Chapter 14

Gastroenterology

Gastroenterology: overview

Gastroenterology: in clinic

Gastroenterology: on the ward

Gastroenterology: in the emergency department

Gastroenterology: in the endoscopy department

Gastroenterology: in exams

Gastroenterology: overview

Gastroenterology is the medical speciality that deals with diseases of the GI system while hepatology deals with diseases of the liver. Although these may be two separate specialties in larger (university) hospitals, liver diseases are managed by general gastroenterologists otherwise. You truly have not looked after a ‘sick’ patient until you have managed liver failure!

On the wards

Paracentesis is drainage of ascitic fluid (accumulation of fluid in the peritoneum due to liver failure, malignancy, and or syndromes). This is usually done when the ascitic volume is so great that it has made the abdomen tense and may lead to abdominal compartment syndrome. Patients may experience abdominal pain, shortness of breath, and difficulty mobilizing at this point. Under aseptic conditions, using local anaesthesia, a plastic drain is inserted through the abdominal wall, usually in the left/right iliac fossa (LIF/RIF) under US guidance to avoid the bowel. IV albumin is given as the ascites is drained to reduce fluid shift and support BP by increasing oncotic pressure. Volumes in excess of 10 L can be drained in one go. Drains are usually removed after 6 hours to reduce the risk of infection. Ascites is an excellent growing medium for microbes image image risk of spontaneous bacterial peritonitis.

Procedures to see

Gastroenterology is a very interventional medical specialty. Most of the procedures will be done in the endoscopy department. Make sure you spend several sessions there so you can see the range of diagnostic and therapeutic work performed.

Things to do

During your placement, ensure you spend time on the wards, in clinic, and in the endoscopy department. Ask about attending MDT meetings. This may include upper or lower GI oncology, nutrition support team, IBD, hepatobiliary, etc. These will give you an impression of the contribution that different professions make to the care of patients with gastroenterological conditions. You may also want to spend time with the MDT members listed in Table 14.1.

Table 14.1 MDT members in GI medicine

Dietician IBD CNS Stoma CNS Nutrition CNS
Colorectal CNS Upper GI CNS Speech and language therapist Alcohol support worker or CNS

Investigations

A day spent in the radiology department seeing patients who have these investigations is a good way to understand what they involve and be able to explain them to your future patients.

Barium/Gastrografin® swallow/meal/enema

Have now largely been replaced by endoscopic investigation, but for patients not able to tolerate endoscopy or in potential oesophageal dysmotility or delayed gastric emptying it remains a useful investigation. The patient drinks a radio-opaque contrast liquid and has serial plain radiographs to show its transit through the GI tract. Distal colorectal pathology can be identified using retrograde PR contrast enema.

CT colonogram

Is an alternative to colonoscopy for some patients who may not tolerate endoscopy. Optimal images may require taking some bowel preparation and drinking an oral contrast agent (faecal tagging). Images are taken in supine and prone positions and compared allowing identification of lesions such as polyps. Biopsies for histological diagnosis or interventions (e.g. polypectomy) are not possible.

MRI

Is used as an investigation modality for complex liver lesions, accurate small bowel imaging in Crohn’s disease (CD), and to assess the biliary tree in magnetic resonance cholangiopancreatography (MRCP) for instance. These procedures often require IV contrast. The presence of metallic implants, claustrophobia, noise intolerance, or inability of the patient to hold their breath for 20 sec may prevent optimal MRI.

Endoscopy

Allows internal visualization of the alimentary canal using a flexible camera. Pictures may also be taken and used for surveillance. It can be used for both diagnostic and therapeutic reasons. Capsule endoscopy has also become popular as a second-line investigation whereby >50,000 images can be recorded from mouth to anus within 8 hours. (See Fig. 14.1)

image

Fig. 14.1 Endoscopic view of an ulcer on the posterior wall of the first part of the duodenum. A gold probe is being used to cauterize bleeding points within the ulcer. Reproduced with permission from Matthew Gardiner and Neil Borley, Training in Surgery: The essential curriculum for the MRCS, 2009, Oxford University Press.

Gastroenterology: in clinic

Non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH)

Fatty deposits within the liver that are not caused by alcohol are called NAFLD. A disease process of fatty change inducing inflammation which progresses to fibrosis then cirrhosis occurs. There is a close relation to metabolic syndrome, obesity, hypercholesterolaemia, and type 2 DM. NASH is the most severe form of NAFLD. Gradual weight loss through image exercise, dieting, or bariatric surgery can improve the histological findings of NAFLD. A third of cases of NASH develop into fibrosis and ~15% progress to cirrhosis over time.

Inflammatory bowel disease (IBD)

Ulcerative colitis (UC)

Affects colonic mucosa diffusely and extends from the rectum proximally in a continuous segment. Rectal disease (proctitis) is the most common form. 10% of patients with UC have total colonic involvement (pan-colitis). Associated with cryptitis and crypt abscess formation. Severe flares can cause toxic megacolon (seen on AXR) or bowel perforation.

Presentation

Presents commonly with diarrhoea, lower abdominal pain, and passing PR blood and mucus. The disease course is relapsing–remitting with acute relapses called ‘flares’. Tools such as the Truelove and Witts' criteria are used to assess the severity of UC activity.

Treatment

Treatment of mild to moderate disease aims to induce then maintain remission and is with local (enema/suppositories) or oral 5-ASAs or steroids and steroid-sparing agents such as azathioprine, mercaptopurine, and ciclosporin. Biological therapies including infliximab, adalimumab, and golimumab can be used in moderately to severely active disease which does not respond to conventional treatment.

Surgical intervention

Is indicated in patients with a poor response to treatment, acute problems such as major bleeds or perforation, necrotizing fasciitis, or if colorectal cancer has developed.

Monitoring

The image risk of colorectal carcinoma in UC makes regular screening using colonoscopy advisable from 10 years post diagnosis of total colitis.1

Crohn’s disease

CD can affect any part of the GI tract in a patchy or discontinuous pattern creating skip lesions.

Pathology

Transmural inflammation with epithelioid, non-caseating granulomata, fibrosis, and stricturing may occur from chronic inflammation. Fistulae (abnormal connections between two epithelial surfaces) can arise as a consequence of fissuring (‘rose thorn’) ulceration.

Presentation

Diarrhoea, malabsorption, weight loss, abdominal pain, and distension due to obstruction or with evidence of fistulae. A relapsing–remitting course is most common with some patients having many years between relapses.

Associations

There is an association with smoking. Genetic predispositions exist, including a link to mutations in the NOD2/CARD15 genes which are found in ~10% of cases.

Treatment

Aims to improve symptoms by inducing and maintaining remission. Oral steroids or an elemental diet are the first-line treatments for an acute flare. Budesonide or 5-ASAs are considered if oral glucocorticosteroids cannot be used. Azathioprine, 6-mercaptopurine, or methotrexate are added in if remission is not gained or steroid dose cannot be tapered down. The biological therapies infliximab, adalimumab, ustekinumab, and vedolizumab can be used in severely active CD which has not responded to conventional treatment. Over half of patients with CD will need surgery at some point to treat obstructing strictures, fistulae, perforations, or if medical therapy fails.2

Honours

Extra-intestinal manifestations of IBD

Include erythroderma nodosum, pyoderma gangrenosum, acute arthritis, uveitis, sacro-ileitis, and ankylosing spondylitis. UC is associated with primary sclerosing cholangitis (PSC).

Most patients with IBD are seen in the outpatient clinic although those with acute severe colitis or complications such as perforations and complex fistulae are managed as inpatients. Aim to see a range of patients with IBD—those in remission and those with active disease as well as those who are pre and post surgery—so that you can understand the spectrum of these diseases.

These are chronic conditions with potentially serious psycho-social effects and the best management is through a MDT approach. Try to understand how the different members of the MDT contribute to the care of patients with IBD. (See Table 14.2.)

Table 14.2 Differences between ulcerative colitis and Crohn’s disease

UC CD
Pathological features
Tissue depth Mucosal (shallow) Transmural (deep)
Pattern Continuous Skip (patchy) lesions
Location Colorectal Oral image anus
Rectal involvement Almost always Sparing
Ileal disease Less common (backwash ileitis) Common
Fistulas Rare Common
Perianal disease Rare Common
Granulomas Rare Common
PR bleed ± mucus +++ +
Smoking Protective Harmful
Colorectal cancer risk Both increase risk (UC >CD)
Endoscopic features
Aphthous ulcers Rare Common
Mucosal friability Common Rare
Vascular pattern Usually normal Commonly distorted
Crypt abscesses Common Rare
Radiological features
Strictures Less common More common (string sign)
Loss of haustra Common (symmetrical)—lead pipe sign Rare (asymmetrical)
Ulceration Collar button Rose thorn
Cobble stone fissuring Rare Common (if severe)

Irritable bowel syndrome (IBS)

A functional disorder of the bowel present for ≥6 months with abdominal pain for ≥1 day/week on average in the last 3 months and ≥2 of the following:

Pain related to defecation.

Change in frequency of stool.

Change in form/appearance of stool.3

Symptoms

Urgency, incomplete evacuation (tenesmus), bloating, and discharge of mucus support the diagnosis. It is important to check for other causes of similar symptoms (e.g. coeliac disease and chronic GI tract infections).

Management

Symptomatic relief with a combination of laxatives (macrogol), antispasmodics (peppermint oil/mebeverine), and antidiarrhoeals (loperamide). Patient education, lifestyle modification, cognitive behavioural therapy, and antidepressants may be effective in reducing symptoms.

Honours

IBS diet

The FODMAP (Fermentable, Oligo-, Di-, Mono-saccharides and Polyols) diet is an exclusion diet that aims to improve symptoms by reducing intake of foods that are poorly digested in the small bowel. Over 75% of patients report an improvement in symptoms after being on the diet.4

Coeliac disease

This is an autoimmune gluten enteropathy. An immunological response to the α-gliadin fraction of gluten, which is a protein found in wheat, rye, barley, and similar grains, causes a lymphocytic enteritis with villous atrophy. Clinical manifestations can include weight loss, abdominal pain, diarrhoea, iron-deficiency anaemia, and other micro-nutrient deficiencies. Diagnosis is based on serology with anti-endomysial or anti-tissue transglutaminase (anti-tTG) levels and histology of duodenal biopsies (Marsh classification) taken at oesophagogastroduodenoscopy (OGD). Treatment is with a life-long gluten-free diet with advice from a dietician.

Honours

Coeliac disease diagnosis

Most people with coeliac disease have human leucocyte antigen (HLA)-DQ2 or HLA-DQ8 serotypes. In cases of diagnostic uncertainty, HLA-DQ haplotyping can be useful. The HLA system is a gene complex encoding MHC cell surface proteins that are responsible for the regulation of the human immune system.

Nutritional deficiencies

Individual micronutrient deficiencies are relatively rare in the general population but may be more common in subgroups such as those with alcohol dependence, concurrent medical problems, hospitalization, or restrictive diets (vegans). Rates of detection of vitamin D deficiency are increasing in the UK.

Gastro-oesophageal reflux disease (GORD)

Recurrent reflux of gastric contents or secretions into the oesophagus can cause heartburn (dyspepsia), regurgitation, and dysphagia or odynophagia. An incompetent lower oesophageal sphincter is often implicated. Lifestyle and diet modifications such as attaining normal weight, eating a low-fat diet, and not eating within 2 hours of going to bed are usually tried first. PPIs such as omeprazole/lansoprazole can reduce gastric acid secretion, raise the pH of the gastric content, and reduce the irritation caused by the proximal reflux. Surgical treatment with Nissen fundoplication is usually reserved for refractory cases (proven by oesophageal pH studies) and has been largely minimized after the introduction of PPIs.

Gastritis

Inflammation of the stomach is very common and may coexist with GORD. Symptoms are those of dyspepsia and include epigastric pain and heartburn. Common causes are Helicobacter pylori infection (Gram-negative, flagellate bacterium), alcohol, and NSAID use. Lifestyle modification such as weight loss, stopping smoking, and moderating alcohol, spicy food, and caffeine intake may reduce symptoms. A PPI is first-line treatment. If symptoms do not improve on high dose PPIs, perform an OGD to assess for other causes.

Peptic ulceration

This term encompasses gastric and duodenal ulceration. An ulcer is the dissolution in continuity of an epithelial surface.

Aetiology

H. pylori is associated with 95% of duodenal ulcers and 70% of gastric ulcers. NSAIDs and smoking (and rarely malignancy) are common causative factors. Gastric ulceration can also be caused by corticosteroids, CD, and TB. Duodenal ulceration has been linked to stress and having blood group O although the mechanism for this is not clear.

Presentation

Epigastric pain ± signs and symptoms of anaemia such as lethargy, shortness of breath, or bleeding including haematemesis or melaena.

Treatment

This is with high-dose PPIs (IV infusion for 72 hours if an actively bleeding ulcer is seen on OGD) and eradication of H. pylori with a triple therapy that combines two antibiotics (clarithromycin/metronidazole/amoxicillin) and a PPI (esomeprazole/lansoprazole/omeprazole/pantoprazole) for 7 days.

Barrett’s oesophagus

Is the replacement of normal squamous epithelium with metaplastic columnar epithelium in the oesophagus visible at ≥1cm from the gastro-oesophageal junction and confirmed on biopsies through OGD.

Screening and surveillance

It is most commonly an incidental finding, however screening endoscopy could be offered to patients with chronic GORD symptoms and three or more factors of age >50 years, white race, male sex, and obesity. Surveillance endoscopies and biopsies are advised (depending on the length of the Barrett’s segment and histological findings) because surveillance correlates with earlier detection and improved survival from oesophageal adenocarcinoma.

Treatment

Involves optimizing antireflux medications (e.g. PPI) and surveillance. If high-grade dysplasia is detected, endoscopic resection or radiofrequency ablation can be offered. Biopsies that detect oesophageal adenocarcinoma should trigger MDT discussion at a centre where both surgical (oesophagectomy) and endoscopic treatment could be offered.

Refeeding syndrome

In patients who have been starved or had very low enteral intake for any reason for a period of time, the possibility of metabolic disturbance (especially low phosphate) known as refeeding syndrome should be considered. Daily blood tests should be done until feeding is established and deficiencies actively corrected. Look out for patients who may be at risk of refeeding on the wards and ask your team about how they are managing them.

Obesity

A BMI >30 kg/m2 is defined as obese. Rates of obesity in the UK are growing and pose a substantial public health problem. Surgical and endoscopic interventions for obesity (bariatric surgery) including gastric banding/balloons and sleeve gastrectomy are also becoming more widespread. Dietician support in conjunction with surgery is usually offered to ensure that the more restrictive postoperative diet meets an individual’s nutritional needs. You may see patients in gastroenterology clinic as part of a MDT approach to management. (See Table 14.3.)

Table 14.3 BMI = weight (kg)/height2 (m)

BMI class Definition
>35 Severely obese
30–34.9 Obese
25–29.9 Overweight
20–24.9 Normal
16–19.9 Underweight
<16 Severely underweight

Diarrhoea

This is a symptom, not a diagnosis. It can be defined as passing more than three unformed (Bristol Stool Chart type 5–7) bowel motions/day.

History

Duration of symptoms, number of stools/day, consistency, colour and presence of blood or mucus mixed in, with or on the paper at the end of a motion. Clues to the cause of the diarrhoea should be sought: unwell contacts, unusual foods (takeaways/buffets), travel, occupational exposure (healthcare workers, jobs with risk of sewage exposure), or recent medications including antibiotics.

Aetiology

The most common cause of acute diarrhoea is gastroenteritis: viral (e.g. norovirus) and bacterial (Escherichia coli, Campylobacter, and Salmonella) causes are common. For those with a recent travel history, parasitic infection should be suspected and stool samples sent for ova cysts and parasites. Patients who have had recent courses of (broad-spectrum) antibiotics (especially the elderly or the immunosuppressed) should be considered at risk of Clostridium difficile until stool samples come back negative.

Recurrent episodes of diarrhoea without a clear cause should be investigated for other differentials including IBD, irritable bowel syndrome, and colorectal cancer (especially in the elderly).

Treatment

Immunocompetent adults who are able to maintain oral fluid intake rarely need to be admitted to hospital. Admission is for supportive care with oral or IV fluids and rehydration solutions (containing Na+ and K+ which can both be lost), especially for those struggling with maintaining oral intake, who are severely dehydrated, or have profound electrolyte disturbances. Empirical antibiotics are not routinely used but may be considered in cases such as suspected C. difficile, outbreaks, IBD, or if immunocompromised.

Constipation

This is another symptom rather than a diagnosis. It should be qualified with a cause or mechanism. Constipation can be defined as passing fewer small-volume stools than the patient usually passes. An objective measure could be fewer than three stools in a week.

Presentation

Some people with constipation may pass very small-volume, hard lumps of faeces more frequently but they will not have complete evacuation with each motion. Constipation can cause abdominal pain, perianal pain, haemorrhoids, and anal fissures if very large, hard stools are passed. Faecal impaction occurs when a build-up of solid faeces in the rectum cannot be passed, and if enemas fail, may require manual evacuation.

Investigations

These include AXR and digital rectal examination.

Aetiology

Constipation is often multifactorial. Causes consist of a diet low in fibre, dehydration, sedentary lifestyle, and anxiety.

Treatment

Chronic constipation that has not improved with lifestyle and laxative treatments may be considered for further investigations including anorectal manometry and input from colorectal or biofeedback nurse specialists. Inpatients are likely to have drug-related constipation. Co-prescription of laxatives and antiemetics with opioids is considered good practice to prevent iatrogenic side effects. Try to address hydration, diet, and mobility as well as prescribing short courses of laxatives if needed for inpatients to prevent recurrence. (See Table 14.4.)

Table 14.4 Laxatives

Class Example Mechanism Notes
Bulk-forming Methylcellulose, ispaghula husk Stimulate peristalsis by increasing stool bulk Must be taken with fluids to prevent obstruction Dietary bran along with liquid such as fruit juice is an alternative
Osmotic Macrogol Lactulose Phosphate enemas Draw or keep water in the bowel to produce soft, large-volume motions Must be taken with fluids to prevent obstruction Can be given in increasing amounts in a disimpaction regimen May cause bloating and abdominal pain Enemas are often used before investigations or if large, hard faecal mass is palpable on rectal exam
Faecal softeners Arachis oil enemas Liquid paraffin Docusate sodium Soften faecal matter—easier to pass especially if haemorrhoids or anal fissure present Arachis oil is peanut oil—avoid in nut allergy Liquid paraffin is rarely used and only suitable for short periods of time Docusate sodium has both stimulant and non-ionic softener effects
Stimulants Senna Docusate sodium Bisacodyl Glycerol suppositories Increase intestinal motility May cause abdominal pain and bloating. Avoid in intestinal obstruction Suppositories cause local irritation encouraging defaecation

Hepatitis B

A double-stranded DNA blood-borne virus. Spontaneous clearance is common in adults, but 5–10% of infected people will be chronic carriers. 3% will have chronic active hepatitis. Two-thirds of patients who are diagnosed with hepatitis B present with jaundice.

Vaccination

In the UK, universal vaccination for infants was introduced in August 2017. In addition, vaccination is offered to high-risk individuals including healthcare workers, injecting drug users, and sexual contacts.

Blood tests

For hepatitis B, include surface and e antigens; surface, core, and e- antibodies; and HBV DNA levels (see Table 14.5).

Table 14.5 Immunology of hepatitis B

Diagnosis HBsAg HBsAb HBcAb HBcIgM HBeAg HBeAb HBV DNA (IU/mL) ALT
Acute HBV + + + + ± image image
Resolved HBV + + ± 0

image

HBV vaccination immunity + 0

image

HBV reactivation + + ± ± ± ≥1 image
Immune tolerant [HBeAg+ chronic infection] +++ + + >107

image

Immune active [HBeAg+ chronic hepatitis] ++ + + ± 104–107 image
Inactive carrier [HBeAg- chronic infection] + + + 1–2000

image

Immune escape [HBeAg- chronic hepatitis] ++ + + >2000 image

ALT, alanine aminotransferase; HBcAb, hepatitis B core antibody; HBcIgM, hepatitis B core immunoglobulin M; HBeAb, hepatitis B e-antibody; HBeAg, hepatitis B e-antigen; HBsAb, hepatitis B surface antibody; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; [new classification].

Treatment

For active hepatitis B (HBV DNA >2000 IU/mL and ALT >40 IU/L) is with nucleos(t)ide analogues (tenofovir/entecavir) which suppress viral replication. Treatment may be lifelong, but can sometimes be stopped if HBeAg seroconversion occurs and HBV DNA is undetectable. See European Association for the Study of the Liver guidelines for further details (image www.easl.eu/medias/cpg/management-of-hepatitis-B-virus-infection/English-report.pdf).

Hepatitis C

A single-stranded enveloped RNA virus. Up to a third of patients are jaundiced at the time of identification indicating hepatic impairment. There is no effective immunization. Tests are antibody levels and viral RNA levels. Genotyping is also necessary to guide treatment. Non-invasive transient elastography (Fibroscan®) can assess the degree of fibrosis/presence of cirrhosis. Traditionally, the immuno-modulators ribavirin and interferon were used over 6–12 months but sustained virological response (SVR) or cure rates were poor. The advent of oral, directly acting antivirals (DAAs) such as Harvoni® (sofosbuvir/ledipasvir) and Zepatier® (elbasvir/grazoprevir) make almost all hepatitis C curable with a short treatment course with few side effects.

References

1. NICE (2013). Ulcerative Colitis: Management. Clinical Guideline 166. London: NICE. image www.nice.org.uk/guidance/cg166

2. NICE (2016). Crohn’s Disease: Management. Clinical Guideline 152. London: NICE. image www.nice.org.uk/guidance/cg152

3. Rome Foundation (2016). Rome IV Diagnostic Criteria for Functional Gastrointestinal Disorders. Raleigh, NC: Rome Foundation. image https://theromefoundation.org/

4. Staudacher HM, Whelan K, Irving PM, Lomer MC. (2011). Comparison of symptom response following advice for a diet low in fermentable carbohydrates (FODMAPs) versus standard dietary advice in patients with irritable bowel syndrome. J Hum Nutr Diet 24(5):487–95.

Gastroenterology: on the ward

Clostridium difficile infection

C. difficile is a spore-forming anaerobe carried in the gut of up to 3% of adults. Infection usually only follows disturbance of normal gut flora because of treatment with antibiotics. Thus C. difficile diarrhoeal illness is almost all iatrogenic.

Prevention

Shorter, narrow-spectrum courses of antibiotics and meticulous attention to infection control including hand washing with soap and water are effective preventative measures.

Treatment

This should be in line with local guidelines but is likely to range from oral metronidazole or vancomycin (for mild disease) to IV vancomycin, IV immunoglobulin, and oral fidaxomicin or adjunctive rifampicin for severe disease. Complications where pseudomembranous colitis develops into a toxic megacolon (colon >10 cm on AXR) is treated with surgical colectomy if the patient is deteriorating.

Liver diseases

There is a growing burden of liver disease in the UK. An estimated one in ten people in the UK have some form of liver disease. Liver disease is the only one of the five leading causes of death in the UK where mortality rates are increasing. The average age of death from cirrhosis is around 20 years lower than that of cardiovascular disease.1

Aetiology

The four leading causes of liver disease in the UK are NAFLD, alcohol-related liver disease, hepatitis C, and hepatitis B. Never judge when enquiring about alcohol intake, or events that may have led to blood-borne virus infection.

Transplant

Unlike in end-stage renal disease, there is no effective mechanical support for liver function in end-stage liver disease. Nearly 800 liver transplants are carried out in the UK each year. Demand for liver transplant exceeds the supply of donor organs and approximately one in ten patients on the waiting list die before they receive a liver transplant.

Treatment

You will find patients with liver disease in gastroenterology/hepatology clinics as well as on general medical and gastroenterology wards. Those with advanced or acute disease may be in HDU/ITU. If your hospital provides treatment for viral hepatitis, these patients may be seen in a dedicated clinic with MDT input. To understand the range of liver disease, try to see a variety of patients in different settings and follow them up.

Cirrhosis

Aetiology

Causes can be remembered as HEPATIC:

Haemochromatosis

ETOH

Post hepatic (drug induced)

Autoimmune

alpha-1 anti-Trypsin deficiency

Infection (hepatitis B or C virus)

Congestive (cardiac, cancer, or cholestatic).

Pathology

Regardless of the cause of chronic liver disease, the final common pathway is fibrosis followed by cirrhosis. Cirrhosis is a diffuse process in which the normal lobular architecture of the liver is destroyed and replaced by structurally abnormal nodules of parenchyma separated by bands of fibrosis. It is irreversible and represents the end stage of liver disease.

Diagnosis

Cirrhosis is traditionally a histological diagnosis, requiring liver biopsy. However, non-invasive imaging modalities such as US, CT, MRI, and transient elastography can often permit diagnosis without risky biopsy.

Complications

Cirrhosis increases resistance in the liver causing portal hypertension which causes complications such as varices and splenomegaly. Severity can be measured by the Child–Pugh scoring system (Table 14.6).

Table 14.6 Child–Pugh score

1 2 3
Bilirubin (µmol/L) <34 35–50 >50
Albumin (g/L) >35 28–35 <28
INR <1.7 1.7–2.3 >2.3
Ascites None Mild Moderate–severe
Encephalopathy None Grade 1–2 Grade 3–4
Scores for each item are added together.
Points 5–6 7–9 10–15
Class A B C
1-year survival (%) 100 81 45
Compensated vs decompensated

Patients with cirrhosis who are stable and have enough liver function to meet essential requirements are described as compensated. Those who have developed jaundice, hepatic encephalopathy, varices (oesophageal, umbilical, or rectal), ascites, or coagulopathy are described as decompensated.

Decompensation can be triggered by a variety of factors such as infection, development of hepatocellular carcinoma, GI tract bleeding, or exposure to toxins including alcohol. When examining patients with liver disease, it is useful to consider the following:

Are they compensated or decompensated?

Are there features of poor synthetic function?

Multiple bruises/oedema/leukonychia.

Are there extra-abdominal stigmata of chronic liver disease?

Clubbing/palmar erythema/Dupuytren’s contracture/leukonychia/more than 5 spider naevi in the SVC distribution/muscle wasting/gynaecomastia (pseudo in obesity)/excoriations from cholestatic pruritus (treated with colestyramine/rifampicin/ opioid antagonists/ursodeoxycholic acid).

Complications of liver disease

Ascites

image Hydrostatic pressure in the portal vein, image sodium and water retention, and reductions in plasma oncotic pressure because of lower levels of albumin result in image transduction. This results in fluid shifts into third spaces including the abdominal cavity. The fluid within the peritoneum is ascitic fluid.

Management

Ascites can be drained by paracentesis, however fluid will re-accumulate so management with a low-salt diet, fluid restriction, and diuretics is preferable to serial drainage. Spontaneous bacterial peritonitis is a risk with ascites. Any patient with ascites who also has signs of sepsis or newly decompensated liver disease, should have a sample taken for urgent MC&S.

Complication

Continuing accumulation image tense abdomen, followed by signs of abdominal compartment syndrome (i.e. intra-abdominal organ ischaemia image reduced urine output).

Peripheral oedema

Low plasma oncotic pressure also results in fluid shifts into peripheral and dependent places causing pitting oedema. Management consists of low-salt diet, fluid restriction, and diuretics.

Hepatic encephalopathy

This is a disturbance of normal cerebral function caused by image toxins including ammonia. Ammonia is produced as proteins are converted to carbohydrates and is usually converted to urea by the liver. In cirrhosis, ammonia levels can rise causing initially lack of attention, tremor, ataxia, and poor coordination.

At higher levels or in acute rises (seen in blood test), ammonia can cause cerebral oedema which can cause coma, decerebration, and death.

Honours

See Table 14.7.

Table 14.7 Hepatic encephalopathy grades

Grade Symptoms Signs GCS score
1 Poor attention Tremor, ataxia, poor coordination 15
2 Lethargy, disorientation, change in personality Asterixis, ataxia, dysarthria 11–15
3 Confusion, somnolence 8–11
4 Coma Decerebration <8
Management

Lactulose should be prescribed to patients with cirrhosis and titrated to give at least two soft bowel motions per day to reduce GI tract protein loading and inhibit the production of ammonia by bacteria in the gut. Rifaximin is an antibiotic that is used for prevention of recurrent encephalopathy.

Oesophageal varices

Portal hypertension causes development of varicosities at the portal–systemic anastomoses (lower oesophagus, rectum, and periumbilicus). The periumbilical varices appear as caput medusae. Oesophageal and gastric varices are seen on OGD. They can obstruct the GI tract and spontaneously burst causing variceal bleeding which can be life-threatening (see image pp. 328329 for details of treatment for upper GI bleeding).

Management

Non-selective beta blockade (propranolol or carvedilol) to reduce pressure in the varices or serial endoscopies to obliterate varices by banding.

Hepatocellular carcinoma (HCC)

This is a primary liver neoplasm (also known as hepatoma). Cirrhosis predisposes to developing HCC with a risk of ~3%/year. Patients with established cirrhosis should undergo surveillance for HCC every 6 months with serial LFTs, alpha-fetoprotein (AFP), and US monitoring.

Alcohol-related liver disease

Repeated exposure to alcohol at hazardous or harmful amounts causes fatty change which can progress to steatohepatitis, then fibrosis and cirrhosis.

Recommendation

Maximum alcohol intake is 14 units per week. If drinking up to 14 units a week, it is best to spread drinking evenly over 3 or more days.

Symptoms

Symptoms of alcohol-related liver disease include fatigue, jaundice, and weight loss. Any feature of cirrhosis may occur as the disease progresses.

Abstinence

Abstinence from alcohol is a worthwhile intervention at any disease stage as there may be incremental improvement in liver function for up to 6 months after stopping alcohol exposure. All patients with cirrhosis should be advised to abstain from alcohol as liver impairment can be multifactorial. Active drinkers are excluded from transplantation waiting lists.

Management

Patients who do show dependent drinking behaviours should have supported alcohol withdrawal (with vitamins, minerals, and chlordiazepoxide or a short-acting benzodiazepine) to avoid delirium tremens which can occur if alcohol intake is rapidly stopped. Ongoing psychological and/or pharmacological (acamprosate/naltrexone/disulfiram) support can help to maintain sobriety.

Acute alcoholic hepatitis

Presents with symptoms of fatigue, weight loss, fever, RUQ pain, and jaundice. The severity of the hepatitis can be assessed using the discriminant function. Scores >32 have the worst prognosis and should be considered for treatment with steroids (if sepsis is excluded) and referral to a local or regional liver unit.

Fulminant liver failure

The time from the onset of jaundice to the development of hepatic encephalopathy is measured to allow categorization of patients (Table 14.8).

Table 14.8 Duration of liver failure

Hyperacute liver failure <7 days
Acute liver failure 8–28 days
Subacute liver failure 4–12 weeks

Paracetamol toxicity remains the leading cause of fulminant liver failure in the UK, despite restrictions on the number of paracetamol tablets that can be sold in a single transaction.

Management

Patients who have toxic levels of paracetamol that are above the treatment line (see image BNF) or who have taken a staggered overdose should be treated urgently with IV N-acetylcysteine. Those with significant overdose and features of liver impairment should also receive supportive care and be discussed with a regional liver unit. Super-urgent liver transplantation is considered for those patients who may not survive more than a few days without transplantation.

Other liver diseases

You may see cases of other liver diseases including haemochromatosis, Wilson’s disease, alpha-1 anti-trypsin deficiency, primary biliary cholangitis (PBC), PSC, autoimmune hepatitis, Budd–Chiari syndrome, and infiltrative diseases such as amyloidosis and sarcoidosis. Useful aspects to think about when seeing patients with these conditions would include general supportive care, specific treatments (such as venesection for haemochromatosis), indications for liver transplant assessment, and when screening of family members is advisable.

Liver function tests (LFTs)

A group of blood tests including bilirubin, albumin (Alb), alkaline phosphatase (ALP), ALT, aspartate transaminase (AST), and gamma glutamyl transpeptidase (GGT) are referred to as LFTs. Other parameters including Hb concentration, mean cell volume (MCV), platelet count, urea, creatinine (Cr), and INR are also useful to assess liver disease. Try to look at the LFTs of patients with a range of causes and stages of liver disease so that the patterns (e.g. obstructive (ALP and GGT rise >ALT and AST rise); hepatitic (AST and ALT rise >ALP or GGT rise)) become familiar. See Table 14.9 for LFT abnormalities.

Table 14.9 Liver function test abnormalities

Disease ALT AST GGT ALP
Viral hepatitis +++ +++ ++

image

/+
Drug hepatitis ++ ++ ++

image

/+
Chronic hepatitis ++ ++ ++ ++
Epstein–Barr virus (EBV) hepatitis ++ ++ ++

image

PBC ++ ++ +++ ++
ETOH cirrhosis

image

++ +++

image

/+
NAFLD/NASH ++ + ++ +
Intrahepatic cholestasis ++ ++ +++ ++
Extrahepatic cholestasis ++ ++ +++ +++
Hepatoma

image

/+
++ ++ ++

Pancreatitis

This is acute or chronic inflammation of the pancreas. Damage to pancreatic cells liberates digestive enzymes which damage tissues causing local inflammation and necrosis.

Aetiology

Common causes are GET SMASHED:

Gallstones

ETOH

Trauma

Steroids

Mumps

Autoimmune

Surgery

Hyperlipidaemia (or hypercalcaemia or hypothermia)

Endoscopic retrograde cholangiopancreatography (ERCP)

Drugs (and toxins).

In most hospitals, acute pancreatitis is managed on surgical wards or in HDU/ITU if very severe. Patients with chronic pancreatitis who experience flares of upper abdominal pain are often managed by gastroenterology teams and so may be found on medical wards.

Presentation

Classically, patients present with severe upper abdominal pain that radiates through to the back. The inflammation may produce a SIRS picture. Those with chronic pancreatitis may also have weight loss, diabetes, steatorrhoea (high fat content in faeces, which may look like slimy stools which float and are difficult to flush), and malabsorption causing micronutrient deficiency (especially of the fat-soluble vitamins).

Scoring

In acute episodes, serum amylase is usually elevated to more than three times normal but is not included in the scoring. All patients who present with acute pancreatitis should have a severity score (e.g. modified Glasgow score) calculated to guide treatment and appropriate place of care (Table 14.10).

Table 14.10 Modified Glasgow Pancreatitis Score: PANCREAS

Metric Value
PaO2 <8 kPa
Age >55 years
Neutrophilia WCC >15
Calcium <2 mmol/L
Renal function Urea >16 mmol/L
Enzymes Lactate dehydrogenase (LDH) >600 IU/L or AST >200 IU/L
Albumin <32 g/L
Sugar >10 mmol/L

Patients with a Glasgow score of 3–4 have ~15% mortality and management in HDU for continuous monitoring is appropriate.

Management

Management of acute pancreatitis is mostly supportive with analgesia (avoid NSAIDs as these can cause pancreatitis), oxygen, IV fluids, jejunal or parenteral nutrition to rest the pancreas, and thromboprophylaxis. ERCP is considered if US and MRCP show obstructing gallstones. Surgical intervention for necrosectomy is rare, only done in severe disease, and a poor prognostic factor. The most important prognostic measurement is CRP which again is not part of the severity score.

Discussion with the boss

When to start antibiotics in pancreatitis? Since the inflammatory process is sterile from gallstones or alcohol, antibiotics are reserved after onset of opportunistic pathogens or necrosis.

Chronic disease

Amylase may be normal in chronic pancreatitis where the disease is burnt out. Faecal elastase testing is used to assess for pancreatic insufficiency. AXR or CT may show calcification of the scarred, fibrotic pancreas. Patients with chronic pancreatitis are supported with analgesia, PPIs, and pancreatic enzyme replacement (e.g. Creon®) that needs to be taken with all meals and snacks. Advice and support to avoid triggers (e.g. alcohol) should be given. Patients need to be monitored for the development of diabetes. Pain in chronic pancreatitis can be difficult to manage and early involvement of specialist chronic pain services can be beneficial.

Pancreatic tumours

Investigations

They are often investigated and managed on urgent suspected cancer or 2-week wait pathways and undergo their investigations (Ca 19-9 tumour markers, CT abdomen, ERCP for histology brushings, endoscopic US) on an urgent outpatient basis. The upper GI MDT is a good opportunity to hear about patients who are being investigated or admitted for ERCP and stent placement if they have obstructive jaundice.

Symptoms

These include weight loss and jaundice ± abdominal pain.

Examination

Courvoisier’s law states that a palpable gallbladder with jaundice is likely due to a pancreatic neoplasm.

Type

Most pancreatic tumours are adenocarcinoma and 80% of these are metastatic (often to the liver) at the time of first presentation.

Management

For metastatic disease, the approach is palliative with the option of chemotherapy if performance status allows. Patients with local disease and good functional status may be offered surgery at specialist centres. A Whipple’s pancreatoduodenectomy is major surgery with mortality ranging from 3% to 15%. 1- and 5-year survival rates for pancreatic cancer in the UK are <20% and <4%, respectively.

Reference

1. Kaner E, Newbury-Birch D, Avery L, et al. (2007). A Rapid Review of Liver Disease Epidemiology, Treatment and Service Provision in England. Newcastle: Institute of Health and Society, Newcastle University.

Gastroenterology: in the emergency department

Acute upper GI bleeding

A patient with an acute upper GI bleed is a medical emergency. Large volumes of blood can be lost before the bleeding becomes apparent.

Presentation

Haematemesis (vomiting fresh or altered blood including ‘coffee grounds’) or melaena (passage of altered blood PR in the form of black, offensively smelling, tar-like stools). Peptic ulceration is the commonest cause.

Aetiology

Peptic ulceration, mucosal inflammation (oesophagitis, gastritis, or duodenitis), oesophageal varices, Mallory–Weiss tear, gastric carcinoma, and coagulation disorders. Ask about alcohol intake and medication history (warfarin, NSAIDs, aspirin, clopidogrel).

Investigations

FBC shows a fall in Hb and U&E may show a rise in urea (especially if melaena present). If an unstable patient has a low Hb but no overt blood loss, a PR exam to assess for occult melaena is mandatory after resuscitation. Patients with prolific haematemesis can be daunting to see but a methodical approach gives critically ill patients the best chance of survival.

Risk scores

The Rockall and Blatchford scores can be used to predict mortality and likelihood of needing blood transfusion/endoscopic intervention in the next 24 hours.

Management

Address Airway, Breathing, and Circulation (ABC).

High-flow O2 and two large (14 G) IV cannulae.

FBC, clotting, U&E, glucose, group & save/X-match (4–6 U).

If SpO2 <93% check ABG. Consider CXR and ECG.

Give IV crystalloid/blood (aim to maintain Hb at >7 g/dL).

If unstable with low Hb, use type-specific or O-negative blood.

Correct coagulopathy (platelets >50 and INR <1.5).

If the patient is anticoagulated or has a clotting disorder (e.g. liver disease), discuss with a haematologist and give vitamin K/clotting factors/fresh frozen plasma accordingly.

If varices are suspected, give terlipressin IV and prophylactic antibiotics.

Keep fasted. Refer to specialist for admission and endoscopy.

Urinary catheter if severe bleeding to measure urine output.

Consider inserting a central line to guide fluid management.

Endoscopy

Patients with acute GI bleeding should undergo OGD within 24 hours or on the next working day. Those who are haemodynamically unstable should have an OGD within 2 hours of being stabilized. This requires team-working and liaison between the ED, medical, gastroenterology, endoscopy, and anaesthetics teams. Patients undergoing emergency endoscopy should be discussed with the surgical team in case endoscopic therapy fails and an open approach is needed. Emergent endoscopy is usually done under GA. Endoscopic treatment depends on the type and site of lesion but may include local injections of adrenaline (epinephrine), applying clips, or thermal coagulation. Patients with non-variceal bleeding with stigmata of recent bleeding on endoscopy should have an IV PPI infusion (pantoprazole/omeprazole).1

Variceal bleeding

Patients with known or suspected cirrhotic liver disease (jaundice, abdominal distension with ascites, stigmata of chronic liver disease) who present with an acute GI bleed should be treated as having variceal bleeding. Resuscitate as for acute GI bleeding and give prophylactic IV antibiotics and terlipressin. If bleeding oesophageal varices are found at endoscopy, elastic bands (‘banding’) can be placed to stop the blood loss. Patients with suspected variceal bleeding who, despite resuscitation, are not stable for endoscopic intervention or where endoscopic intervention does not control bleeding can have a Sengstaken–Blakemore/Minnesota tube inserted to attempt to tamponade the bleeding point. Endoscopy is then attempted 12 hours later. Transjugular intrahepatic portosystemic shunt (TIPS, Fig. 14.2) is a rescue interventional radiological procedure for intractable variceal bleeding.

image

Fig. 14.2 An illustration of a TIPS placed for portal decompression. Reproduced with permission from Bhogal HK, Sanyal AJ. Using transjugular intrahepatic portosystemic shunts for complications of cirrhosis. Clin Gastroenterol Hepatol. 2011 Nov;9(11):936–46; quiz e123.

Reference

1. NICE (2016). Acute Upper gastrointestinal Bleeding in Over 16s: Management. Clinical Guideline 161. London: NICE. image www.guidance.nice.org.uk/CG141

Gastroenterology: in the endoscopy department

Endoscopy means looking at the inside. Flexible digital cameras (endoscopes) are used which allow specifically designed instruments to be passed down an internal channel in the endoscope to allow interventions such as taking biopsies and removing polyps. All endoscopies require written informed consent. It is useful to see this aspect of the procedure so you can understand the risks and benefits. Risks include infection, perforation, bleeding, failure of diagnosis and treatment, need for future endoscopies, and a small risk of mortality.

Oesophagogastroduodenoscopy (OGD)

OGD of the upper GI tract is used to investigate symptoms such as dyspepsia, dysphagia, epigastric pain, anaemia, or to treat GI tract bleeding or obstruction. Local anaesthetic to the pharynx ± conscious sedation (with e.g. midazolam) is used.

Colonoscopy

Requires patients to take bowel preparation (strong laxatives) prior to endoscopy to ensure the colon is empty and the mucosa can be clearly seen. IV analgesia ± sedation or Entonox® is given. It is used to investigate a change in bowel habit, PR bleeding, anaemia, and lower abdominal pain, as surveillance in those at high risk of colonic polyps, and as a treatment for volvulus or obstruction where palliative stenting is the only option. The aim is to visualize the entire colon and terminal ileum. Polyps can be snared and retrieved (polypectomy) and tissue biopsies can be taken for histological diagnosis of cancer, IBD subtype, and other causes of colitis. (See Fig. 14.3.)

image

Fig. 14.3 Colonoscopy. Reproduced with permission from Graham J MacKay et al, Colorectal Surgery, 2010, Oxford University Press, and from Daniel Marks and Marcus Harbord, Emergencies in Gastroenterology and Hepatology, 2013, Oxford University Press, and with kind permission from the Chelsea and Westminster Hospital.

Flexible sigmoidoscopy

Examines the left side of the colon up to the splenic flexure, usually without sedation. Can be done after bowel preparation or in cases of possible acute colitis unprepared or after a single enema. This is the procedure used for the UK-wide bowel scope screening programme.

Percutaneous endoscopic gastrostomy (PEG)

This is the insertion of a permanent feeding tube through the abdominal wall into the stomach using PO endoscopic guidance. Sedation and local anaesthesia are used. Indications include swallowing problems after CVA, neurodegenerative diseases, or extensive head and neck carcinoma excisions.

Endoscopic retrograde cholangiopancreatography (ERCP)

ERCP is a combined endoscopic and radiological procedure treating problems of the biliary tree (e.g. gallstones) which obstruct the common bile duct or masses compressing the biliary tree image obstructive jaundice. Stenting maintains duct patency. Risk of pancreatitis is notable.

Gastroenterology: in exams

See the full history and examination sequences for an abdominal assessment on image pp. 910916. The following are some more detailed pointers.

History

Abdominal pain: use a system (e.g. SOCRATES, see image pp. 148149, p. 893) to get a full assessment of pain. Also ask about associations with meals, particular types of food, and bowel motions.

Ensure the following areas are covered in a general gastroenterological history:

Bowels: frequency, type (Bristol Stool Chart), blood or mucus passed.

Upper GI symptoms: dysphagia, reflux, heart burn/indigestion, waterbrash.

Weight loss: how much over how long? Intentional or unintentional?

Diet: is the patient vegetarian, vegan, or following any other special diet?

It may also be pertinent to ask about genitourinary symptoms.

Liver risk factors should be addressed in patients who present with liver problems. They mostly relate to the risks of viral hepatitis. Testing for viral hepatitis would almost always be part of the first-line investigations for abnormal liver function, but asking about these risk factors may help direct investigations:

Blood transfusions

Travel overseas

Tattoos/piercings

Surgery overseas

IV drug use

Family history of liver or metabolic disorders

Previous jaundice

Alcohol history

Drug history

PMHx of diabetes, hyperlipidaemia, obesity.

Some patients may find discussing their bowel habits, genitourinary symptoms, or sexual history difficult. It is useful to give the patient a warning before asking personal questions (e.g. ‘I’d like to ask you some personal questions now so I can work out what tests we need to do to find the cause of your problem. Is that OK?’).

Alcohol history

Always take a full alcohol history. Patients who have a high alcohol intake should be assessed for hazardous or harmful drinking (e.g. AUDIT-C questionnaire). Maximum recommended alcohol intake is 14 units per week. Documenting that someone is a ‘social drinker’ is not enough as this can range from one unit twice a year (Christmas and birthday) to 10+ units in a binge every Friday night with friends. Aim to get an estimate of average weekly or daily alcohol. Also ask about duration of this pattern of drinking. Know your units!

See Fig. 14.4 for units of alcohol.

image

Fig. 14.4 Units of alcohol. Reproduced with permission from Alcohol Learning Centre. AUDIT-C questions, available from www.alcohollearningcentre.org.uk/_library/AUDIT-C.doc

Things to practise beforehand

Use time on clinical placements to practise taking an alcohol history, assessing for peripheral stigmata of gastroenterological disease, palpating for solid organs, and percussing for shifting dullness.

Make sure you have talked to lots of patients about their bowels so you are comfortable discussing this with future patients.

It is useful to have two ways of asking your patients to do any manoeuvres you may need them to do. For example, to check for asterixis ask your patient ‘Please put your arms out straight in front of you and cock your wrists back’. If they do not follow you could say ‘Like you’re stopping traffic’ and if that does not work a demonstration and request to ‘Please copy me’ may work.

Present your histories and examination findings to any member of the team you are working with for practice. Aim for a coherent summary of your findings. Make eye contact with the person you are presenting to with hands behind your back.

Be logical when answering questions, e.g. if asked for the causes of pancreatitis, although ‘scorpion venom’ may spring to mind, a more appropriate answer would be ‘In the UK, most cases are caused by gallstones and alcohol, and rarer causes include scorpion venom, steroids, mumps, autoimmune diseases, and certain drugs’. Remember that common things are common and you are expected to identify them to demonstrate clinical competency.

Common abdominal cases in OSCE can be IBD, stomas, hepato/splenomegaly, renal transplant, and polycystic kidney disease.