeptic symptoms may also result from other problems, such as medication intolerance, pancreatitis, biliary tract disease or motility disorders (e.g. gastroparesis or gastric dumping).Clinical guidelines recommend that endoscopy is not always required for diagnosis; a positive diagnosis of GORD and functional dyspepsia can be based on clinical presentation in the absence of alarm symptoms or features (see below).3,4 In many cases symptoms are increased after meal ingestion (postprandial distress syndrome), being triggered by impaired gastric accommodation and visceral hypersensitivity to gastric distension.5 Other patients have an epigastric pain syndrome in which discomfort is independent of food intake and gastrointestinal function.6 There is an important overlap between functional dyspepsia and other functional gastrointestinal diseases (e.g. irritable bowel syndrome [IBS]) and chronic pain syndromes (e.g. fibromyalgia).7 Psychological disease (e.g. anxiety or somatization disorder) and/or psychosocial stress are also present in a significant proportion of patients who seek medical attention.8,9 Notwithstanding the constructive advice provided by published reviews and guidelines, the broad definition of dyspepsia, lack of diagnostic investigations, uncertain cause of disease, psychosocial issues and paucity of specific treatments make the management of dyspepsia challenging. Here, I discuss 10 common and/or high-impact mistakes that are made in the diagnosis and treatment of patients with dyspeptic symptoms: five related to diagnosis, five related to treatment.
Mistakes in coeliac disease diagnosis and how to avoid them
Learn from leaders in the field!