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CHAPTER 0 | MISCELLANEOUS
15. A 45- year- old man presented with abdominal bloating, watery diarrhoea, and atulence. Aglucose- hydrogen breath test was arranged.
Which statement regarding glucose- hydrogen breath testing is correct?
A. Adouble peak in expired breath hydrogen should be considered normal
B. Arise in breath hydrogen by more than 20 ppm from baseline within 90 minutes would be
consistent with a positive test result
C. Glucose- hydrogen breath testing correlates well with jejunal aspirates
D. Lactulose is well absorbed across the small intestinal mucosa
E. The test is not aected by small bowel transit time
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MISCELLANEOUS
0
ANSWERS
1. B. Stop apixaban 48 hours before, continue aspirin
• Aspirin is safe to continue prior to routine endoscopic procedures
• Apixaban should be stopped 48 hours prior to high- risk procedures
• Cardiology advice should be sought for patients with high- risk conditions
AF and ischaemic heart disease with long- standing stents are low- risk conditions for stopping anticoagulant and antiplatelet agents. Therefore, consulting a cardiologist is not required. Diagnostic gastroscopy is a low- risk procedure. However, the colonoscopy should best be considered a high­risk procedure to allow for polypectomy, given the patient’s preference. Aspirin is safe to continue prior to routine endoscopy.
High- riskconditions
• <12months after drug eluting coronary stent
• <1month after bare metal coronary stent
• AF + prosthetic heart valve
• Prosthetic mitral valve
• AF + mitral stenosis
• <3months after VTE
Low- riskconditions
• IHD with no recent stents
• Cerebral vascular disease
• Peripheral vascular disease
• Tissue heart valve
• Prosthetic aortic valve
• Non- valvular AF
• >3months after venous thromboembolism (VTE)
Direct oral anticoagulants (apixaban,dabigatran, edoxaban, rivaroxaban)
Low- risk procedures:omit on the morning of procedure High- risk procedures:stop 48 hours before procedure (72 hours for dabigatran with CrCl 30– 50 ml/ min)
Warfarin
Low- risk procedures:continue therapy, check international normalized ratio (INR) does not exceed therapeutic range
Best of Five MCQs for the European Specialty Examination in Gastroenterology and Hepatology. Thomas Marjot, Colleen G C McGregor, Tim Ambrose, Aminda N De Silva, Jeremy Cobbold, and Simon Travis, Oxford University Press (2021). © Oxford University Press. DOI: 10.1093/oso/9780198834373.003.0010
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High- risk procedures:assess risk of underlying condition
• If low- risk condition, stop ve days before procedure, check INR <1.5
• If high- risk condition, stop ve days before procedure and bridge with low molecular weight heparin (LMWH)
P2Y12 receptor antagonists (clopidogrel, prasugrel, ticagrelor)
Low- risk procedures:continue High risk procedures:
• If low- risk condition, stop ve days before procedure
• If high- risk condition, consult cardiologist
Veitch AM 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. 206;65:374– 389. Doi:0.36/ gutjnl- 205- 30.
2. B. CT abdomen
Post- polypectomy syndrome:
• Presents similarly to colonic perforation and often requires a CT to dierentiate
• Occurs more commonly in larger polypectomies (>2cm)
• Is managed conservatively in the majority of cases
The most likely diagnosis in this case is post- polypectomy syndrome (or post- polypectomy electrocoagulation syndrome). The electrical current arising from diathermy extends beyond the mucosa and muscularis propria into the serosal surface of the colon. Thermal injury ensues, without evidence of colonic perforation, and results in a localized inammatory reaction. The syndrome occurs after large amounts of sustained thermal energy have been applied, so it is more commonly seen after larger polypectomies (>2cm in diameter), or when normal mucosa is inadvertently caught within the snare alongside the polyp. Anecdotal evidence suggests the injection of uid submucosally prior to polypectomy may reduce the risk of developing post- polypectomy syndrome.
Post- polypectomy syndrome occurs in 0.5%– 1% of polypectomies, and in 7%– 8% after endoscopic submucosal dissection. Patients can present acutely (within 12 hours) or delayed (up to 5days post procedure). Clinical presentation includes fever, tachycardia, abdominal pain, and leucocytosis. The main dierential is colonic perforation. As such, the denitive investigation to dierentiate is a CT scan, which may show focal thickening of the colon and periluminal fat stranding. In contrast to perforation, there will be no evidence of pneumoperitoneum. Therefore, an erect chest radiograph is unhelpful.
Management is conservative and includes nil by mouth, intravenous uids, and antibiotics until symptoms and inammatory markers settle. If symptoms and signs are mild, some patients may even be managed as outpatients. There is a very low risk of evolution to frank perforation, and the prognosis is generally excellent.
In this case, repeating a colonoscopy would be inappropriate given the concern of perforation. Equally, surgical intervention would only be indicated if a large perforation were conrmed radiologically.
Cha JM. Clinical outcomes and risk factors of post- polypectomy coagulation syndrome:a multicenter, retrospective, case- control study. Endoscopy. 203;45:202– 207. Doi:0.055/ s- 0032- 32604.
3. A. Endoscopic retrograde cholangiopancreatography (ERCP) for jaundice secondary to a hilar cholangiocarcinoma
• Some endoscopic interventions may cause bacteraemia; however, complications from bacteraemia are fortunately uncommon
• Antibiotics are no longer routinely required for the prevention of infective endocarditis
• Antibiotics are required in ERCP when adequate biliary decompression is unlikely to be achieved
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There are specic situations in endoscopy where antibiotics are indicated. These are summarized in Table 10.1.
Allison MC, Sandow JAT etal. Antibiotic prophylaxis in gastrointestinal endoscopy. Gut. 2009;58:869–
880. Doi:0.36/ gut.2007.36580.
Table10.1 Summary ofprophylactic antibiotic regimens recommended forgastrointestinal endoscopy
Scenario Rationale Antibiotics Dose/ route
1. Patients with valvular heart disease, valve replacement, and/ or surgically constructed systemic– pulmonary shunt or conduit or vascular graft
2. ERCP in the following:
a. Ongoing cholangitis or
sepsis elsewhere
b. Biliary obstruction and/ or
CBD stones
c. When complete biliary
drainage is unlikely to be achieved (e.g. PSC, hilar cholangiocarcinoma) (may need to consider alternative antibiotic prophylaxis if repeated procedures are needed)
d. Communicating pancreatic
cyst or pseudocyst
e. Biliary complications
following liver transplant
3. EUS in the following:
a. FNA solid lesions
b. FNA cystic lesions in or
near the pancreas or drainage of a cystic cavity
4. PEG Prevention of
Prevention of infective endocarditis or conduit/ graft infection
Prevention of procedure- related bacteraemia Prevention of cholangitis
Prevention of cholangitis
Reducing risk of introducing infection into cavity Prevention of cholangitis
Prevention of local infections Prevention of cyst infections
peristomal infection
Possible reduction in risk of other infections, such as aspiration pneumonia
Not indicated
Guide by culture results. Patients should already be established on antibiotics Not indicated unless biliary decompression is not achieved. If biliary decompression is not achieved during the procedure, a full course of antibiotics is indicated Ciprooxacin
or
Gentamycin
As (c)
As (c)+ amoxicillin
or
vancomycin
Not indicated
Co- amoxiclav
or
Ciprooxacin
Co- amoxiclav
or
Cefuroxime
Microbiology advice
750 mg PO 60– 90 mins before procedure
1.5 mg/ kg IV over 2– 3 mins As (c)
1 g IV single dose
20 mg/ kg IV infused over at least 1 hour
1.2 g IV single dose
750 mg PO single dose
1.2 g IV injection or infusion just before procedure 750 mg IV injection or infusion just before procedure
(continued)
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Table10.1 Continued
Scenario Rationale Antibiotics Dose/ route
Teicoplanin can be used if there is a past history of anaphylaxis or angioedema with penicillin/ cephalosporin
5. Variceal bleeding (not strictly prophylaxis)
6. Profound immunocompromise
(e.g. neutropenia <0.5 × 109/ L or advanced haematological malignancy)
CBD, common bile duct; PO, by mouth; IV, intravenous; PSC, primary sclerosing cholangitis; ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasound; FNA, ne- needle aspiration; PEG, percutaneous endoscopic gastrostomy.
Prevention of infections such as spontaneous bacterial peritonitis
Prevention of procedure- related bacteraemia
Piperacillin/ tazobactam
or
Third- generation cephalosporin Seek microbiology or regional liver unit advice in cases of penicillin allergy
Only indicated in procedures with a high rate of bacteraemia (e.g. sclerotherapy, dilatation, ERCP with obstructed system)
400 mg IV for adults
4.5 g IV 3 times a day
e.g. cefotaxime 2 g IV 3 times a day
Discuss with haematologist and/ or clinical microbiologist
4. B. Grade II A
• Gastroscopy should be performed between 12 and 48 hours post caustic ingestion
• Zargar’s classication is the most common endoscopic tool for assessing caustic injury
• There is a ninefold increase in morbidity and mortality with every increased injury grade
Gastroscopy is an important diagnostic and prognostic tool in the evaluation of a caustic injury, especially during the rst 12– 48 hours of caustic ingestion. It is contraindicated in patients with haemodynamic instability, severe respiratory compromise, and suspected perforations. In the absence of symptoms, signicant lesions are typically not seen endoscopically. Emergent endoscopy is recommended in symptomatic individuals and in those with intentional ingestions of caustic substances.
Endoscopy is the gold standard in diagnosis and prognostication in caustic ingestions. It also guides management. Zargar’s classication (Table 10.2) is most commonly used to grade severity of caustic injury. Grades 0– II Agenerally recover without sequelae. Grades IIB– III eventually develop oesophageal or gastric scarring, which may result in stricture formation. The degree of oesophageal injury endoscopically is a predictor of morbidity and mortality with a ninefold increase with each injury grade.
Table10.2 Zargar classication
Zargar classication Endoscopic description
Grade 0 Normal mucosa
Grade I Oedema and erythema of the mucosa
Grade II A Haemorrhage, erosions, blisters, supercial ulcers
Grade II B Circumferential lesions
Grade III A Focal deep grey or brownish- black ulcers
Grade III B Extensive deep grey or brownish- black ulcers
Grade IV Perforation
De Lusong MAA, Tombol ABG, Tuazon DJS. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 207 May 6;8(2):90– 98. Doi:0.4292/ wjgpt.v8.i2.90.
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283
5. D. Obesity
• Sedation- related complication is the leading factor in endoscopy- related mortality
• Assessment of risk factors for sedation- related complications is paramount
• Opiates and benzodiazepines have a synergistic eect
Conscious sedation is dened as the use of medication to depress the central nervous system without the loss of verbal communication. Sedation is the leading factor in endoscopy- related mortality.
Risk factors for complications of sedation include the following:
• Advanced age
• Obesity
• Comorbidities including cirrhosis, cardiac disease, respiratory disease, renal disease
• Prior administration of sedation or opiates
• Known drug allergies
• Low resting oxygen saturations
• Emergency endoscopy
Complications of sedation include over- sedation, paradoxical excitement, respiratory depression, aspiration, cardiac arrhythmias, acute coronary events, hypertension, hypotension, cerebrovascular events, nausea, vomiting, and ushing (Table 10.3). Risk factors for complications should warrant discussion of un- sedated endoscopy and, if sedation is undertaken, adjustment of doses should be considered.
6. C. Bile duct cannulation rate in at least 90%
The ESGE and United European Gastroenterology have identied quality of endoscopy as a major priority. They recommend that endoscopy services adopt the following key performance measures for ERCP and EUS:
1. Adequate antibiotic prophylaxis before ERCP (key performance measure, at least 90%)
2. Antibiotic prophylaxis before EUS- guided puncture of cystic lesions (key performance measure, at least 95%)
3. Bile duct cannulation rate (key performance measure, at least 90%)
4. Tissue sampling during EUS (key performance measure, at least 85%)
5. Appropriate stent placement in patients with biliary obstruction below the hilum (key performance measure, at least 95%)
6. Bile duct stone extraction (key performance measure, at least 90%)
7. Post- ERCP pancreatitis (key performance measure, less than 10%)
Minor performancemeasure
8. Adequate documentation of EUS landmarks (at least 90%)
Domagk D, Oppong KW etal. Performance measures for ERCP and endoscopic ultrasound:a European Society of Gastrointestinal Endoscopy (ESGE) quality improvement initiative. Endoscopy. 208;50:6– 27. Doi:0.055/ a- 0749- 8767.
7. D. The formal consent process should be completed before entry into the procedure room
• All endoscopic procedures require written consent, except in an emergency
Table10.3 Sedatives, analgesics and adjuncts used inendoscopy
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Drug Eect Contra- indications Side eects (SE) Onset
Benzodiazepines
e.g. Midazolam
Opiates
e.g. Pethidine*, Fentanyl
Buscopan Relief of smooth
Xylocaine Throat Spray (Topical lidocaine)
Sedation with amnesia, and no analgesic eect
Prevention, reduction, and relief of pain
Opiates have a synergistic eect with benzodiazepines
Give 3 minutes before benzodiazepines, as doses may need to be reduced by up to fourfold
muscle spasm
Analgesia of oropharynx
Neuromuscular respiratory weakness Severe respiratory depression
Acute respiratory depression Phaeochromocytoma
Myasthenia gravis, acute closed- angle glaucoma
Unsafe swallow (Relative)
Confusion Paradoxical excitement or agitation Nausea Vomiting Reduced respiratory eort Hypoxia Hypotension Cardiac or respiratory arrest
Confusion Nausea Vomiting Decreased responsiveness Reduced respiratory eort Hypoxia Hypotension Cardiac or respiratory arrest
Tachycardia Arrhythmias Anti- muscarinic side eects
Risk of aspiration Peak:1
(minutes)
Initial:1 Peak:1- 2
Initial:1- 2 Peak:3
Peak:4 Duration of action (hours):5
Duration of action:15– 60
Dose Reversal agent
<70 yrs:0– 2 mg, increment 0– 1 mg, max 5 mg
>70years:0– 1 mg, increment 0– 0.5 mg, max 2 mg
<70years old: Pethidine:initial dose 25 mg, increment 25 mg, max 50 mg Fentanyl:initial dose 50 mg, increment 25 mg, max 100 mg
>70years old: Pethidine:initial dose
12.5 mg, increment
12.5 mg, max 25 mg Fentanyl:initial dose 25 mg, increment
12.5 mg, max 50 mg
20 mg can be repeated every 30 minutes up to a max of 100 mg in 24 hours.
Max 20 applications (200 mg lidocaine base)
Flumazenil:0.2– 0.5 mg, increment 0.1 mg, peak eect in up to 1 minute, duration of action 1– 2 hours
SE:ushing, seizures, and late re- sedation.
Naloxone: Dosage 0.1– 0.2 mg, maximum 10 mg, peak eect in 1– 2 minutes, duration of action 1– 3 hours
SE: Pain, agitation, arrhythmias, pulmonary oedema, and late re- sedation.
-
-
*Pethidine is metabolized to fentanyl and therefore has less predictable eects, including a higher risk of hypotension, and hallucinations Dumonceau JM, Riphaus Aetal. European Society of Gastrointestinal Endoscopy, European Society of Gastroenterology and Endoscopy Nurses and Associates, and the European Society of
Anaesthesiology Guideline:Non- anesthesiologist administration of propofol for GI endoscopy. Endoscopy. 200 Nov;42():960- 74. Doi:0.055/ s- 0030- 255728
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• Abest interest decision should be taken for those who lack capacity
• The consent process should be completed before entry into the procedure room
All endoscopic procedures require written consent, except in an emergency. The endoscopist performing the procedure is ultimately responsible for ensuring that the consent process is appropriate for the procedure being undertaken. The endoscopist performing the procedure should assess capacity to consent. If a patient lacks capacity, delaying the procedure to allow the patient to regain capacity may be appropriate. If the patient is unlikely to regain capacity or the procedure is an emergency, the endoscopist should make a decision to proceed in the patient’s best interests. In such instances, where possible, the next of kin should be informed. However, this should not delay emergency treatment. Patients who lack capacity may have a proxy decision maker (e.g. Lasting Power of Attorney) or may require appointment of an Independent Mental Capacity Advocate. In non- emergency cases where the patient lacks capacity, the decision regarding endoscopy is best decided in a multi- disciplinary discussion with best interests in mind. Patients physically unable to sign their consent may have their consent countersigned by a witness (relative or healthcare professional (not the consenting healthcare professional).
All patients should receive written information explaining the procedure, and its intended benets and risks, in a format that they can understand. Written information should be provided in advance of the procedure. The consent process should be performed by a suitably trained individual before entry into the procedure room. Final validation of the consent process should be completed before the procedure starts. Endoscopic photo- and video- documentation as part of routine clinical care does not require additional consent. If a patient, with capacity, withdraws consent during an endoscopic procedure, the procedure should be stopped. The person’s concerns should be explored. If they clearly indicate a wish for the procedure to be discontinued, this must occur without delay unless doing so would result in a risk of serious harm to the patient.
Everett SM, Griths H etal. Guideline for obtaining valid consent for gastrointestinal endoscopy procedures. Gut. 206;65(0):585– 60. Doi:0.36/ gutjnl- 206- 3904.
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8. D. Neoplastic lesions account for two- thirds of cases
• Intussusception is a rare cause of intestinal obstruction in adults
• It typically occurs in the small bowel and is associated with structural lesions in 90% of which
two- thirds are neoplastic
Intussusception is the invagination of one segment of bowel into an immediately adjacent segment. It is most commonly found in children and represents the second most common cause of intestinal obstruction in this group after pyloric stenosis. The majority of paediatric intussusception is idiopathic (90%) and is usually ileocolic. Conversely, adult intussusception is rare, accounting for 1– 5% of cases of bowel obstruction and usually occurs in the ileum. Ninety per cent of adult cases will have an underlying structural cause, two- thirds of which will be due to benign or malignant neoplasms. The remainder are caused by infections, adhesions, intestinal ulceration, and congenital abnormalities such as Meckel’s diverticulum. These lesions act as a focal area of traction, or ‘lead point’, which draws the proximal bowel within the peristalsing distal bowel, which can ultimately lead to bowel ischaemia and perforation. Intussusception in adults is usually diagnosed on CT, which classically demonstrates a concentric hyperdense double ring or ‘target- sign’. In children, most ileocolic intussusception is successfully managed with ultrasound or uoroscopy guided pneumatic/ hydrostatic enema. In adults, because of the majority of cases arising from structural pathology in the small bowel, surgery remains the mainstay of treatment.
Marsicovetere P, Ivatury SJ, White B etal. Intestinal intussusception:etiology, diagnosis, and treatment. Clin Colon Rectal Surg. 207 Feb;30():30– 39. Doi:0.055/ s- 0036- 593429.
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9. D. Rubber band ligation (RBL)
• RBL is currently the rst- line intervention in Grades I– III haemorrhoids, with a long- term
success rate of >80%
• Surgical haemorrhoidectomy is associated with the lowest rate of recurrence but should be
reserved for when RBL has failed because of higher complication rates (pain, anal stenosis, incontinence)
Haemorrhoids are dened as the symptomatic enlargement and displacement of the anal cushions which are prominences of anal mucosa formed by connective tissue, smooth muscle, and blood vessels. Contributing factors include lack of dietary bre, chronic straining, excess time on the commode, constipation, and pregnancy. Haemorrhoids can be classied as internal (covered by columnar epithelium) or external (covered by squamous epithelium), and internal haemorrhoids can be graded from I– IV depending on the degree of prolapse during defecation. Conservative management of haemorrhoids includes lifestyle advice (adequate uid and bre intake, reduce straining, good anal hygiene), and treatment with laxatives and topical analgesics.
RBL is currently rst- line therapy in Grade I– III haemorrhoids with a long- term success rate of >80%. Pain is the most common complication of RBL but can be minimized by proximal placement and single banding at a session. Sclerotherapy and heater probe coagulation can be used in Grade I– II haemorrhoids with variable success and higher complication rates respectively, when compared to RBL. While surgical haemorrhoidectomy is more eective than RBL in the treatment of Grade III haemorrhoids, it is associated with higher rates of complications, pain, and disability, and should therefore be reserved for cases when band ligation has failed. Lord’s procedure involves anal dilation to decrease sphincteric pressure but is now an outdated technique because of high rates of post­procedural incontinence.
Ganz RA etal. The evaluation and treatment of hemorrhoids:a guide for the gastroenterologist. Clin Gastroenterol Hepatol 203;(6):593– 603. Doi:0.06/ j.cgh.202.2.020.
10. C. Topical diltiazem
• Topical diltiazem and GTN have a similar ecacy for chronic anal ssures
• Topical diltiazem has a superior side eect prole
• Surgical options, including sphincterotomy, are reserved for cases refractory to conservative
and medical therapy
Following the initial development of an anal ssure, passage of subsequent stool will continue to irritate the area. The internal sphincter may be involved and can go into spasm, causing further pain. It also pulls the edges of the ssure further apart, impairing wound healing, leading to the development of a chronic ssure.
Although conservative treatment may be sucient for some acute ssures, other patients will need medical or surgical therapy. Stool softeners may reduce the pain and progression of a ssure, warm baths may relax the sphincter, and topical anaesthetic gel can provide pain relief. Topical diltiazem would be the next treatment of choice. This has the same ecacy as GTN— however with a superior side eect prole (30% of patients who use topical GTN suer from headache). Topical diltiazem has been associated with healing rates of 65%– 95%. Fifty per cent of patients treated with topical GTN may experience recurrent ssures. Treatment with botulinum toxin has a similar ecacy to that of GTN and diltiazem. However, it is more expensive and therefore may be used in patients whose ssures do not heal with topical (diltiazem or GTN) therapy or in cases of recurrence.
With regard to surgical treatment, lateral internal sphincterotomy has consistently superior healing rates and less recurrence when compared with medical therapy. However, there is a higher rate of faecal incontinence following treatment. In general, sphincterotomy and the
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various alternative surgical techniques available should only be used if the patient does not respond to medical treatment.
Stewart D, Gaertner W etal. Clinical Practice Guideline for the management of anal ssures. Dis Colon Rectum. 207;60():7– 4. Doi:0.097/ DCR.0000000000000735
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11. B. Rectal bleeding on defaecation is a hallmark feature
• SRUS is a chronic, benign disorder in young adults
• Only 20% of patients have a solitary ulcer
• Patient education and conservative measures, including biofeedback, are the mainstay of
treatment
SRUS is a rare, benign disorder characterized by a combination of clinical, endoscopic, and histological ndings. Although denoted as a ‘solitary rectal ulcer’, only 20% of patients have a single ulcer endoscopically. It is a rare and often underdiagnosed disorder, with an annual prevalence of 1 in 100,000 persons. Adisorder of young adults, occurring most commonly in the third and fourth decade in men and women respectively. Men and women are aected equally, however. The aetiology is not well understood but is thought to be multifactorial. Characterized by single or multiple ulcerations of the rectal mucosa, symptoms include rectal bleeding and mucus discharge, usually associated with excessive straining or abnormal defaecation. The passage of blood during defaecation is a hallmark feature. However, over a quarter of patients are asymptomatic, diagnosed incidentally.
According to anorectal manometry studies, dyssynergic defaecation is associated with SRUS in 25%– 82% of patients. Defaecatory disorders with excessive straining are signicantly associated with SRUS. Diagnosis is made on clinical features, endoscopy, and histology. Proctosigmoidoscopy reveals shallow rectal ulcer(s) of varying sizes covered by white or yellow slough. Surrounding rectal mucosa may appear hyperemic. Key histological features include bromuscular obliteration of the lamina propria, hypertrophied muscularis mucosa, and glandular crypt abnormalities. Defaecatory proctogram and/ or anorectal manometry are useful for determining the presence of intussusception, rectal prolapse, or dyssynergic defaecation. Several treatment options include conservative measures (high- bre diet, patient education), biofeedback, medical therapy (topical sucralfate, mesalazine), and surgery (in presence of prolapse). Conservative measures and biofeedback are the mainstays of treatment.
Zhu Q, Shen R etal. Solitary rectal ulcer syndrome:clinical features, pathophysiology, diagnosis and treatment strategies. World J Gastroenterol. 204;20(3):738– 744. Doi:0.3748/ wjg.v20.i3.738.
12. A. Chlamydia lymphogranuloma venereum (LGV)
• LGV proctitis may mimic Crohn’s disease
• All patients with LGV proctitis should be screened for HIV
• Treatment is with macrolides— doxycycline or erythromycin
All the infections listed can cause proctitis, and often there will be coexisting infections. Patients should be tested for HIV, especially in cases of LGV, syphilis, and herpes simplex virus (Table 10.4). Where positive, contact tracing should be instigated.
LGV has re- emerged among European MSM in the past decade and is a relatively common cause of proctitis in this population. Anorectal LGV is generally a symptomatic infection, although asymptomatic infection does occur. Proctitis is the primary manifestation of LGV infection, usually occurring within a few weeks of sexual contact. It is characterized by symptoms of anorectal pain, mucopurulent discharge, bleeding per rectum, tenesmus, and constipation. Endoscopic examination may reveal distal granular or haemorrhagic proctitis with purulent exudate, inammatory inltrate,