http://www.bsg.org.uk/attachments/960_obca_draft_10.pdf.Flexible sigmoidoscopy and colonoscopy
Endoscopic retrograde cholangiopancreatography
Faecal and serological testing in inflammatory bowel disease
Investigations for small bowel pathology
Tests of small bowel absorption
Tests for bacterial overgrowth
Tests of pancreatic exocrine function
Testing for neuroendocrine tumours
This allows direct visualization of the GIT mucosa and offers further diagnostic investigations to obtain tissue for histology, cytology, or microbiology, as well as therapeutic possibilities.
Consent is a vital component of the endoscopy process. Patients should receive written information before attending for the procedure. This should describe pretest preparation, the procedure itself, risks and possible complications, after-care advice (particularly for those patients requiring sedation), and contact details in the event of problems and include the consent form that the patient will be asked to sign. In the UK, the Montgomery v Lanarkshire case of 2015 has established that the patient should be told whatever they want to know rather than what the clinician thinks they should be told, so covering issues of importance to the patient is paramount.
Whilst the majority of OGD procedures can be performed using a local anaesthetic spray to the oropharynx, either sedation or patient-controlled Entonox® (an inhaled mix of medical nitrous oxide and O2) will be required for more complex or prolonged procedures. An IV combination of a sedative with amnesic effects, such as midazolam, is usually combined with an analgesic such as fentanyl. Addition of hyoscine butylbromide may act to reduce intestinal motility, which is useful for colonoscopy, ERCP, or enteroscopy. An alternative to hyoscine is glucagon, which may be used for patients with glaucoma or IHD where hyoscine is contraindicated. Rarely, for patients who are relatively intolerant of procedures and require prolonged interventions at ERCP or enteroscopy, general anaesthetic (GAn) is an option, depending on patient fitness and the availability of an anaesthetist and anaesthetic support.
Pre-procedure prophylaxis is only indicated for patients undergoing:
•Percutaneous endoscopic gastrostomy or jejunostomy placement.
•ERCP where biliary drainage is unlikely to be achieved at the first procedure.
•Severe neutropenia (<0.5 × 109/L) and/or severe immunocompromise undergoing procedures with a high risk of bacteraemia such as oesophageal dilatation or variceal sclerotherapy.
With the advent of novel oral anticoagulants and greater use of PY212 receptor antagonists (including clopidogrel and ticagrelor). this has become a more complex area. Please see British Society of Gastroenterology (BSG) guidelines for further details.
In summary, procedures are divided into:
•Low risk: diagnostic procedures (OGD, colonoscopy, flexible sigmoidoscopy, enteroscopy), with simple mucosal biopsies possible if needed.
•High risk: polypectomy, ERCP with sphincterotomy, dilatation of strictures, variceal therapy, percutaneous endoscopic gastrostomy (PEG) placement, endoscopic ultrasound (EUS) with FNA, stenting of the GIT.
Can be continued (± aspirin) for low-risk procedures but should be discontinued 5 days before high-risk cases. If there is a high thrombotic risk, continue aspirin and liaise with a cardiologist about risk/benefit of discontinuing.
For low-risk procedures, continue the usual dose of warfarin and go ahead if the INR is within the normal range. For high-risk procedures, stop warfarin 5 days beforehand. If there is a low risk of thrombosis, then check INR pre-procedure and go ahead if INR <1.5. If there is a high thrombosis risk, then cover with low-molecular-weight heparin from 2 days after stopping warfarin, with the last dose ≥24h pre-procedure.
For low-risk procedures, omit on the morning of the procedure. For high-risk procedures, the last dose should be taken ≥48h pre-procedure. For patients on dabigatran with an estimated glomerular filtration rate (eGFR) of 30–50mL/min, the last dose should be taken 72h pre-procedure. Specialist haematology advice should be sought if renal function is worse than this.
Table 7.1 shows the common complications of endoscopic procedures.
In view of the risk of electrolyte disturbance and renal failure using oral bowel-cleansing agents, the National Patient Safety Agency (NPSA) advice from 2009 suggests the following:
•Check U&E, creatinine, and eGFR before oral bowel cleansing. If evidence of renal impairment (eGFR <30mL/min), then assess risks and benefits of procedure. Polyethylene glycol-based preparations (Klean-Prep® or Moviprep®) are safer if eGFR 30–50mL/min.
•If safe to do so, omit ACE inhibitors, angiotensin-2 inhibitors, diuretics, and/or NSAIDs on the day of starting oral bowel preparation for 3 days. If unable to stop (e.g. heart failure), then consider the risks and benefits of the procedure and seek advice from a cardiologist.
Table 7.1 Risks and complications of the most commonly performed endoscopic procedures
Allison M, Sandoe ATM, Tighe R, et al. Antibiotic prophylaxis in gastrointestinal endoscopy. Gut 2009; 58: 869–80.
Connor A, Tolan D, Hughes S, Carr N, Tomson C (2009). Consensus guidelines for the prescription and administration of oral bowel cleansing agents. http://www.bsg.org.uk/attachments/960_obca_draft_10.pdf.
Veitch AM, Vanbiervliet Gj, Gershlick AH, et al. Endoscopy in patients on antiplatelet or anticoagulant therapy, including direct oral anticoagulants: British Society of Gastroenterology (BSG) and European Society of Gastrointestinal Endoscopy (ESGE) guidelines. Gut 2016; 65: 374–89.
•Endoluminal visualization: oropharynx to second part of duodenum.
•Allows direct testing for Helicobacter pylori.
•In preparation for OGD, patients should not eat for 4–6h beforehand, with clear fluids allowed up to 2h before the procedure.
•They should remain nil by mouth for at least 30min afterwards to allow the LAn spray or sedation to wear off.
•Stop proton pump inhibitors 2 weeks before an elective diagnostic OGD to prevent masking of appearances (risk of partial healing and thus misdiagnosing malignant oesophageal or gastric ulcers).
As an alternative procedure to OGD or enteroscopy, barium swallow, meal, or follow-through may be performed, depending upon symptoms (for oesophageal, gastric, or duodenal pathology, respectively). Investigations are limited by their lower sensitivity for mucosal pathology and inability to obtain tissue for histology or undertake therapeutic procedures.
•Dyspepsia despite appropriate therapy.
•Iron deficiency anaemia (see Fig. 7.1a).
•Investigation of suspected giardia or bacterial overgrowth to obtain duodenal aspirates.
•Obtaining duodenal biopsies in suspected coeliac disease.
•Investigation to obtain histology and cultures of H. pylori.
•Abnormal barium swallow, meal, or early follow-through.
•Ensures healing of oesophageal and gastric ulceration.
•Establishes response to a gluten-free diet in coeliac disease.
•Diagnosis of polyps in familial polyposis syndromes.
•Treatment of bleeding lesions (peptic ulceration, angiodysplasia, varices, vascular malformations).
•Palliation of oesophageal cancers using stent placement, argon plasma coagulation, or Nd:Yag laser therapy.
•Placement of PEG or jejunostomy tubes (see Fig. 7.1b).
•Direct placement of nasogastric or nasojejunal feeding tubes.
•Dilatation of strictures of the oesophagus or pylorus.
Fig. 7.1 (a) Endoscopic view of gastric antral vascular ectasia, one cause for blood transfusion-dependent iron deficiency anaemia, which may be treated using argon plasma coagulation. (
Colour plate 4.) (b) Endoscopic view of internal bumper of percutaneous endoscopic gastrostomy (PEG) holding this in situ in the stomach to allow feeding. PEG placement is a therapeutic possibility by using OGD to allow direct visualization.
•Similar to OGD, but allows views of the distal duodenum and jejunum using a 2.4m instrument.
•An overtube allows less looping but ↑ complications.
•Preparation as for OGD; usually requires sedation, analgesia, and hyoscine butylbromide.
•Allows views of the entire small bowel from an oral or rectal approach.
•Preparation is as for OGD or colonoscopy and requires deep sedation or GAn, with the addition of hyoscine butylbromide.
•Consists of one or two balloons, respectively. For single- and double-balloon procedures, one is attached to a transparent overtube sliding over the endoscope, allowing movement forward by telescoping the small bowel by gripping and pleating it over the endoscope. For the double balloon, the second balloon is attached to the distal endoscope to act as an anchor.
Barium investigations (follow-through or small bowel enema) are limited by a lower sensitivity for mucosal pathology.
MRI small bowel studies are good for young patients, as these present no radiation risk, with contrast allowing clear serosal and mucosal images and views of the whole length of the small bowel.
Wireless capsule endoscopy (WCE) is a more effective (but less frequently available) alternative. However, each of these is limited by an inability to obtain tissue or provide therapeutic intervention.
Single- or double-balloon enteroscopy allows visualization and treatment of lesions within the full length of the small bowel and may replace conventional enteroscopy, although procedure length and intensity will require deep sedation or GAn. Conventional enteroscopy will diagnose and treat lesions within the upper small bowel (to the jejunum) but is limited by patient tolerance as conscious sedation is used.
•Investigation and/or treatment of obscure GI bleeding or severe anaemia (following non-diagnostic OGD and colonoscopy).
•Investigation and/or removal of lesions found on CT scan abdomen/MRI small bowel/capsule endoscopy/barium investigation (e.g. polypectomy).
•Treatment of bleeding lesions found at enteroscopy or by WCE.
•Allows examination from anus to splenic flexure (flexible sigmoidoscopy) or from anus to caecum/terminal ileum (colonoscopy).
•Preparation for flexible sigmoidoscopy: phosphate enema 30–60min prior to the procedure.
•Preparation for colonoscopy: oral preparation using an oral bowel-cleansing agent. Need to bear in mind both the patient’s fitness and willingness to undergo the purgative preparation, and also the risk of renal failure and electrolyte disturbance associated with administration of these agents (for advice, Endoscopy, pp. 498–501). Ideally, a low-residue diet should be followed for the 3 days pre-procedure to obtain the best views.
•Whilst colonoscopy usually requires sedation/analgesia, and ideally a smooth muscle relaxant (hyoscine butylbromide), both colonoscopy and flexible sigmoidoscopy are possible using Entonox® with or without hyoscine butylbromide. For patients who are intolerant of such procedures, GAn may rarely be available with appropriate anaesthetic specialist support.
Alternative procedures are radiological—mainly CT colonography, which has largely superseded barium enema. Neither allows tissue or polypectomy to be taken for histology nor other therapeutic procedures to be performed. For these reasons, colonoscopy is considered the ‘gold standard’ for investigating likely colon cancer, diarrhoea, anaemia, and rectal bleeding. Sensitivity is lower for detecting adenomas of ≤10mm using CT colonography (90%) than colonoscopy (99%). These alternative procedures all require the use of oral bowel-cleansing agents too.
For patients not fit to undergo oral bowel cleansing, then an unprepared CT abdomen and pelvis is a possibility. However, it is significantly less sensitive for lesions of <10mm; it may have a role for elderly or medically unfit patients where prognosis is important.
•Rectal bleeding (bright red = flexible sigmoidoscopy, and dark red = colonoscopy), but beware as some right-sided colonic lesions do present with bright red bleeding.
•+ve faecal occult bloods (colonoscopy).
•Abnormal barium enema (depends upon site of pathology found).
•Iron deficiency anaemia (colonoscopy).
•Diarrhoea (colonoscopy with biopsies from right and left colon).
•Extensive ulcerative colitis or colonic Crohn’s disease for >10 years, then ongoing follow-up determined by disease extent and severity.
•High risk of adenomatous colonic polyps or carcinoma, or previous history of adenomatous polyps or carcinoma.
•Familial polyposis syndrome (FAP), hereditary non-polyposis colorectal carcinoma (HNPCC), or other family cancer syndromes.
•For further information, please see BSG guidelines.1
•Treatment of bleeding lesions (angiodysplasia, vascular abnormalities, haemorrhoids).
•Dilatation of benign strictures.
•Palliation of malignant strictures (placement of stents, argon plasma coagulation, or Nd:Yag laser therapy).
•Decompression of sigmoid volvulus and non-malignant toxic megacolon.
•Endoscopic mucosal resection of tumours.
Offers 2-yearly screening using FOB testing (due to change to faecal immunochemical testing shortly) with kits sent to everyone from 60–74 years of age. Face-to-face review for all patients with a +ve result allows either colonoscopy or CT colonography to be offered, depending on patient fitness and wishes. Aim: to allow diagnosis and removal of polyps (adenomas) before development of carcinoma.
Currently in roll-out phase across the UK to offer one-off flexible sigmoidoscopy for all 55-year-olds. Aim: to diagnose and remove polyps (adenomas) and reduce future bowel cancer risk. Full colonoscopy is offered to those with >3 adenomas, those with a villous component to one or more polyps, and anyone with an adenoma of >1cm.
•Side-viewing endoscope used to find the ampulla of Vater and guide cannulation of the biliary and pancreatic ducts by injecting radio-opaque contrast medium using fluoroscopy.
•MRCP has replaced ERCP in 1° diagnosis. ERCP is used for interventional procedures and to obtain biopsy and cytology specimens.
•ERCP requires sedation, analgesia, and hyoscine butylbromide or GAn (which requires anaesthetic support).
MRCP allows imaging of the biliary and pancreatic systems and is the best (and safest) option for diagnosis, although no therapeutic procedures are possible. A percutaneous transhepatic cholangiogram (PTC) allows imaging, stent placement, and drainage of a dilated biliary tree using a transabdominal approach. PTC is indicated if therapeutic ERCP fails, albeit with greater risk of complications.
•Endoscopic diagnosis of periampullary polyps and tumours.
•Obtain bile/brushings for cytology in suspected cholangiocarcinoma.
•Investigation of dilated biliary ducts found on USS with contraindications to MRCP.
•Assessment of the sphincter of Oddi pressures in suspected sphincter of Oddi dysfunction (SOD) syndromes—at specialist centres.
•Palliation of pancreatic, ampullary, and cholangiocarcinomas.
•Treatment of a biliary leak following surgery.
•Gaining access to perform diagnostic or therapeutic procedures.
•Treatment of a biliary leak following surgery.
•Treatment of SOD (types I and possibly II only)
•Treatment of acute severe pancreatitis 2° to gallstones.
•Drainage of pseudocysts (via the stomach).
•Following sphincterotomy for SOD.
•Gaining access prior to stent placement.
•Minor duct papillotomy in pancreatic divisum.
•Combines endoscopy with US imaging to allow visualization of organs, such as the pancreas, and accurate assessment of the degree of invasion of luminal tumours in the oesophagus, stomach, and duodenum.
•Higher-frequency US probe allowed by proximity of the probe to the organ results in ↑ spatial resolution, compared with transabdominal US, CT, or MR scanning.
•Two different modes of imaging are possible: radial (which allows a 360° view around the shaft of the instrument) or linear (which is in line with the endoscope and allows 90° and up to 270° views).
•Pre-procedure preparation is as for OGD.
•Consent procedures differ, depending upon indications and potential pathology.
Transabdominal US, CT, and MRI scanning allow views of the pancreas and liver but do not allow such fine detail for diagnosis or therapy.
•Staging of oesophageal, gastric, pancreatic, and distal biliary tumours.
•Diagnosis and staging for GI stromal tumours.
•FNA of ‘Trucut’ biopsy of mediastinal or coeliac axis lymph nodes, pancreatic lesions, or submucosal lesions.
•Defining mucosal abnormalities such as Barrett’s oesophagus.
•Coeliac axis nerve block to treat pancreatic pain (chronic pancreatitis or pancreatic carcinoma).
•Evaluation and treatment of pancreatic pseudocysts.
Allum WH, Blazeby JM, Griffin SM, et al. Guidelines for the management of oesophageal and gastric cancer. Gut 2011; 60: 1449–72.
•Allows imaging of the entire small bowel by using an 11 × 27mm capsule (e.g. PillCam® SB) with up to 7.5h of battery life.
•When swallowed, the capsule transmits images to aerials attached by adhesive pads to the abdominal wall and stored on a recorder attached round the waist.
•Propelled by the patient’s own peristalsis, so symptom-free.
•Specialist procedure, but with a higher diagnostic yield for mucosa pathology than other small bowel investigations (see Table 7.2).
•If there is suspicion of stricturing where WCE could precipitate obstruction, then a dissolvable patency pill will verify adequate patency, allowing subsequent WCE. Prior barium radiology would also rule out stricturing.
•New capsules for investigation of the colon and oesophagus (PillCam® COLON and PillCam® ESO) are not in widespread use.
•WCE has a role in visual diagnosis but is unable to obtain samples for subsequent analysis or allow therapeutic management.
•Occult GI bleeding undiagnosed at endoscopy.
•Possible small bowel polyposis (e.g. Peutz–Jegher syndrome).
•Unexplained diarrhoea or malabsorption undiagnosed at endoscopy.
•A 0.5% risk of obstruction reported, especially if stricturing (e.g. small bowel Crohn’s disease) or previous small bowel surgery. However, prior use of the patency pill will rule out stricturing significant enough to cause capsule retention.
Table 7.2 Diagnostic yield of small bowel investigations for occult bleeding lesions
| Sensitivity (%) | Specificity (%) | Diagnostic yield (%) | |
| Enteroscopy | 37 | 97 | 30–32 |
| WCE | 64 | 92 | 55–68 |
Mylonaki M, Fritscher-Raven A, Swain CP. Wireless capsule endoscopy: a comparison with push enteroscopy in patients with gastroscopy and colonoscopy negative gastrointestinal bleeding. Gut 2003; 52: 1122–6.
Swain P. Wireless capsule endoscopy. Gut 2003; 52: 48–50.
•‘Test and treat’: patients <55 years of age with a low probability of significant pathology and dyspeptic symptoms do not require OGD. Non-invasive testing for H. pylori allows treatment of those found to be +ve, with acid suppression using a proton pump inhibitor to assess response for all patients.
•Ensure effective eradication in patients with confirmed peptic ulceration or mucosa-associated lymphoid tumour (MALT) lymphoma.
•H. pylori antigens in faeces measured using an immunochromatographic test.
•Sensitivity exceeds 91%, and specificity exceeds 92%.
•Commercially available kits make an initial diagnosis and confirm eradication.
•Expired air is collected after ingestion of 13C-labelled urea.
•If H. pylori present, bacterial urease breaks down urea → ammonium and bicarbonate, then → CO2 and ammonia.
•Expired 13CO2 is collected into a tube 30min after ingestion, measured by a mass spectrophotometer, and compared with one collected prior to ingestion.
•Test almost 100% sensitive and specific, and remains the gold standard to confirm eradication.
•Serum IgG antibodies to H. pylori may be detected by ELISA with sensitivity of 90% and specificity of 70–90%.
•IgG levels persist up to 1 year, so fail to confirm eradication.
•Other organisms may cause cross-reactivity.
•False −ves occur in elderly or immunocompromised patients.
•Investigations are based on biopsy samples.
•H. pylori density is usually the greatest in the antrum, but during acid suppression, the greatest concentration is found in the corpus.
•Colonization is patchy so may yield sampling errors.
•So for patients taking proton pump inhibitors, one biopsy should be taken from each area (two in total) for the greatest yield for each of the tests below.
•H. pylori can be detected on routine histology using the modified Giemsa stain.
•Sensitivity is 85%, with a specificity of almost 100%.
•This is useful in those few patients who have failed eradication to establish antibiotic sensitivities.
•Sensitivity is over 95%, with specificity of almost 100%.
•Biopsy is placed into a urea solution containing phenol red.
•H. pylori contains urease, releasing ammonia from urea, thus changing the pH and detected as a colour change with phenol red dye turning from straw to pink/purple.
•Commercial kits, such as the Campylobacter-like organism (CLO) test, are available.
•Specificity is 97%, and sensitivity between 70 and 95%.
National Institute of Health and Care Excellence (2014). Gastro-oesophageal reflux disease and dyspepsia in adults: investigation and management. Clinical guideline CG184. https://www.nice.org.uk/guidance/cg184.
•Used in the current National Health Service (NHS) England National Bowel Cancer Screening Programme as population screening for 60- to 74-year-olds every 2 years.
•Early diagnosis of cancer pathway for primary care (NICE guidelines, 2015). General practitioners advised to offer testing for adults without rectal bleeding if:
•50 years or over with unexplained abdominal pain or weight loss.
•Under 60 years with a change in bowel habit or iron deficiency anaemia.
•Aged 60 or over with anaemia in the absence of iron deficiency.
•Simple and inexpensive, performed by the patient in their own home.
•Samples taken onto a test card from three consecutive bowel motions and card sent to a screening centre.
•Test card uses the ‘guaiac’ reaction with pseudoperoxidase in Hb, causing a colour change in an indicator dye.
•Dietary changes advised to avoid red meat, horseradish, broccoli, and turnips, as their high peroxidase activity may cause false +ve results, and avoid vitamin C tablets (high ascorbic acid activity).
•Sensitivity of the non-hydrated test is 70%; this ↑ to 90% with rehydration, but at the loss of specificity. Sensitivity improves with the number of samples taken.
•Individuals who are +ve require full colonoscopy.
•Multicentre UK trial invited 486,355 for screening using FOB (take up 56%), finding 2% FOB +ve, and of these, 10.9% have carcinoma, 35% adenoma, and 54.1% normal.
Polyps and carcinomas may bleed intermittently, but FOB are more likely to be +ve with early-stage cancers than polyps.
Non-colorectal blood source such as the upper GIT or nosebleed; diet containing red meat, broccoli, or turnips (peroxidase activity).
‘Old’ sample with bacterial degradation of Hb, the presence of ascorbic acid, and reduced or absent bleeding at time of testing.
•This will replace FOB testing used by the NHS England National Bowel Cancer Screening Programme and has already happened in Scotland.
•A single sample is collected via a brush into a pot; this appears to encourage more people to take part in screening (currently just 55% of those invited to participate).
•Tests for human Hb protein from the colon in stool, with less reactivity for blood from the upper GIT or nose.
•+ve result means that colonoscopy or CT colonography is required.
•Higher sensitivity to lower concentrations of blood than FOB.
Hardcastle JD, Chamberlain JO, Robinson MHE, et al. Randomised controlled trial of faecal-occult-blood screening for colorectal cancer. Lancet 1996; 348: 1472–7.
National Institute of Health and Care Excellence (2015). Suspected cancer: recognition and referral. NICE guideline NG12. http://www.nice.org.uk/guidance/ng12.
Tappenden P, Chilcott J, Eggington S, Patnick J, Sakai H, Karnon J. Option appraisal of population-based colorectal cancer screening programme in England. Gut 2007; 56: 677–84.
Valori R (2007). Bowel cancer screening. http://www.18weeks.co.uk..
•Neutrophil granulocyte cytosol protein, which acts as a marker of intestinal inflammation.
•+ve correlation with inflammation in Crohn’s disease and ulcerative colitis.
•Non-specifically elevated in neoplasia and radiation proctitis too.
•Sensitivity for diagnosing pathology is 93%, with specificity of 100%, with a result of ≤50μg/g classed as −ve, effectively excluding IBD.
•A normal result of ≤50μg/g reduces the need for invasive investigations, such as colonoscopy, for patients of 16–40 years of age with no alarm symptoms of pathology (weight loss, bleeding, anaemia, nocturnal diarrhea, or a significant family history of bowel cancer).
•Neutrophil-derived protein; marker of intestinal inflammation.
•May be used for non-invasive testing to differentiate those who require colonoscopy from those more likely to have functional disease such as IBS.
•Not as effective as calprotectin, as sensitivity for diagnosing pathology is 82% and specificity is 84%.
•Occur in the serum of 50–80% of patients with histologically confirmed ulcerative colitis, but only 10% of those with Crohn’s disease. This is likely to be genetically determined.
•Antibodies are particularly associated with 1° sclerosing cholangitis in association with ulcerative colitis.
•Overall sensitivity is 55.3%, with a specificity of 88.5%.
•In a paediatric cohort with −ve antibodies to Saccharomyces cerevisiae (ASCA), sensitivity ↑ to 70.3%, with 93.4% sensitivity.
•Found in 60% of patients with Crohn’s disease, but only 5% of those with ulcerative colitis.
•In Crohn’s disease, the presence of high titres of ASCA is associated with early age of onset, fibrostenosing and fistulating disease types.
•Sensitivity is 54.6%, with specificity of 92.8% if pANCA is −ve.
National Institute of Health and Care Excellence (2013). Faecal calprotectin diagnostic tests for inflammatory disease of the bowel. Diagnostics guidance DG11. https://www.nice.org.uk/guidance/dg11.
Reese GE, Constantinides VA, Simillis C, et al. Diagnostic precision of anti-Saccharomyces cerevisiae antibodies and perinuclear antineutrophil cytoplasmic antibodies in inflammatory bowel disease. Am J Gastroenterol 2006; 101: 2410–22.
•As a result of generally low sensitivities and specificities, these should not be first-line investigations.
•They are best used for tracking patients following a diagnosis of carcinoma through subsequent surgery, and chemo-radiotherapy when levels should fall to normal unless disease recurs.
•↑ in 60% of those with localized colorectal carcinoma (CRC) and 80–100% of those with metastatic disease.
•Non-specific and non-diagnostic—also ↑ in bronchial carcinoma, heavy smokers, and IBD.
•Levels do not relate to tumour load, but rising levels, which were previously low/normal, may imply recurrence of CRC.
•Normally produced by fetal liver.
•High levels in non-pregnant adults imply hepatocellular carcinoma (raised in over 90% cases).
•↑ serological concentrations in pregnancy suggest neural tube defect.
•Blood levels may be ↑ in hepatocyte regeneration, acute viral hepatitis, cirrhosis, choriocarcinoma, and teratoma.
•May be used 6-monthly (with liver USS) to screen cirrhotic patients for development of hepatocellular carcinoma.
•↑ in pancreaticobiliary obstruction, with the highest levels in pancreatic carcinoma.
•Levels >40IU/L have 75–90% sensitivity and 80–95% specificity for ductal pancreatic carcinoma.
•Serum levels may be elevated in jaundice, cholangitis, choledocholithiasis, and chronic pancreatitis.
•Glycoprotein antigen to an epidermal growth factor receptor (p110 sEGFR).
•Blood levels ↑ with menstruation, endometriosis, pelvic inflammatory disease, pregnancy, and ascites of all types.
•Highest levels with ovarian malignancy, but also ↑ with ovarian, pancreas, breast, lung, and colon cancers.
•20% of ovarian cancers have little/no expression of Ca-125.
•Useful in monitoring response of ovarian carcinoma to treatment (if initially +ve), as rising level of Ca-125 precedes clinical recurrence by up to 3 months (>90% of cases).
•As isolated values lack sensitivity and specificity, serial Ca-125 readings may be used to achieve specificity of 99.6%, but with a sensitivity of only 80%.
•Presenting features of small bowel pathology include diarrhoea, steatorrhoea, abdominal pain, weight loss, and nutritional deficiencies.
•Investigation of diarrhoea is shown in Fig. 7.4.
•Occasionally, occult GI bleeding may originate in the small bowel, and an algorithm for investigation of anaemia is shown in Fig. 7.5.
•Anti-tTG antibodies have almost 100% sensitivity for coeliac disease but may be false −ve in presence of low IgA.
•Diagnosis should be confirmed using duodenal or jejunal biopsies taken at OGD, which would reveal partial or total villous atrophy.
•OGD and enteroscopy allow views of the proximal small intestine to obtain tissue and allow therapeutic possibilities.
•WCE permits diagnosis from the whole small intestine but does not allow therapeutic options.
•MRI of the small bowel has mostly replaced barium radiology, particularly in younger patients, with a lack of radiation, greater sensitivity for mucosal detail by using contrast, and abilities to use cine views to determine motility.
•Barium follow-through involves ingestion of dilute barium, with images taken every 10–30min until barium reaches the caecum.
•Small bowel enema (enteroclysis) uses insertion of a nasoduodenal tube to infuse barium slowly, creating a column, which may be followed continuously using fluoroscopy. This allows focusing on areas including the terminal ileum (see Fig. 7.2).
•Uses 99mtechnetium–hexamethyl-propylene-amine-oxime (99mTc-HMPAO) to show intensity and extent of inflammation or infection 1 and 3h after injection of autologous radiolabelled leucocytes.
•Delineates disease extent in Crohn’s disease and ulcerative colitis (see Fig. 7.3).
•False −ve results may occur in small bowel Crohn’s disease.
•Sensitivity of 96% and specificity of 97% for IBD, and sensitivity of 85–100% and specificity of 100% for detecting abscesses.
Fig. 7.3 Radiolabelled white cell scintigraphy using 99mTc-HMPAO to show inflammation of the terminal ileum consistent with Crohn’s disease (taken at 3h).
•IV 99mTc pertechnate accumulates in gastric mucosa with a time course of 5–60min.
•Uptake in ectopic mucosa (e.g. Meckel’s diverticulum) occurs simultaneously.
•Imaging at 5–10min intervals up to 2h after injection allows localization of the site of ectopic mucosa.
•False +ves are caused by early gastric emptying.
•Sensitivities vary from 90% in children to 60% in adults.
•The labelled bile acid 75selenium homotaurocholate (SeHCAT) is administered orally. Retention measured at 7 days by whole body counting.
•Retention of >15% SeHCAT is normal (less indicates malabsorption).
•Commonest reason for abnormal result is post-cholecystectomy, presence of ileal disease, or post-ileal resection.
•Useful second-line investigation in patients with diarrhoea of unknown aetiology.
Xylose is absorbed from the proximal small bowel, and urinary excretion and blood levels reflect absorption. It is used mainly in paediatric practice and has a low sensitivity.
Oral administration of 50g of lactose is followed by blood sampling every 30min for 2h. A rise in blood glucose of <1.1mmol/L suggests deficiency of disaccharidases, especially with colicky abdominal pain and diarrhoea.
This is similar to the hydrogen breath test for bacterial overgrowth. Lactase-deficient individuals fail to metabolize lactose, which then undergoes luminal metabolism by lactase-producing colonic bacteria to yield hydrogen. Glucose and fructose may be used as alternative short-chain carbohydrates to determine the presence of malabsorption.
Patients with fat malabsorption 2° to small bowel diseases, such as coeliac disease or tropical sprue, may malabsorb between 10 and 20g/day of fat, whilst patients with pancreatic insufficiency may malabsorb 30–50g/24h. A normal faecal fat excretion is <6g/day (17mmol/day).
•Unpleasant test, fallen into disuse, but remains gold standard.
•Fat content measured in a 3-day faecal collection.
•Patient takes a standard diet of 100g of fat per day.
•Does not differentiate small bowel and pancreatic malabsorption.
•Samples may be collected through the biopsy channel at OGD.
•Scanty bacteria are present in normal upper small bowel.
•Numbers in excess of 106/mL of aspirated fluid are pathological.
•This technique may culture Giardia and Strongyloides species.
In mammals, the only source of breath hydrogen is bacterial fermentation of carbohydrates. Hydrogen is absorbed from the intestinal lumen and expired during breathing. In bacterial overgrowth, hydrogen production can occur in the small intestine, as well as in the colon.
•A mouthwash is given beforehand to reduce contamination by oral bacteria.
•Test dose of glucose/lactose (50g of either) or lactulose (10–15mL) and breath hydrogen measured.
•An early peak (e.g. 40min) suggests bacterial overgrowth.
•This test can be used for other short-chain carbohydrates, such as fructose or lactose, to determine if a patient is malabsorbing one or more.
•Sensitivity 60–90%, with specificity of 80%.
•False −ves result from variations in microflora present in the small intestine or antibiotic administration within 3 weeks.
•False +ves occur in patients with IGT, those with rapid transit to the colon, and smokers.
•Patients should avoid eating pulses for 48h prior to the test (normal digestion of pulses liberates excess hydrogen).
•Symptoms of pancreatic exocrine dysfunction include diarrhoea or steatorrhoea and weight loss.
•Investigations aim to determine the degree of pancreatic insufficiency, although biochemical and radiological investigations are more reliable with greater sensitivity and specificity in advanced disease.
•Proteinase produced by pancreatic acinar cells and remains un-degraded during gut transit.
•Measured using immunoassay of non-liquid faeces sample.
•Levels of >200µg/g of faeces being normal, 100–200 representing mild insufficiency, and <100 being diagnostic of severe disease.
•Specificity is 93%, whilst sensitivity is 63% and 100% for mild and severe disease, respectively.
•False +ves may occur with high-volume watery stools.
•The result is not affected by pancreatic enzyme supplements.
•Less sensitive (64%) and specific (89%) than elastase.
•Used mainly in children to screen for cystic fibrosis.
•Result is affected by pancreatic enzyme supplements.
•Direct intubation of the duodenum allows collection of pancreatic juice, following IV injection of either secretin (allowing measurement of volume and bicarbonate content) or cholecystokinin (allowing measurement of amylase, trypsin, and lipase).
•Whilst highly sensitive and specific, even with mild pancreatic disease, this is only available in specialist centres.
•Synthetic peptide, which is given orally.
•In normal patients, pancreatic chymotrypsin hydrolyses this peptide, yielding free PABA, which is absorbed, metabolized, and excreted in urine.
•In pancreatic insufficiency, free PABA levels are reduced, resulting in reduced absorption and excretion with lower urinary and serum PABA concentrations.
•Fluorescein dilaurate (an ester) is taken orally with a set diet.
•In the presence of normal pancreatic function, aryl esterases release fluorescein, which is absorbed, partially conjugated in liver, and excreted in urine.
•A 24h urine collection for excreted levels shows close correlation with pancreatic exocrine function.
•Specialist area where clinical suspicion results from baseline investigations, and radiology should allow targeting of more specific biochemical investigations, depending on which syndrome is suspected.
•Histology is required to confirm the diagnosis.
•24h collection of urine for 5-hydroxyindole acetic acid (5HIAA).
•High levels imply carcinoid syndrome.
•High specificity, but false +ves result from serotonin-rich bananas, tomatoes, or drugs such as phenothiazines.
•Marker of neuroendocrine tumours (NETs) found in high concentrations, regardless of presence or absence of hormone-related clinical features.
•May be falsely elevated in proton pump inhibitor use and atrophic gastritis.
•CT or MRI of the chest, abdomen, and pelvis. The 1° tumour is identified in only 50–70%.
•Radiolabelled somatostatin receptor scintigraphy (OctreoScan).
•Positron emission tomography (PET) using gallium-68 with concurrent CT (PET/CT) if unknown 1° or to look for 2°.
•Endoscopy or EUS may allow tissue diagnosis.
•Measured using fasting serum gut hormone assays: insulin (paired with a serum glucose sample), glucagon, chromogranin A and B, VIP, pancreatic polypeptide (PP), gastrin, and somatostatin.
•Single tumours often secrete >1 type of hormone.
•Up to 50% of slow-growing tumours are thought to be non-functional.
•Several types of tumour occur as part of MEN-1.
•Concurrent therapy with a proton pump inhibitor will falsely raise serum gastrin and chromogranin A levels, so these should be stopped for at least 1 week prior to measuring serum levels.
Ramage JK, Ahmed A, Ardill J, et al. Guidelines for the management of gastroenteropancreatic neuroendocrine (including carcinoid) tumours (NETs). Gut 2012; 61: 6–32.
•A water-perfused pressure catheter is used during ERCP to measure sphincter of Oddi pressures to formally diagnose SOD.
•SOD is triad of abnormal liver function, biliary-type abdominal pain, and dilatation of the biliary tree in the absence of gallstone disease.
•Diagnosis is confirmed by high resting pressure, retrograde peristalsis, and failure of contrast to drain from the biliary tree within 45min.
•Whilst patients with SOD have an ↑ risk of pancreatitis post-ERCP, biliary sphincterotomy may relieve symptoms of pain in selected cases.
•Assessment of gastro-oesophageal reflux disease (GORD).
•Atypical symptoms such as asthma or non-cardiac chest pain.
•Before consideration of anti-reflux surgery.
•Poorly controlled GORD to confirm diagnosis on or off treatment.
•Ambulatory 24h test that places a pH electrode through the nose to sit 5cm above the lower oesophageal sphincter.
•Connected to a portable microprocessor that records episodes where the pH dips below 4.
•Patient fills in a simultaneous event diary to correlate symptoms and episodes of low pH.
•For most patients, H2 receptor antagonists and proton pump inhibitors are stopped 7 days beforehand. A few patients require testing on medication to establish treatment response.
•Measure frequency and duration of episodes of pH <4.
•Assess correlation between symptoms and pH.
•Excessive oesophageal acid reflux is defined as a total duration of pH <4 of 4–6% of recording time.
•Diagnosis and assessment of motility disorders suggested by symptoms/OGD/barium swallow findings.
•Defining the precise location of the lower oesophageal sphincter prior to 24h pH monitoring.
•Before consideration of anti-reflux surgery.
•Static test using a nasogastrically placed multiple channel, water-perfused catheter, which is gradually withdrawn during a series of wet and dry swallows.
•Pressure is measured through the length of the oesophagus, at the upper and lower oesophageal sphincter, and the duration and frequency of contractions are recorded (see Table 7.3).
Table 7.3 Results from oesophageal manometry studies
| Non-specific motility disorder | Abnormal and incomplete peristalsis with normal body contractions |
| Achalasia | Incomplete relaxation and high pressure of lower oesophageal sphincter with aperistalsis of the oesophageal body |
| Nutcracker oesophagus | High amplitude and duration of contractions, normal peristalsis |
| Oesophageal spasm | Disordered peristalsis with simultaneous prolonged contractions throughout |
•Scintigraphy using the radioactive tracer 99mtechnetium displays gastric movements with a range of test meals (liquid to solid) to quantify gastric emptying and intestinal filling over time.
•In practice, barium and endoscopic studies often provide enough information when investigating patients with vomiting.
•Intestinal transit is measured using 50 radio-opaque plastic markers inside a pH-sensitive gel capsule, swallowed by the patient and designed to release its contents in the terminal ileum. An abdominal radiograph at 100h should show <20% of markers present in the colon.
•Measures colonic transit in suspected slow transit constipation.
•Water-perfused catheter measures anorectal pressures to assess voluntary and involuntary sphincter squeeze pressures and reflex responses to balloon distension in the rectum.
•Readings allow assessment of rectal sensation, spinal reflexes, and internal and external sphincter integrity.
•Assesses symptoms of faecal soiling, incontinence, and chronic constipation.
These are basic serological screening tests that establish whether liver inflammation, infection, or obstruction is present.
Alanine transaminase (ALT: cytosol enzyme specific to the liver) and aspartate transaminase (AST: mitochondrial enzyme also present in the heart, muscle, kidney, and brain)—both enzymes are present in hepatocytes and leak into blood with liver cell damage.
Alkaline phosphatase (ALP: canalicular and sinusoidal membranes of the liver, but also bone, intestine, placenta)—specific isoenzymes for ALP are produced by different tissues, but simultaneously raised γ-glutamyl transpeptidase (γGT) and ALP implies a hepatic origin. Extra- and intra-hepatic cholestasis may cause raised ALP and results from benign or malignant disease with or without raised bilirubin. The highest levels result from PBC and hepatic metastases.
γGT (microsomal enzyme)—activity can be induced by drugs, such as phenytoin and rifampicin, and alcohol. Mild elevation of γGT is common with even a small alcohol intake, and isolated elevation does not imply liver disease. It rises in parallel with ALP in cholestasis.
A protein that is synthesized in the liver. Plasma concentration partially results from functional capacity within the liver. However, it has a serum half-life of 20 days and may be normal in early phases of acute liver disease. Hypoalbuminaemia may also arise from ↑ volume of distribution (sepsis, overhydration, pregnancy), ↑ excretion or degradation (nephrotic syndrome, protein-losing enteropathy), haemorrhage, or catabolic states such as malignancy or burns.
Test of plasma clotting activity and reflects the activity of vitamin K-dependent clotting factors synthesized by the liver. PT may be elevated in acute or chronic liver disease. In vitamin K deficiency with normal liver function, PT will return to normal within 18h of administration of parenteral vitamin K.
In liver disease, a raised bilirubin is usually associated with other liver function abnormalities. There are many causes of raised serum bilirubin. Bilirubin may be conjugated or unconjugated, although in practice, this conjugation state only differentiates congenital hyperbilirubinaemias. In Gilbert’s syndrome (the commonest benign cause of an isolated raised serum bilirubin), an elevated unconjugated bilirubin, which rises during fasting and mild illness, diagnoses the condition. Haemolysis is another cause of hyperbilirubinaemia, which is covered in Chapter 3.
•IgG ↑ in viral hepatitis, chronic AIH, and cirrhosis.
•IgM ↑ in PBC, non-biliary cirrhosis, and acute viral hepatitis.
•IgA is ↑ in alcoholic liver disease, with β–γ fusion seen on electrophoresis.
These are summarized in Table 7.4, with serological tests, diagnosis, and definitive investigations required to confirm the diagnosis. The best investigations for an individual patient are established from history, examination, and basic biochemical parameters.
•Acute infection: +ve IgM antibodies to HAV.
•Chronic infection: does not occur.
•Markers of clearing virus: +ve IgG antibodies to HAV and anti-HAV IgM.
•HBsAg appears in blood from 6–12 weeks after infection, then disappears.
•HBeAg appears early, then declines rapidly.
•Anti-HBs appears late and indicates immunity.
•Anti-HBc is the first antibody to appear, and IgM anti-HBc may persist for many months as the only marker of ongoing viral replication when HBsAg has disappeared and anti-HBs is not yet detectable.
•Anti-HBe appears after anti-HBc and indicates ↓ infectivity.
•HBsAg persists and indicates chronic carrier state.
•HBeAg persists, correlating with ↑ severity and infectivity.
•Anti-HBe indicates seroconversion (if this occurs) with disappearance of HBeAg and a rise in ALT.
•HBV DNA suggests continued viral replication.
•Acute infection: hepatitis C HCV RNA is +ve 1–2 weeks after infection, with HCV antibodies developing after ~12 weeks.
•Chronic infection: >50% of patients with persistent HCV RNA, which can be measured as viral load.
•Hepatitis C has six genotypes that determine response to treatment.
•Similar to hepatitis A with no chronic or carrier state.
Figure 7.6 shows an algorithm for investigation of liver disease. This differentiates obstructive from parenchymal liver disease to suggest further investigation and treatment.
•Stages liver disease by assessing stiffness using the velocity of a vibration wave.
•Measures liver inflammation and fibrosis, with ↑ stiffness correlating with disease severity.
•Requires a minimum of ten valid readings; results are expressed in kPa.
•Fibrosis: >7.0kPa (with an 85% probability).
•Cirrhosis: >14.0kPa (with a 90% probability).
•Falsely high results: liver inflammation (active hepatitis), cholestasis, mass lesion or tumour, liver congestion in heart failure.
•Unreliable results: presence of ascites.
•Not suitable: pregnancy and patients with a pacemaker.
•Benefit: avoid risks of liver biopsy.
Table 7.4 Specific biochemical tests
| Test | Condition | Findings | More specific tests |
| Haemochromatosis | HFE gene testing (83–90% of patients have Cys 282 Tyr mutation; 25% have His 63 Asp; 187G in complete linkage disequilibrium with Cys 282 Tyr). Liver biopsy—with dry weight of iron | ||
| Wilson’s disease | Serum copper and caeruloplasmin levels are usually reduced but can be normal | Liver biopsy—with dry weight of copper | |
| α1-antitrypsin | α1-antitrypsin deficiency | Levels of <10% of normal in homozygotes and 60% in heterozygotes | Liver biopsy and lung function testing for emphysema |
| AMA | PBC | Liver biopsy | |
| ANA/SMA | Type I AIH | Liver biopsy | |
| Anti-LKM1 or anti-liver cytosol antibodies | Type II AIH | Liver biopsy | |
| Fasting cholesterol and glucose, glycosylated Hb | IGT | Fibroscan®/fibrosis score/liver biopsy |
•Obtains tissue for diagnosis of diffuse or localized parenchymal disease.
•Severity of histological liver dysfunction cannot be predicted from basic LFTs.
•Consent should be obtained based on risks.
•Transjugular liver biopsy overcomes many contraindications.
•Unexplained persistently abnormal LFTs.
•Staging of disease in hepatitis B or C infection, and prior to considering antiviral treatment.
•Acute hepatitis of unknown aetiology.
•Cirrhosis of unknown aetiology.
•Alcohol-related liver disease.
•PBC/chronic active hepatitis.
•Targeted liver biopsy of lesions (not if resection/transplant is a possibility).
•Haemochromatosis/Wilson’s disease.
•Post-liver transplant to rule out acute or chronic rejection.
(See Table 7.5.)
•Standard method for obtaining tissue.
•Ultrasonography of liver and biliary tree pre-procedure to identify anatomical variations ↑ risk and to rule out obstruction.
•Most complications <2h but can occur up to 24h.
•No evidence that direct US-guided biopsy is safer, but US should definitely be used if a targeted biopsy is required.
•An uncooperative or confused patient.
•PT prolonged by >3s, platelets <80 × 109/L, or bleeding diathesis.
•Hydatid cysts (risks of anaphylaxis and abdominal seeding).
•Higher risk of bleeding if amyloidosis present.
Shoulder tip pain, minor intra-abdominal bleeding, or mild abdominal pain (up to 30%)—usually settles with analgesia.
•Perforation (0.01–0.001%: pneumothorax, gall bladder puncture, kidney, colon).
•Intra-abdominal haemorrhage; haemobilia (0.05%: a triad of biliary colic, jaundice, and melaena within 3 days of liver biopsy).
•Mortality varies between 0.001 and 0.0001% and results from intraperitoneal haemorrhage or biliary peritonitis.
•Risk of tumour seeding if a malignant lesion is biopsied; if curative resection/transplantation is planned, needle biopsy should be avoided.
•Specialist technique carried out using fluoroscopic guidance.
•Catheter passes from the right internal jugular vein, through the right atrium and IVC, and into the hepatic veins.
•Patient holds his/her breath, whilst the biopsy needle is advanced through the catheter then rapidly pushed forward by 1–2cm into the liver to obtain a small core of liver parenchyma.
•Safe technique with few complications (1.3–2% morbidity and 0.5% mortality), usually performed in higher-risk patients.
•Complications range from neck haematoma, puncture of intrathoracic arteries, transient Horner’s syndrome, cardiac arrhythmias, infection, and perforation of the liver capsule.
•Test of choice in patients excluded from percutaneous biopsy by coagulopathy, bleeding diathesis, ascites, portal hypertension, and amyloidosis.
•Transjugular cannulation allows measurement of portal venous pressures.
•Allows sampling of the liver when an operation is planned.
•Allows targeted biopsies, as well as parenchymal biopsies.
•Bleeding is directly controlled and perforation is avoided.
•Risks of surgery and anaesthesia should be considered.
Table 7.5 Percutaneous liver biopsy—practical procedure
| Procedure | Should be carried out by an experienced doctor using aseptic precautions |
| Check | Clotting, FBC, and take group and save (G&S) within 24h before procedure (cancel if platelets <80 × 109/L or PT prolonged >3s) |
| Patient | Lies flat on his/her back |
| Liver margins | Delineated using percussion and/or US |
| 1% lidocaine | 5mL injected at the point of maximal dullness down to the liver capsule through intercostal space in expiration |
| Menghini or Trucut needle | Used to obtain sample with patient’s breath held in expiration (up to two passes may be used). Menghini needles use suction, have a lower rate of complications, and allow more rapid biopsy, but they have a lower yield for tissue than Trucut (a cutting needle) |
| Sample | Placed into 10% formalin (or into a dry pot to estimate dry weight of iron or copper or for culture) |
| Patient | Nurse in supine position or right lateral for >6h, with regular BP and pulse measurements (every 15min for 2h, every 30min for the next 2h, then hourly), with urgent medical review if any sign of deterioration |
| If stable | At 6h, the patient can be discharged home as long as s/he can return to hospital within 30min and have a responsible adult with him/her overnight |
Grant A, Neuberger J, Day C, Saxseena S (2004). Guidelines on the use of liver biopsy in clinical practice. http://www.bsg.org.uk/images/stories/docs/clinical/guidelines/liver/liver_biopsy.pdf.
(See Table 7.6.)
•10mL is sent for cell count, Gram stain, ZN stain culture (add 10mL to a pair of blood culture bottles to ↑ diagnostic yield).
•10mL for biochemical investigation of protein, glucose, LDH, TGs (if chylous ascites is suspected), and amylase (if pancreatic ascites is suspected).
•Polymorphonuclear leucocytes (neutrophils) of >250 cells/mm3 suggest underlying spontaneous bacterial peritonitis (SBP) (or 2° infection).
•Total leucocytes of >500 cells/mm3 imply bacterial peritonitis (SBP) if a specific neutrophil count is not available.
•Lymphocyte count of >500 cells/mm3 implies tuberculous peritonitis (with raised protein, positive ZN stain/TB culture, and low glucose).
•Gram staining for early identification of bacteria and bacterial culture allow targeting of antimicrobial therapy.
•Using ascitic fluid protein levels to aid diagnosis is best achieved using the serum ascites albumin gradient (SAAG) by subtracting ascites albumin concentration from serum albumin concentration. Levels of ≥11g/L suggest cardiac failure, cirrhosis, and nephrotic syndrome, whilst levels of <11g/L suggest malignancy, TB, or pancreatitis as causes.
•Risk of SBP is greatest if ascitic protein <10g/L.
May be diagnostic in cases of peritoneal malignancy.
↑ ascitic amylase (>2000IU/L) is typical of pancreatic ascites.
↑ in chylous ascites.
Table 7.6 Ascitic fluid aspiration—practical procedure
| Patient | Lies on his/her back, tilting towards side planned for aspiration |
| Percussion | Used to find shifting dullness in left or right lower quadrant |
| Chlorhexidine | Used to clean the site |
| Lidocaine | 2–3mL of 1% used to infiltrate a site in the left or right lower quadrant where shifting dullness is detected. It should be possible to aspirate ascitic fluid using a standard 19G needle |
| 50mL syringe | Sterile 19G needle placed through the same site to obtain the samples required |
| Rare complications | Include bowel perforation, 2° bacterial peritonitis, or haemorrhage |
1 Cairns SR, Scholefield JH, Steele R, et al. Guidelines for colorectal cancer screening and surveillance in moderate and high risk groups (update from 2002). Gut 2010; 59: 666–90.
