Colorectal Flashcards
82 How are anal fissures treated?
Conservative
- High fibre diet
- Adequate fluid intake
- Sitz bath (bathing perianal area in water/saline)
- Stool softeners
Medical
- Topical analgesia
- Topical muscle relaxants (PR GTN, topical diltiazem, topical nifedipine) to target internal anal sphincter
- Botulinum toxin injection
Surgical (very rarely done)
- Partial lateral internal sphincterotomy (risk of faecal incontinence)
- Anal advancement flap (less effective but less risk)
83 What is an anal fissure?
How does if develop?
What causes it to persist?
Longitudinal tear in the skin and mucosa of the anal canal, distal to the dendate line
Primary causes = trauma (hard stool, prolonged diarrhoea, vaginal delivery, anal sex)
Secondary causes = previous anal surgical procedures, IBD, malignancy, communicable diseases (HIV, syphilis, chlamydia)
In chronic anal fissure, persistent IAS spasm prevents healing and causes repeated tearing open of the fissure
84 How would you go about investigating a previously well 63 yoa man who presented to you with a short history of rectal bleeding?
All rectal bleeding is assumed to be due to a rectal tumour until proven otherwise
History:
- Characterise bleeding (duration, frequency, volume, colour, relationship to stool)
- PMH pain, constipation, weight loss, diarrhoea
- Fx colorectal cancer
- Medications (esp. anticoagulants)
- Prev colonoscopy findings
- Smoking
Examination
- Vitals
- Abdominal exam incl. PR
- Signs of chronic anaemia (conjunctival pallor, SOB)
Investigation
- Bloods: FBC, iron studies
- Stool MCS OCP
- Sigmoidoscopy/colonoscopy
Ddx
- Anorectal: haemorrhoids, acute anal fissure, distal proctitis, rectal prolapse
- Rectosigmoid: rectal tumour, proctocolitis, diverticular disease
- Proximal colon: colonic tumour, colitis, angiodysplasia, NSAID- induced ulceration
85 How would you go about investigating a previously well 63 yoa man who presented to you with a short history of anaemia?
History
Dizziness, SOB, chest pain
Constitutional symptoms
PR bleeding, change in bowel habits
PMHx
PUD, GORD, malignancy, haematology, IBD, liver disease, coeliac
Dietary, smoking, EtOH
iFOBT, colonoscopies
Medications
NSAIDs, anticoagulants
Ix
FBC, iron, B12, folate, DAT
ECG
iFOBT
86 How would you go about investigating a previously well 63 yoa man who presented to you with a short history of a change in bowel habit to more frequent evacuation of loose stools with mucus?
Mucus is suggestive of an inflammatory diarrhoea
Causes
- Irritable bowel syndrome
- Villous adenoma
- Inflammatory bowel disorders
- Diverticular disease (occasionally)
- Haemorrhoids (maybe)
History
- Change in bowel habits (duration, frequency)
- Associated symptoms: PR bleeding, abdo pain, weight loss, fatigue
- Constitutional symptoms
- PMH: IBD
- Fx IBD, colorectal cancer
- Social: smoking, EtOH, recent gastro contacts, change in diet
Examination
- General inspection and vitals
- Abdo exam incl. PR
Investigation
- FBC, iron studies, serum B12 and folate
- Faecal calprotectin (released into the intestines in excess when there is any inflammation)
- Colonoscopy
87 What are the major risk factors for colorectal cancer?
There are non-modifiable, medical and lifestyle risk factors for colorectal cancer
Colorectal adeonomas are the most significant risk factor as cancer is thought to progress from them
Non-modifiable
Family history
Increasing age
Hereditary syndromes (FAP, HNPCC, SPS)
Medical comorbidities
IBD
Diet and lifestyle
Smoking
Alcohol
Obesity
Processed meat, high fat, low-fibre diet
88 What method is used for population screening for Colorectal cancer in Australia?
FOBT - used in asymptomatic average risk population 2-yearly between the ages of 50 and 75. It will be fully implemented by 2020
Average risk (no personal hx/fx/polyps/IBD, 1 x 1st/2nd degree relative with CRC \>55yo) - FOBT 2-yearly from age 50 to 75
Moderate risk (1 x 1st degree relative with CRC >55yo OR 2 x 1st degree on same side of family with CRC at any age OR 1 1st 1 2nd same side any age)
- Colonoscopy/sigmoidoscopy+CT colonography 5-yearly from age 50 (or 10 years younger than dx age in relative)
- FOBT every non-colonoscopy year
High risk (3+ 1st or 2nd same side with CRC/Lynch syndrome OR 2+ with CRC + high risk features OR suspected FAP OR confirmed fx of APC mutation)
- Genetic screening
- Flexi sig (FAP) or colonoscopy (attentuated FAP)every year between ages 12-35, 3-yearly after 35yo
- Colonoscopy + prophylactic aspirin (Lynch syndrome) 1-2 yearly from age 25 or 5 years younger than earliest family dx
89 What is neoadjuvant therapy for rectal cancer?
Neo-adjuvant therapy is the administration of therapeutic agents prior to the main surgical treatment. Surgical resection is the mainstay curative treatment of rectal adenocarcinomas.
Benefits:
- Improvement in resectability
- Tumour regression
- Higher rate of sphincter preservation
Indications:
- Usually only for T3 or T4
- Clinically node-positive T1 or T2 staged by MRI or trans-rectal USS (relative)
- Distal rectal tumour requiring abdominoperineal resection (relative)
- Tumour appears to invade mesorectal fascia on pre-op imaging (relative, decreased likelihood of achieving clear margins)
No established best regimen
- “Long course” = conventional fractionation RT + long-course concurrent chemo (5-FU)
- “Short course” = short-course RT only
90 Where are the common sites that metastatic disease from a colorectal primary are found?
Common:
- Liver (venous drainage via portal system)
- Lungs (next organ in the venous pathway)
- Peritoneum (proximity)
- Regional lymph nodes
Less common:
- Bone
- Brain
- Adrenal glands
- Kidneys
91 What are the treatment options for liver metastases from a colorectal primary?
Different from the normal approach to metastasis - 1/3 of CRC patients with mets have isolation to the liver, therefore curative treatment can still actively be pursued
Some general rules:
1) Resect where possible
2) RFA where surgically resectable lesion but patient not fit for surgery
3) Neo-adjuvant chemo or palliative chemo where surgically unresectable
Pre-op management
1) Neo-adjuvant chemo (unresectable -> resectable) - 5-FU, leucovorin, oxaliplatin (by HIA)
2) Portal vein branch embolisation (block flow to diseased portions, increases remnant liver volume due to post-embolisation regeneration, enabling hepatectomy while reducing risk of post-op liver failure)
Surgical resection
- Only treatment with definitive survival benefit
- MRI and PET to identify hepatic lesions and occult mets
- Procedure: segmentectomy/lobectomy OR wedge resection (smaller, non-anatomical)
- Can be done at same time as resection of CRC primary
Resection eligibility:
1) Primary cancer is being resected for cure
2) No extra-hepatic mets
3) Adequate post-resection hepatic function (at least 2 of 8 segments)
4) No involvement of major structures (portal vein, hepatic artery)
Radiofrequency ablation (RFA)
- Insertion of image-guided probe percutaneously into the tumour which produces high energy current into the tumour bed to effectively burn cancer cells
- Limited evidence (no RCT assessing efficacy)
Selective Internal Radiation Therapy (SIRT)
- Catheter-guided injection of small radioactive particles into the hepatic blood vessels and the blocking of hepatic vessels to trap beads in the tumour bed
- Targeted approach minimises damage to healthy parenchyma
- BUT, lack of evidence (no RCT)
92 What is the adenoma-carcinoma sequence?
The adenoma-carcinoma sequence is the progressive accumulation of mutations in oncogenes (e.g., KRAS) and tumour suppressor genes (e.g., APC, TP53) that results in the slow transformation of adenomas into carcinomas
It is based on the hypothesis that CRCs develop from intermediate pre-cancerous precursors such as adenomas/adenomatous polyps that become dysplastic over the course of 5-10 years.
During the normal growth process, epithelial cell proliferation occurs at the crypt base. As the cells migrate luminally they cease proliferating and then terminally differentiate.
In the adenoma-carcinoma sequence, the normal growth pattern becomes increasingly disrupted, with normal epithelium transforming into dysplastic aberrant crypt foci into adenoma as the tissue increases in size. This may be due to genetic predisposition (e.g. APC gene) or inactivation of DNA repair mechanisms.
Eventually, sufficient changes to oncogenes and tumour suppressor genes cause progression to a carcinoma which gains invasive potential
93 What is Crohn’s disease?
Crohn’s disease is an incurable chronic inflammatory bowel disease that can affect any part of the GIT from mouth to anus, characterised by unpredictable flares and remissions.
Epidemiology
- Males = females
- Peak age of symptom onset is teens to early 20s (with a second smaller peak 60-80yo)
- 4-10 per 100,000 annually
Aetiology is unclear but genetic factors and environmental factors are thought to play a role. These include familial histories of the disease, smoking, NSAIDs, and nutritional factors.
Pathology:
- Most commonly involves TERMINAL ILEUM and CAECUM (hence RLQ pain)
- Transmural inflammation
- Skip lesions, luminal stricturing, fistulation
- Deep ulceration creating cobblestone appearance
- Mesenteric “fat creeping” on small bowel
Clinical features: diarrhoea (non-bloody), malabsorption/weight loss, abdominal pain (usually RLQ), N/V, extra-intestinal manifestations (e.g. arthritis, skin disorders, vitamin B12 deficiency)
Investigations: colonoscopy + biopsy, CT/MRI enterography, exclusion of other inflammatory diarrhoea causes (stool MCS & OCP, c. diff toxin assay)
Management:
- Conservative: nutrition supplementation/elimination diet/low carb + symptomatic therapy (loperamide, paracetamol)
- Medical: prednisone, oral corticosteroids (budesonide), IV corticosteroids (hydrocortisone. methylprednisone), immunosuppression (azathioprine, methotrexate, mercaptopurine), immunomodulators (TNF-a inhibitors e.g. infliximab)
- Surgical: resection of obstructed areas (but NOT curative)
Antibiotics (metronidazole and ciprofloxacin) should only be used in perianal and fistulising disease.
94 What is diverticular disease?
Acquired outpouchings of colonic mucosa and overlying connective tissue through colonic wall
Mostly asymptomatic, but may present as diverticulitis or bleeding diverticular disease
Diverticulitis: LIF pain, nausea, fever, loose stools
Bleeding: large volume dark red, clotted blood. Due to rupture of a peridiverticular submucosal blood vessel
Environmental factors: chronic lack of dietary fibre, decreased physical activity, obesity, red meat consumption, excess alcohol/caffeine
Genetic factors: altered colonic wall structure (e.g. increased collagen synthesis and elastin deposition), connective tissue abnormalities
Commonly affected areas are sites of potential defect between teniae coli where mucosal blood vessels penetrate the wall. The sigmoid colon is most commonly affected.
Right-sided diverticular disease commonly affects Japanese, Chinese, Polynesian, and Hawaiian patients.
Isolated caecal diverticula are common in westernised countries and are susceptible to perforation.
95 What is diverticulitis?
How does it present clinically?
Diverticulitis is the inflammation of one or more diverticulum. It can be acute or chronic, uncomplicated or complicated by diverticular abscess, fistula, bowel obstruction, or free perforation.
Incidence increases with age and is increasing with low-fibre diets being prevalent in westernised society.
Signs and symptoms: LLQ pain (70%), change in bowel habits, N/V, flatulence, bloating
On examination: fever, localised tenderness, tender palpable mass (where diverticular abscess present), signs of perforation (peritonism, distension, absent/reduced bowel sounds), signs of fistula (PV discharge, UTI)
96 What are the major complications that can result from diverticulitis?
- Abscess
- Perforation (frank or contained/micro)
- Fistula (between bladder, vagina, uterus, other bowel segments, and the abdominal wall
- Obstruction
97 What are haemorrhoids and how are they classified or described?
Haemorrhoids are vascular-rich connective tissue cushions located within the anal canal
Can be classified as external or internal, or graded I-IV
- External = originate distal to the dentate line, covered by sensate anoderm or skin
- Internal = originate proximal to the dentate line, covered by insensate transitional epithelium
NB: dentate line is the anatomical landmark demarcating the upper two-thirds of the anal canal from the lower third, where columnar epithelium (above line) meets stratified squamous epithelium (below)
- *Grade I**: no prolapse, often bleed
- *Grade II**: prolapse only with straining/defecation, spontaneous reduction
- *Grade III**: prolapse spontaneously, manually reducible
- *Grade IV**: chronically prolapsed, irreducible, internal and external components, presents acutely as a strangulation or thrombosis.
98 How are symptomatic haemorrhoids treated?
Conservative (grade I-II and external)
- Weight loss, exercise, high-fibre diet
- Avoid excessive straining and > 5 minutes on the toilet
- Sitz baths
- Stool softeners
- Topical analgesia, anti-inflammatories or antispasmodics
Outpatient (grade III)
- Rubber band ligation
- Sclerotherapy
- Infrared coagulation
Surgical (grade IV)
- Arterial ligation
- Submucosal haemorrhoidectomy
- Stapled haemorrhoidopexy
99 What are the indications for elective surgery in a patient with Ulcerative Colitis?
Surgery is considered curative in UC
Acute:
- Fulminant cases non-responsive to medical management
- Acute exacerbation progressing to toxic megacolon/perforation/major haemorrhage
Elective:
- Chronic disabling symptoms (intractable diarrhoea w/ urgency, recurring anaemia, unable to maintain weight and nutrition)
- Children with FTT or growth retardation
- Longstanding UC w/ progression to dysplasia/malignancy (increased risk of 0.5-1.0% per year after the first 10 years)
Options: subtotal + ileostomy, proctocolectomy + permanent ileostomy, spincter-preserving proctocolectomy
100 What are the indications for elective surgery in a patient with Crohn’s?
Surgery is NOT curative in Crohn’s disease. Every attempt should be made to preserve as much bowel as possible and not necessarily resect all disease
Up to 70% of patients with Crohn’s will eventually need surgery, of whom half will need further surgery within 5 years
Elective indications:
- Fistulising disease
- Strictures/obstruction
- Abscess formation
- Small bowel or colonic cancer/dysplasia
- Failure of medical therapy
- Growth retardation in children
101 What are the indications for emergency surgery in a patient with inflammatory bowel disease?
Toxic megacolon
- Total or segmental non-obstructive colonic distension ≥6cm with systemic toxicity
- Mx: intestinal resection + faecal diversion
Haemorrhage
- Rectal blood loss
- Mx: colectomy + rectal preservation + ileostomy (UC), segmental resection (Crohn’s)
Perforation
- Peritonism, abdominal pain, fever/chills, N/V
- Mx: intestinal resection + faecal diversion
Intra-abdominal abscess with sepsis
- Malaise, swinging fever, abdominal pain, N/A, paralytic ileus
- Mx: CT-guided percutaneous drainage OR definitive resection
Intestinal obstruction
- Abdominal pain, vomiting, distension, obstipation, palpable mass
- Mx: non-operative, reserve surgery for complete obstruction or intractability
102 You are the ED intern on duty. You are asked to see a 20 yoa man who has presented with perianal pain that started 24 hours ago and has got worse despite appropriate analgesia. The pain is worse when he walks or sits. This has not happened before. He has no other relevant history. On examination you find a fluctuant, warm, red 3cmx3cm swelling at the anal margin. What is the likely diagnosis?
Likely diagnosis = anorectal abscess
Ddx: pilonidal abscess, anal fissure, thrombosed haemorrhoid, infected epidermal inclusion cyst
Very common, 1/3 of Crohn’s patients, 2-3x more likely in men, 20-40yo peak age, highest occurrence in spring and summer
Begins as an acute purulent infection of the anal glands which lie in the intersphincteric (intramuscular) space. Their ducts pass through the internal sphincters and drain into the anal crypts at the dentate line. Occlusion of these crypts by impacted food matter, by oedema secondary to hard stool/foreign body, or adjacent inflammation (e.g. Crohn’s) results in infection.
The infection rarely stays in the intramuscular space, spreading in any of three possible directions:
1) Inferiorly = perianal abscess
2) Laterally = ischiorectal/ischioanal abscess
3) Superiorly = supralevator abscess
Symptoms: localised pain (1-2 days prior, progressively more severe), swelling and warmth, pain exacerbated by movement/coughing/sneezing/bowel motion
Signs: tender indurated area, may only be felt PR
Management: surgical drainage
103 You are the ED intern on duty. You are asked to see a 20 yoa man who has presented with perianal pain that started 24 hours ago and has got worse despite appropriate analgesia. The pain is worse when he walks or sits. This has not happened before. He has no other relevant history. On examination you find a fluctuant, warm, red 3cmx3cm swelling at the anal margin. What is the likely diagnosis? What aetiological factors are associated with this condition?
Likely diagnosis = anorectal abscess
Ddx: pilonidal abscess, anal fissure, thrombosed haemorrhoid, infected epidermal inclusion cyst
Very common, 1/3 of Crohn’s patients, 2-3x more likely in men, 20-40yo peak age, highest occurrence in spring and summer
Begins as an acute purulent infection of the anal glands which lie in the intersphincteric (intramuscular) space. Their ducts pass through the internal sphincters and drain into the anal crypts at the dentate line. Occlusion of these crypts by impacted food matter, by oedema secondary to hard stool/foreign body, or adjacent inflammation (e.g. Crohn’s) results in infection.
The infection rarely stays in the intramuscular space, spreading in any of three possible directions:
1) Inferiorly = perianal abscess
2) Laterally = ischiorectal/ischioanal abscess
3) Superiorly = supralevator abscess
Symptoms: localised pain (1-2 days prior, progressively more severe), swelling and warmth, pain exacerbated by movement/coughing/sneezing/bowel motion
Signs: tender indurated area, may only be felt PR
Management: surgical drainage
104 You are the ED intern on duty. You are asked to see a 20 yoa man who has presented with perianal pain that started 24 hours ago and has got worse despite appropriate analgesia. The pain is worse when he walks or sits. This has not happened before. He has no other relevant history. On examination you find a fluctuant, warm, red 3cmx3cm swelling at the anal margin. What is the likely diagnosis?
Likely diagnosis = anorectal abscess
Ddx: pilonidal abscess, anal fissure, thrombosed haemorrhoid, infected epidermal inclusion cyst
Very common, 1/3 of Crohn’s patients, 2-3x more likely in men, 20-40yo peak age, highest occurrence in spring and summer
Begins as an acute purulent infection of the anal glands which lie in the intersphincteric (intramuscular) space. Their ducts pass through the internal sphincters and drain into the anal crypts at the dentate line. Occlusion of these crypts by impacted food matter, by oedema secondary to hard stool/foreign body, or adjacent inflammation (e.g. Crohn’s) results in infection.
The infection rarely stays in the intramuscular space, spreading in any of three possible directions:
1) Inferiorly = perianal abscess
2) Laterally = ischiorectal/ischioanal abscess
3) Superiorly = supralevator abscess
Symptoms: localised pain (1-2 days prior, progressively more severe), swelling and warmth, pain exacerbated by movement/coughing/sneezing/bowel motion
Signs: tender indurated area, may only be felt PR
Management: surgical drainage
105 What is Ulcerative Colitis?
Def: A chronic inflammatory bowel disease affecting any part of the large bowel but restricted to the mucosa and submucosa. The rectum is always involved (proctitis), the lesion is continuous, and the disease is characterised by exacerbations and remissions.
Epidemiology: 2/3 cases develop by age 30, slightly more common than Crohn’s (2-10 per 100,000)
Aetiology: Unclear - possible genetic predisposition (first-degree fx of IBD), possible environmental triggers (diet, bacterial antigens)
Pathophysiology:
- Initial colonic mucosa inflammation
- Neutrophils accumulate in tubular colonic glands → crypt abscesses
- Sloughing of overlying mucosa → superficial ulceration, denuded appearance
- Residual islands of intact but oedematous mucosa = pseudopolyps
- “Goblet cell depletion” in colonic glands due to chronic inflammation
- Over time → dysplasia → neoplasia (adenocarcinoma), so greatest risk of malignancy with early onset and extensive disease
- Long-standing colitis → fibrosis → loss of haustration and colonic shortening (“lead pipe” colon)
Clinical features:
- PR bleeding
- Stool changes: diarrhoea, tenesmus (feeling of incomplete voiding), urgency, incontinence
- Abdominal cramping or pain esp. preceding defecation
- Systemic symptoms: fever, weight loss, anorexia, fatigue
- Extra-intestinal features: jaundice, uveitis, arthritis
Investigations: sigmoidoscopy + mucosal biopsy, colonoscopy, CT colonography, stool MCS & OCP, stool c. diff toxin
Management:
- Conservative often not helpful
- Medical: 5-ASA, corticosteroids, immunosuppressants (azathioprine), immunomodulators (infliximab)
- Surgical: colectomy (required in 20-30%, curative, stoma may be required)
Prognosis:
- Normal life expectancy
- Greater risk of colorectal cancer
- Toxic megacolon can be a complication
106 This lesion is found at colonoscopy in the proximal colon. What is it? How should it be treated? Is follow up or surveillance needed?
What = pedunculated or sessile polyp (depending on look)
Treatment:
1) Polypectomy OR representative sample biopsy where numerous small polyps are encountered
2) Send sample for biopsy
Follow-up and surveillance:
1) Follow-up in clinic for biopsy results 4-6 weeks
2) Surveillance time-frames according to risk
107 This 22 year old female patient presents with vague intermittent right sided abdominal discomfort and some mild diarrhoea.
What abnormality is evident here in the terminal Ileum and right colon at colonoscopy?
What histopathological findings are anticipated in the biopsy findings of this lesion?
What are possible diagnoses?
Abnormality
Cobblestoning, linear ulcers, granulomas, stricture
Histopathological findings
Transmural inflammation, non-caseating granulomas, cobblestoning, skip lesions, hypertrophic lymph nodes, giant cells
DDx
Crohn’s, UC, infectious colitis, IBD
108 This lesion is found at colonoscopy in the sigmoid colon of an 85 year old male admitted acutely with a near complete large bowel obstruction.
What is the lesion?
What initial treatment is most appropriate for this patient whose CT scan shows a large number of bilobar hepatic metastases?
What are the major risks of this approach?
Lesion = colorectal cancer
Considerations in this case:
Priority #1: decompress bowel with stenting +/- resection
Priority #2: liver mets
Liver resection eligibility:
1) Primary cancer is being resected for cure
2) No extra-hepatic mets
3) Adequate post-resection hepatic function (at least 2 of 8 segments)
4) No involvement of major structures (portal vein, hepatic artery)
In this case it does not appear that the liver is immediately resectable. Therefore, a decision would need to be made as to pursuing neo-adjuvant therapy with an aim to future resectability, or to palliate.
Treatment:
- Neo-adjuvant chemo in attempt to shrink liver mets to a size where liver may be resectable
- Chemo options include 5-FU (pyrimidine analogue) ± leucovorin, oxaliplatin (platinum compound), Bevacizumab (VEGF inhibitor), Cetuxumab (EGFR inhibitor)
Major risks of approach:
- Stenting: perforation, stent migration, bleeding, abdominal pain
- Chemo: hepato-/oto-/nephro-/neuro-toxicity (Oxaliplatin), myelosuppression (5-FU), stroke/arterial thromboembolism/bleeding (bevacizumab)
109 What is the obvious abnormality on this X-ray and in this operative photo?
In the presence of symptoms of large bowel obstruction what initial treatment options exist?
What can be done to prevent recurrence?
Obvious large bowel x-ray abnormalities
Dilatation:
Coffee-bean (volvulus):
Initial treatment:
- Volvulus = decompression (flexi sig), Hartmann’s procedure if unsuccessful
- Any other LBO = colonoscopic stenting, resection + stoma if unsuccessful
Recurrence prevention:
- Hartmann’s for volvulus (very high recurrence rate)
- Stool softeners, high-fibre diet for faecal impaction LBO
110 This is a photo of a patient with a loop defunctioning colostomy.
What is the abnormality seen here?
What is the mechanism?
What treatment options are there?
Parastomal hernia/prolapse
- Common complication among colostomy patients
- Mechanism: protrusion of bowel loop through abdominal wall around the stoma site; risk factors include obesity, stoma aperture is too large or placed outside rectus sheath, multiple previous incisions in the abdominal wall around the stoma
- Treatment = primary vs mesh repair (hernia), cool compress/osmotic agent/manual reduction/binder (prolapse)
111 What is the lesion visible here at colonoscopy and what has been done?
What is the possible histology?
What additional endoscopic manoever is needed before completion of the colonoscopy?
112 This patient presents with anal discharge and pain.
What is the likely nature of this lesion?
What does the initial management involve?
How is it usually treated?
What is the role of surgery?
Perianal abscess draining into anal canal via fistula
Initial management: analgesia, I&D of the abscess
Treat cause if possible - Crohn’s disease, constipation
Surgery
Abscess: I&D
Fistula: fistulotomy if small, seton placement
113 This patient presented with severe anal pain after lifting a heavy piece of furniture. He feels this perianal swelling but does not present to his GP for a couple of days.
What is the diagnosis?
What is the treatment?
Prolapsed internal haemorrhoid
Depends on grade:
I = infrared photocoagulation, sclerosing agent II = rubber band, arterial ligation III = haemorrhoidopexy \> rubber band IV = haemorrhoidectomy
114 This man had had an abscess drained in the perianal region.
Q1: What is the common presentation of this problem?
Q2: What is the first line of management?
Q3: What bacteria are usually cultured?
Q4: What is the usual cause of this?
Q1. Perianal pain worse on sitting or walking, fluctuant warm red swelling at anal margin
Q2. Analgesia + drainage
Q3. Aerobes (E. Coli, staph, strep), anaerobes (clostridium, bacteriodes, peptostreptococcus)
Q4. Begins as an acute purulent infection of the anal glands which lie in the intersphincteric (intramuscular) space. Their ducts pass through the internal sphincters and drain into the anal crypts at the dentate line. Occlusion of these crypts by impacted food matter, by oedema secondary to hard stool/foreign body, or adjacent inflammation (e.g. Crohn’s) results in infection.
115 This patient had had an endoscopic mucosal resection (EMR) of a colonic polyp.
- What are the complications of this procedure?
- What is the likely pathology here?
- What would normally occur if there is found to be a tiny focus of completely excised, well differentiated invasive cancer in the specimen that is far from the resection line?
- Bleeding and perforation, minor risk of bleeding from irritated haemorrhoids
- Most polyps needing EMR are sessile - villious adenomas or sessile serrated
- Management of malignant polyps by polypectomy alone is now standard practice and is generally acknowledged to be safe, providing that the cancer is completely contained within the resected tissue, the margins are free of cancer and there is no lymphovascular invasion
Follow up is required to detect residual adenoma or recurrence in 6-12 months, then 3 years, then 5 yearly
116 This is a photo of the anal canal taken at colonoscopy by retroflexion of the scope.
Q1. What does this show?
Q2. How do these present clinically?
Q3. How are they treated?
Q1. Haemorrhoid
Q2. Bright PR bleeding, pain/painless, prolapse, pruritus
Q3. Depends on grade
117 This patient presents with perianal itching.
Q1. What are the lesions you can see in the perianal area?
Q2. What is the responsible agent that causes this condition?
Q3. What treatments are available?
