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Junior surgery > General - Large bowel > Flashcards

General - Large bowel Flashcards

1
Q

Give some of the risk factors for developing acute appendicitis?

A
  • Family History
  • Ethnicity - More common in caucasians but ethnic minorities at higher risk of perforation
  • Environmental - seasonal presentation during summer
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2
Q

Name 2 specific signs for acute appendicitis

A
  1. Rosving’s sign: RIF pain when palpating the LIF
  2. Psoas signs: RIF pain with extension of the right hip
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3
Q

What imaging should be done for suspicion of acute appendicitis?

A
  • CT scan is best type of imaging
  • USS can be done but only works well in children or slim adults
    • Can help rule of gynaecological pathology if this is a differential
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4
Q

How is acute appendicitis managed?

A
  • Definitive treatment is laparascopic appendicetomy
  • Can try on antibiotics to see if settles but studies show best to remove the appendix
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5
Q

What is the best way to manage a appendicular mass?

A
  • In this case surgery does more harm than good
  • Pt needs prologned antibiotic therapy (augmentin/co-amoxicav) and then offered surgery to remove appendix at a later date
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6
Q

What are some of the complications of acute appendiciits?

A
  • Perforation - if left untreated, can cause peritoneal contamination
  • Surgical site infection
  • Appendix mass - where omentum and small bowel adhere to the appendix
  • Pelvic abscess - presents with feveer and a palpable RIF mass
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7
Q

What is the most commonly used scoring system for acute appendicitis?

A

The Alvarado score

Score 1-4 dischage

Score 5-6 admit for observation/ admission

Score 7-10 surgery

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8
Q

Describe the pathophysiology behind diverticular disease

A
  • Aging bowel naturaly weakens over time
  • Stool movements increase lumenal pressure and can cause outpouchings of mucosa through weaker areas of bowel wall
  • Bacteria can grow in the outputchings leading to inflammation, potentially perforation
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9
Q

What are some of the complications of someone with chronic diverticular disease?

A

Chronic disease can cause fistulae to form

Most commonly colovesical or colovaginal

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10
Q

Give some risk factors for developing diverticular disease

A
  • Increasing age
  • Low dietary fibre
  • Obesity
  • Smoking
  • Family history
  • NSAID use
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11
Q

What are the 4 different manifestations of diverticular disease?

A
  1. Diverticulosis - presence of diverticula (can be asymptomatic and incidental finding)
  2. Diverticular disease - when symptoms start to arise from diverticula
  3. Diverticulitis - inflammation of diverticula
  4. Diverticular bleed - when diverticula erode into a blood vessel - causes a large volume but painless bleed
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12
Q

How does acute diverticulitis present?

A
  • acute abdominal pain - typically sharp and localised to LIF, worse on movement
  • Decreased appetite
  • Pyrexia
  • N+V
  • Change in bowel habit
  • Bleeding
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13
Q

What investigations should be done if suspecting acute diverticulitis?

A
  • Routine bloods: FBS, CRP, U+E, consider faecal calprotectin if diagnosis less clear
  • Group and Save
  • Venous blood gas
  • Urine dipstick to exclude urological causes
  • CT abdomen pelvis - best imaging
  • Flexible sigmoidoscopy suitable if diverticular disease is uncomplicated
    • CT colonography is the alternative if patient not suitable
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14
Q

What CT findings may suggest diverticulitis?

A
  • Thickening of the colonic wall
  • Pericolonic fat stranding
  • Abscesses
  • Localise air bubbles
  • Or free air
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15
Q

What staging is used for classifying acute diverticulitis based on CT findings?

A

Hinchey Classification

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16
Q

How should patients with uncomplicated diverticular disease be managed?

A
  • Manage as outpatient with simple analgesia and encourage oral intake
  • Encourage high fibre diet
  • Outpatient colonsocopy arranged to exclude any masked malignancies
    *
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17
Q

How should patients with acute diverticulitis be managed?

A
  • First conservatively: antibiotics, IV fluids, analgesia, encourage oral intake
  • Symtpoms typically improve within 2-3 days
  • If pt clinically deteriorates then repeat imaging
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18
Q

When is surgical intervention for acute diverticulitis required?

A

Only if there is perforation with faecal peritonitis or overwhelming sepsis

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19
Q

What procedure is performed in perforated cases of acute diverticulitis?

A

Hartmann’s procedure

Sigmoid colectomy with formation of an end colostomy

(Reversal of colostomy can be done at a later date but only in 50% of cases)

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20
Q

What are some of the complications of acute diverticulitis?

A
  • Recurrence (10-35%)
  • Stricture (have to do a biopsy to check it’s not a malignant stricture)
  • Obstruction
  • Fistula formation
  • Perforation
  • Bleed
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21
Q

What is a fistula?

A

An abnormal connection between 2 epithelial surfaces

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22
Q

What is a sinus?

A

An open ended cavity

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23
Q

What is Crohn’s Disease?

A

An inflammatory bowel disease affecting anywhere from mouth to anus but commonly tarets the distal ileum and proximal colon

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24
Q

Describe the features of inflammation in Crohn’s disease

A
  • Transmural (affects full thickness of bowel wall)
  • Cobblestone appearance of deep ulcers and fistulas
  • Skip lesions (non-continuous)
  • Perianal disease
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25
Q

What microscopic features are seen in Crohn’s disease?

A

Non- Caseating granulomas

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26
Q

What types of fistulas can form in Crohn’s disease?

A
  • Perianal
  • Entero-enteric
  • Recto-vaginal
  • Entero-vesicular
  • Entero-cutaneous
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27
Q

What are some of the risk factors for developing Crohn’s disease?

A
  • Family history (20% have 1st degree affected relative)
  • Smoking
  • White European
  • Appendectomy
    • increases risk directly after surgery
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28
Q

What are some of the extra-intestinal features seen in Crohn’s disease?

A
  • MSK - arthritis
  • Skin- eythema nodosum, pyoderma gangrenous
  • Eyes- uveitis, episcleritis, iritis
  • HBP - primary sclerosing cholangitis, cholangiocarcinoma, gall stones
  • Renal - stones
29
Q

How does Crohn’s disease present clinically?

A
  • Bimodal ages: 15-30 and 60-80
  • Episodic abdominal pain and diarrhoea
  • May contain mucus and blood in stool
  • Low grade Fever
  • Malaise
  • Anorexia
  • Oral aphthous ulcers
  • Perianal disease
30
Q

What investigations should you do if suspecting Crohn’s disease?

A
  • Routine bloods: for anemia, low albumin (secondary to malabsorption), evidence of inflammation in CRP/WCC
  • Fecal calprotectin - good sensitivity
  • Abdominal X-ray to exlude any features of toxic megacolon
  • Stool sample for any possible infective causes
  • Colonoscopy with biopsy: Gold Standard
  • CT abdo pelvis for sever chrohn’s disease
    • can demonstrate bowel obstruction, fistula formation, perforation, collection formation
  • MRI if looking for enteric fistulae
31
Q

Which drugs should be avoided in Crohn’s disease patients and why?

A

Any anti-motility drugs e.g. loperamide

Why? Can induce toxic megacolon

32
Q

How should acute attacks of Crohn’s be managed?

A
  • Fluids
  • Nutritional support
  • Prohphylactic heparin
    • IBD flares cause pro-thrombotic state
  • Medications
    • corticosteroids
    • immunosuppresives - azothioprine, mesalazine
    • biologics- inflximab can be trialled as rescue therapy
33
Q

How often is surgery needed for Crohn’s disease patients?

What types of surgery are done?

A

70-80% will need surgery at some point in their lives

  • Ileocaecal resection
  • Surgery for peri-anal disease
    • abscess draining, senton insertion, laying open of fistula
  • Stricturoplasty
    • division of strictures causing bowel obstruction
  • Small or large bowel resections
34
Q

What are some of GI complications of Crohn’s disease?

A
  • Fistulae
  • Stricture formation
  • Recurrent peri-anal abscess
  • GI malignancy (3% chance of colorectal cancer, x30 more likely to develop small bowel CA)
35
Q

What are some of the extra-intestinal complications of Crohn’s?

A
  • Malabsorption
  • Osteoporosis
    • secondary to malabsorption or long term steroid use
  • Increased risk of gallstones (reduced absorption of bile salts at terminal ileum)
  • Increased risk of renal stones
36
Q

What are the typical demographics of patients with UC?

A
  • Caucasian
  • Bimodal distribution: 15-25yrs, 55-65yrs
  • Males and Females affected equally
37
Q

Describe the pattern of inflammtion seen in UC

A
  • Diffuse continual inflammation of mucosa starting at the rectum and spreading proximally (potentially affecting the entire large bowel
  • Histologically shows inflammation of the mucosa and submucosa
  • Pseudopolyps can form from repeated episodes of ulceration and healing
38
Q

What microscopic changes are seen in UC?

A
  • Crypt abscesses
  • Reduced goblet cells
  • Non-granulomatous inflammation
39
Q

What is meant by the term backwash ileitis?

A
  • Seen in UC
  • If the ileoceacal valve is incompetent a portion of the distal ileum
40
Q

How does UC typically present?

A
  • Blood diarrhoea (90% of cases)
  • Increased frequency and urgency of defecation
  • Tenesmus
  • PR bleeding
  • Mucus discharge
  • May be clinically dehydrated +/- electroylyte imbalance if more widespread colonic involvement
  • Malaise
  • Anorexia
  • Low grade fever
41
Q

Which criteria is used to classify the severity of an UC exacerbation

A

Truelove & Witts criteria

42
Q

What extra-intestinal complications can be seen in UC?

A
  • MSK - enteropathic arthritis (typically affects nail joints), nail clubbing
  • Skin - erythema nodosum
  • Eyes - episcleritis, anterior uveitis, iritis
  • Hepatobiliary - primary sclerosing cholangitis
43
Q

Which investigations should be done for investigating UC?

A
  • Routine bloods: FBC, U&Es, CRP, LFTs, clotting
  • Faecal Calprotectin - raised in IBD but normal in IBS
  • Stool sample - for microscopy and culture
  • Colonoscopy with biopsy - for definitive diagnosis - flexi sig may be sufficient
    • avoid in acute severe exacerbations
  • Abdominal Xray or CT scan in acute flares to assess for toxic megacolon/ bowel perforation
44
Q

What features may you find on an X-ray of a patient with UC?

A
  • Mural thickening
  • Lead pipe colon / loss of haustra (with barium studies)
45
Q

How are flares of UC managed medically?

A
  • Corticosteroid therapy and immunosuppresive agents (mesalazine or azothioprine)
  • Add infliximab as rescue therapy if no response to the above
46
Q

What are the indications for surgery in patients with UC?

A
  • Disease non responsive to medical management
  • Toxic megacolon
  • Bowel perforation
  • To reduce risk of colonic carcinoma if dysplastic cells detected on routine monitoring
47
Q

Which surgical procedures can be done for patients with UC?

A
  • Total proctocolectomy- curative, patient requires ileostomy
  • Many patients first undego a subtotal colectomy which preserves the rectum
48
Q

What complications can occur in UC?

A
  • Toxic megacolon
  • Colorectal carcinoma
  • Osteoporosis
  • Pouchitis - inflammation of ileal pouch
    • symptoms: abdo pain, bloody diarrhoea, nausea
    • treated with metronidazole and ciprofloxacin
49
Q

What is toxic megacolon?

How does it present?

A

An acute form of colonic distension

Severe abdominal pain, abdominal pain, abdominal distension, pyrexia and systemic toxicity

50
Q

How should toxic megacolon be managed?

A

Decompression of the bowel ASAP due to high risk of perforation

51
Q

What is a volvulus

A

The twisting of a loop of intestine around its mesenteric attachment causing closed loop opstruction

Affected bowel can become ischemic leading to bowel necrosis and perforation

52
Q

Where do volvuli most common occur and why?

A

At the sigmoid colon due to the long mesentry which increases with age makes it more prone to twisting

(can also occur at the caceum, stomach, small intestine and transverse colon)

53
Q

Give some of the risk factors for developing a volvulus

A
  • Increasing age
  • Neuropsychiatric disorders
  • Resident in nursing home
  • Chronic constipation or laxative use
  • Previous abdominal operations
  • Male
54
Q

How do patients with a volvulus present clinically?

A

Clinical features of bowel obstruction:

  • colicky pain
  • abdominal distension
  • absolute constipation
  • usually rapid onset
  • vomiting occurs as a late sign (due to sigmoid being distal in GI tract)
  • O/E: abdomen is often tympanic to percussion
55
Q

Which investigations should be done if suspecting volvulus?

A
  • Routine bloods: including electrolytes, Ca2+ and TFTs to rule out any pseduo-obstruction
  • CT scan abdo pelvis with contrast
  • Abdominal radiograph
56
Q

What will you seen on abdominal xray if patient has a volvulus?

A

Coffee bean sign

57
Q

What will you seen on CT scan if patient has a volvulus?

A

whirl sign

58
Q

How are patients with sigmoid volvulus managed?

A

Mainly conservatively with initial decompression by sigmoidoscope and instertus of flatus tube

Sigmoidoscope decompression - patient placed in left lateral position and sigmoidscope inserted, twisted bowel is located, there will be a rush of air and liquid faeces as obstruction relieved

Flatus tube - left in situ for up to 24 hours to allow continued passage of contents. Unsuccessful in 25-50% of patients so formal flexi sig decompression required

59
Q

When is surgery required for sigmoid volvulus?

A

When conservative management fails or:

  • Colonic ischaemia or perforation
  • Repeated failed attemps at decompression
  • Bowel is necrotic on endoscopy
60
Q

What are some of the complications of a sigmoid volvulus?

A
  • Bowel ischemia
  • Perforation
  • Risk of recurrence
  • Complications of stoma needed
  • Overal mortality is high as patients are generally old, frail and multi-morbid
61
Q

What is the typical age of onset for caecal volvulus?

A

Bimodal: 10-29 years and 60-79 years

62
Q

How do the pre-disposing factors for caecal volvulus differ between the older and younger age groups?

A

Younger patients: intestinal malformation or excessive exercise

Older patients: chronic constipation, distal obstruction or dementia

63
Q

What is pseduo-obstruction of the bowel?

A

Dilation of the colon due to an adynamic bowel in the absence of mechanical obstruction

64
Q

What is believed to be the pathophysiology behind pseudo-obstruction?

A

Believed to be due to interruption of the autonomic nervous supply to the colon resulting in absence of smooth muscle contraction

65
Q

What are some of the causes of pseudo-obstruction?

A
  • Electrolyte imbalces or endocrine disorders
    • including hypercalcaemia, hypothyroidism, hypomagnesaemia
  • Medication
    • opioids, calcium channel blockers, anti-depressants
  • Recent surgery, severe illness or trauma
  • Neurological diseases:
    • Parkinson’s, MS, Hirschsprung’s disease
66
Q

How do patients present with pseudo-obstruction?

A
  • Abdominal pain
  • Abdominal distension
  • Constipation (but can have paradoxical diarrhoea)
  • Vomiting (typically a late feature)
  • O/E: abdomen is distended and tympanic
    • Focal tenderness indicated ischemia
67
Q

Which investigations should be done if suspecting pseudo-obstruction?

A
  • Bloods for biochemical or endocrine causes
    • U&E, Ca2+, Mg2+, TFTs
  • Abdominal X-ray will show bowel distension but appears no different to a mechanical cause
  • CT abdo-pelvis with contrast will show dilation of colon and exclude any mechanical twist and show any complications .g. perforation
68
Q

How is pseudo-obstruction managed?

A

Mostly conservatively

  • Make NBM
  • Start IV fluids - monitor input and output
  • NG tube if vomiting and aid decompression
  • If does not resolve in 24-48hours needs endoscopic decompression and insertion of flatus tube
  • If there is limited resolution try IV neostigmine (anticholinesterase)
  • Consider TPN
69
Q

When is surgery performed for pseudo-obstruction?

A

In the absence of ischemia or perforation, non-responsive cases may require segmental resection +/- anastamosis

Alternatively bowel can be decompressed long term e.g. caecostomy or ileostomy

Junior surgery (8 decks)

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