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Yr3 Surgery: General > Colon > Flashcards

Colon Flashcards

1
Q

What is appendicitis?

What age range does it commonly affect?

A
  • Inflammation of appendix
  • Age: 10-30yrs
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2
Q

Remind yourself of the pathophysiology of appendicitis

A
  • Luminal obstruction due to:
    • Faecolith
    • Lymphoid hyperplasia
    • Impacted stool
    • Foreign object
    • Appendiceal or caecal tumour (rare)
  • Obstruction causes mucus in appendix to become blocked
  • Increase in intra-luminal pressure
  • Results in increased venous pressure
  • Leads to mucosal oedema
  • Mucosal oedema impairs arterial supply to appendix
  • Ischaemia allows bacteria to invade the appendix wall
  • Immune response to bacteria invading wall causes further swelling further impairing blood supply
  • If ischaemia untreated then necrosis of wall can occur
  • Necrosis of wall can laed to perforation
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3
Q

What are the most common bacteria in the appendix? (2)

A

Bacteroides fragilis

Escherichia coli

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4
Q

State some risk factors for appendicitis

A
  • Family history
  • Caucasian (however ethnic minorities, when they do get it, are at greater risk of perforation)
  • Environmental (seasonal presentation during summer)
  • Low fibre diet (increased constipation risk)
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5
Q

Describe the clinical features/presentation of acute appendicitis

A
  • Abdominal pain
    • Starts peri-umbilical, dull, poorly localised
    • Migrates to RIF, sharp, well localised
  • Anorexia
  • Vomitting (occurs after pain has started)
  • Diarrhoea or constipation
  • Rebound tenderness & percussion tenderness at McBurney’s point
  • Rovsing’s sign
  • Psoas sign
  • Guarding (if perforated)
  • Rebound tenderness all over (if perforated)
  • Lie very still (if perforated)
  • RIF mass (if appendiceal mass)
  • May have signs of sepsis
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6
Q

What is Rovsing’s sign?

What is psoas sign?

A
  • Rovsing’s sign= RIF pain on palpation of LIF
  • Psoas sign= RIF pain when extend right hip (specifically suggests inflamed appendix abutting psoas major in retrocaecal position)
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7
Q

Children with acute appendicitis often present in an atypical manner; true or false?

A
  • True
  • E.g. diarrhoea, urinary symptoms, left sided pain
  • Examian GI, urinary, CV systems & genitals in boys
  • If had symptoms for >48hrs more likely to be perforated appendix so need a period of active observation
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8
Q

What investigations are required if you suspect acute appendicits?

A

Bedside

  • Urine dipstick: exclude urological cause. NOTE: may find leucocytes in urine dip if have appendicitis
  • Pregnancy test: exclude pregnancy

Bloods

  • FBC: infection
  • CRP: infection
  • U&Es: baseline
  • Serum b-hCG: exclude pregnancy if not already excluded

Imaging (not essential to diagnose)

  • Ultrasound: can help exclude other causes e.g. gynaecological
  • Abdominal CT: rule out other GI and gynaecological causes
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9
Q

If a pt has a clinical presentation suggestive of appendicits but investigations are negative what should you do?

A

Diagnostic laparoscopy (can proceed to appendectomy if indicated)

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10
Q

Several risk stratification scors have been devloped to try and help aid diagnosis of appendicits; different models have been compared to find the best models for prediction (based on clinical and radiological) evidence in men, women and children.

State the model/score used for each

A
  • Men= appendicitis inflammatory response score
  • Women= adult appendicitis score
  • Children= Shera score
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11
Q

Discuss the management of acute appendicits with no appendiceal mass

A
  • Supportive:
    • Analgesia
    • Fluids
    • NBM
  • Fit for surgery= Laparscopic appendicectomy with single dose prophylactic abx *GOLD STANDARD
  • Unfit for surgery= IV abx (amoxicillin & metronidazole)

Send appendix for histopathology to look for any malignancy!

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12
Q

Discuss the management of appendicits with an appendiceal mass

A
  • Supportive
    • Analgesia
    • Fluids
    • NBM
  • Abx therapy initially then…
  • Interval laparoscopic appendicectomy

Send appendix for histopathology to look for any malignancy!

*NOTE: there is controversy about how to approach appendicitis with appendiceal mass; one option is the above, others include conservative management or early appendicetcomy.

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13
Q

Why is appendicetomy the gold standard over abx therapy for acute appendicits?

A
  • Abx therapy as failure rate of 25-30% at one year
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14
Q

State some potential complications of acute appendicitis

A
  • Perforation
  • Pevlic abscess
  • Appendix mass (omentum & small bowel adhere to appendix)
  • Usual surgical risks
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15
Q

Discuss the difference between:

  • Diverticulosis
  • Diverticular disease
  • Diverticulitis
  • Diverticular bleed
A
  • Diverticulosis: presence of diverticula
  • Diverticular disease: diverticula causing symptoms
  • Diverticulitis: inflammation of diverticula
  • Diverticular bleed: diverticulum erodes into a vessel and causes large volume painless bleed
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16
Q

What is a diverticulum?

Where in bowel are they most common?

What are range are they common in?

What gender is diverticulosis common in?

Where in world more prevelant (developed or undeveloped countries)?

A
  • Outpouching of bowel wall
  • Sigmoid colon
  • 50+ years (many people have them but only 25% symptomatic)
  • Men>women
  • Developed countries
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17
Q

Discuss the pathophysiolofy of diverticula

A
  • In bowel we have circular layer of muscle and then 3 longitudinal bands of muslce (taeniae coli)
  • Where blood vessels penetrate the circular layer of muscle are areas of weakness
  • Increased pressure inside lumen over time alongside weakening of muscle can cause a gap to form in these areas
  • These gaps then allow mucosa to herniate through the muscle layer and form pouches a.k.a. diverticula
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18
Q

State some risk factors for the formation of diverticula

A
  • Age
  • Low fibre diet
  • Obesity
  • Smoking
  • Family history
  • NSAID use
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19
Q

Describe the clinical presentation of diverticular disease

A
  • Intermittent lower abdo pain
    • Colicky
    • Relieved by passing faeces
  • Altered bowel habits
  • Nausea
  • Flatulence
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20
Q

What investigation is used to diagnose uncomplicated divertiular disease?

A
  • Flexible sigmoidoscopy
  • It pt not suitable for sigmoidoscopy, do CT colonography or bariun enema
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21
Q

Discuss the management of diverticular disease

A
  • Analgesia e.g. paracetamol
  • Increased fibre diets
  • Increased fluid intake
  • Laxatives
    • e.g. Bulk forming such as ispaghula husk
    • AVOID STIMULANTS
  • Weight loss
  • Stop smoking
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22
Q

Dicsuss the pathophysiology of diverticulitis

A
  • Bacterial overgrowth in diverticula
  • Leading to inflammation (diverticulitis)
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23
Q

Diveriticulitis can be simple or complicated; explain the difference

A
  • Simple: inflammation without any of the below
  • Complicated: abscess, perforation, fistula, intestinal obstruction, haemorrhage, or sepsis
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24
Q

Describ the clinical presentation of acute diverticulitis

A
  • Acute abdo pain
    • Sharp
    • Usually LIF
    • Worsened by movement
  • Localised tenderness LIF
  • Anorexia
  • Pyrexia
  • Nausea
  • PR bleeding
  • Urinary symptoms (dysuria, frequency or urgency) due to irritation of bladder by inflammed bowel
  • Signs of peritonism e.g. rebound tenderness, guarding, lying still (if perforated)
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25
Q

Two classes of drug can mask the symptoms of diverticulitis; state these two drug classes

A
  • Corticosteroids
  • Immunosupressants
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26
Q

Why might a pt with diverticulitis present with right lower quadrant or suprapubic pain?

A

If pt has redudant colong (colon longer than usual) the sigmoid colon may not be localised to the LIF)

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27
Q

What investigations should you do if you suspect diverticulitis?

A

Bedside

  • Urine dipstick: rule out urological patholgy
  • Pregnancy test: any abdo pain in woman of child bearing age
  • VBG:

Bloods

  • FBC: infection
  • CRP: infection
  • U&Es: baseline
  • Group & save: may require surgery

Imaging

  • CT abdomen-pelvis: findings suggestive of diverticulitis
  • AXR: may show dilated loops of bowel, obstruction or abscesses
  • Erect CXR: if suspect pneumoperitoneum
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28
Q

What might you see on CT abdomen pelvis of someone with diverticulitis?

A
  • Thickening of colonic wall
  • Pericolonic fat stranding
  • Abscesses
  • Localised air bubble or free air
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29
Q

What investigation should you NEVER perform in a suspected case of diverticulitis?

A

Colonscopy due to risk of perforation

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30
Q

What classification is used to stage diverticulitis based on CT findings?

A
  • Hinchey classification
    • Higher stages= higher morbidity & mortality

Stage 1a= phlegmon

Stage 1b= diverticulitis with pericolic or mesenteric abscess

Stage 2= diverticulitis with walled off pelvic abscess

Stage 3= diverticulitis with generalised pustular peritiontis

Stage 4= diverticulitis with generalised faecal peritionitis

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31
Q

Discuss the management of uncomplicated acute diverticulitis

A

Uncomplicated diverticulitis

Can be managed in primary care with:

  • Oral co-amoxiclav (at least 5 days)
  • Analgesia (avoid NSAIDs & opiates)
  • Taking clear fluids (no solid foods) until symptoms improve (usually 2-3 days)
  • Follow up in 2 days to review symptoms

If the symptoms don’t settle within 72 hours, or the patient intiially presents with more severe symptoms, the patient should be admitted to hospital for IV antibiotics (IV ceftriaxone and IV metronidazole)

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32
Q

Discuss the management of complicated acute diverticulitis

A

If have severe pain or complications then pts needs admitting to hospital for treatment:

  • NBM or clear fluids only
  • IV abx e.g. ciprofloxacin & metronidazole
  • IV fluids
  • Analgesia
  • Urgent investigations (CT scan)

Localised abscess >3cm can be drained via ultrasound or CT guidance

Surgery required if complictions such as abscess that can’t be drained, perforation with faecal peritoinitis, fistula, obstruction, overwhelming sepsis or failure to respond to conservative therapy requires Hartmann’s procedure

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33
Q

What is a Hartmann’s procedure?

A

Sigmoid colectomy with formation of end colostomy

*An anastomosis with reversal of colostomy may be possible at later date (~50% cases)

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34
Q

What is an alternative term for a diverticular abscess?

A

Pericolic abscess

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35
Q

Discuss the management of diverticular bleeds

A
  • Most will resolve spontaenously
  • Significant bleeds will need resuscitation using blood products
  • Failure to respond to conservative may require embolisation or surgical resection
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36
Q

State some potential complications of diverticulitis

A
  • Recurrence
  • Diverticular stricture
    • May result in large bowel obstruction which then requires sigmoid colectomy
  • Fistula formation
    • Colovesical
    • Colovaginal
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37
Q

How may the following present:

  • Colovesical fistula
  • Colovaginal fistula
A

Colovesical

  • Recurrent UTIs
  • Pneumoturia (gas bubbles in urine)
  • Passing faecal matter in urine

Colovaginal

  • Copious vaginal disharge
  • Recurrent vaginal infections
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38
Q

What age does crohn’s disease usually present?

A

Bimodal

  • 15-30yrs
  • 60-80yrs
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39
Q

State some risk factors for Crohn’s disease

A
  • Family history
  • Smoking
  • White european descent
  • Appendicetomy (increases risk of developing CD directly after surgery)
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40
Q

Discuss clinical features of Crohn’s disease

A
  • Abdominal pain
    • Colikcy
    • Varying site
  • Diarrhoea
    • Blood
    • Mucus
    • Malaena
  • Malaise
  • Anorexia
  • Low grade fever
  • Oral apthous ulcers
  • Perianal diseas
  • Extra-intestinal features:
    • Enteropathic arthritis
    • Metabolic bone disease (secondary to absorption)
    • Erythema nodosum
    • Pyoderma gangrenosum
    • Episclertis, anterior uveitis, iritis
    • PSC (more associated with UC)
    • Renal stones
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41
Q

See Yr3 Medicine Gastroenterology for medical management

A
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42
Q

What investigations are required if you suspect Crohn’s disease?

A

Bedside

  • Faecal calprotectin
  • Stool sample for M&C

Bloods​

  • FBC: may find anaemia, increased WCC
  • CRP: inflammation
  • LFTs: may find low albumin, deranged if PSC
  • U&Es: check renal func
  • Clotting: inflammation may affect coagulation cascade

Imaging

  • Abdominal radiograph: rule out toxic megacolon, obstruction
  • CT abdomen pelvis: rule out toxic megaolon, obstruction, perforation, fistulae
  • MRI small bowel and/or pelvis: look for fistulae
  • Colonoscopy with biopsy: GOLD STANDARD/DEFINITIVE DIAGNOSIS
  • Proctosigmoidoscopy: if perianal fistula present
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43
Q

What % of patients with Crohn’s disease will require surgery in their life?

A

70-80%

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44
Q

What are some indications for surgery in Crohn’s disease?

A

Complications e.g. stricutures, fistulas, growth impairment in younger pt

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45
Q

What operations can be offered to patients with Crohn’s disease?

A
  • Ileocaecal resection: removal of terminal ileum and caecum with primary anastomosis
  • Surgery for peri-anal disease
    • Abscess drainage
    • Seton insertion (thin silicone thread that is passed through fistula to keep it open to allow it to drain and then heal from inside out)
    • Laying open of fistula (cut open fistula, with probe so can see inside, wash out then pack and allow to heal)
  • Stricturoplasty (shown on image)
  • Small or large bowel resection
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46
Q

Crohn’s disease pts are low risk to operate on; true or false?

A

False

must attempt optimisation prior to surgery

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47
Q

Why must surgeons take a bowel sparing approach when doing surgery in pts with crohn’s?

A

Prevent short guy syndrome in later years

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48
Q

State some potential complications of Crohn’s disease

A
  • Fistula
  • Stricutures
  • Perianal abscesses/fistula
  • GI malignancy
    • Colorectal= 3% risk
    • Small bowel cancer= 30x more common in crohn’s
  • Malabsorption
  • Osteoporosis
  • Increased risk of gallstones
  • Increased risk of renal stones
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49
Q

Explain why Crohn’s patients have increased risk of:

  • Gallstones
  • Renal stones
A
  • Gallstones: decreased reabsorption of bile salts at inflamed terminal ileum
  • Renal stones: malabsorption of fats in small intestine results in excess lipids in SI. Calcium binds to lipids. Usually, calcium would bind to oxalate and both be excreted in stool. Since calcium is bound to lipids more oxalate is free hence get hyperoxaluria and formation of oxalate stones in renal tract
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50
Q

What age does UC usually present?

A

Bimodal

  • 15-25yrs
  • 55-65yrs
51
Q

UC only affects the colon however in a small number of cases you can get something called backwash ileitis; what is this and why does it occur?

A

Portion of distal ileum involved

Occurs due to incompetent ileocaecal valve

52
Q

Describe clinical features of UC

A
  • Bloody diarrhoea
  • Mucus discharge
  • Increased frequency of defaecation
  • Urgency of defaecation
  • Tenesmus
  • Malaise
  • Anorexia
  • Low grade fever
  • Extra-intestinal:
    • Enteropathic arthritis
    • Erythema nodosum
    • Episcleritis, anterior uveitis, irititis
    • PSC
53
Q

The most common presentation of colitis if proctitis; what is this?

A

Inflammation confined to rectum

54
Q

Remind yourself what criteria can be used to assess severity of UC exacerbation

A

Truelove & Witts criteria

55
Q

Other than UC state some potential causes of colitis

A
  • Crohn’s
  • Chronic infections (schistomiasis, giardiasis, TB)
  • Mesenteric ischaemia
  • Radiation colitis
56
Q

What investigations should you do if you suspect UC?

A

Bedside

  • Faecal calprotectin
  • Stool sample for M&C

Bloods

  • FBC: anaemia, raised WCC
  • CRP: inflammation
  • U&Es: baseline
  • LFTs: hypoalbuminaemia due to malabsorption, deranged LFTs due to meds or PSC
  • Clotting: clotting may be deranged in severe attacks due to inflammatory response affecting coagulation cascade

Imaging

  • Colonoscopy with biopsy: GOLD STANDARD?DEFINITIVE
  • Flexible sigmoidoscopy:may be sufficient as opppose to full colonscopy
  • AXR: lead pipe colon, toxic megacolon or perforation
  • CT abdo-pelvis: toxic megacolon or perforation
57
Q

What may you see on AXR of pt with UC?

A
  • Mural thickening
  • Thumbprinting
  • Lead pipe colon in chronic UC

*image shows toxic megacolon with lead pipe colon

58
Q

See Yr3 Medicine Gastroenterology FC for medical management

A
59
Q

What % of pts with UC will require surgery?

A

30%

60
Q

State some indications for surgery in UC

A
  • Refractory to medical management
  • Toxic megacolon
  • Bowel perforation
  • To reduce risk of colonic carcinoma if dysplastic cells detected on monitoring
61
Q

State some surgeries that may be offered to pts with UC

A
  • Total proctocolectomy is curative (require ileostomy)
  • Sub-total colectomy (require ileostomy. Preserve rectum. May be excised later)
  • Ileal pouch-anal anastomosis (form pouch from ileum loops- acts as reservoir for intestinal contents and is anastomosed with anus to achieve faecal continence)
62
Q

State some potential complications of UC

A
  • Toxic megacolon
  • Colorectal carcinoma
  • Osteoporosis
  • Pouchitis (inflammation of ileal pouch)
63
Q

How does toxic megacolon present?

How is it managed?

A
  • Presentation:
    • Severe abdo pain
    • Abdo distension
    • Pyrexia
    • Systemic toxicity
  • Urgent decompression of bowel due to high risk of perforation
    • Dependent on cause use abx, IV steroids (as in UC)
    • If no improvement after 72hrs then colectomy with end ileostomy
64
Q

How does pouchitis present?

What is the management?

A
  • Presentation:
    • Abdo pain
    • Blood diarrhoea
    • Nausea
  • Managment:
    • Metronidazole & ciprofloxacin
65
Q

For pseudo-obstruction of colon (also known as Ogilvie syndrome), state:

  • What it is
  • Causes
  • Clinical features
  • Investigations
    *
A
  • Acute dilation of colon due to adynamic bowel in the absence of mechanical obstruction thought to be due to interupption of autonomic nerve supply to colon resulting in absence of smooth muscle contraction. Typically in caecum & ascending colon. Rare condition.
  • Causes:
    • Electrolyte imbalances
    • Medication (opiods, CCBs, antidepressants)
    • Recetn surgery, illness or trauma
    • Neurological disease e.g. MS, Parkinson’s, Hirschsprung’s disease
  • Clinial features:
    • Pain
    • Distension
    • Constipation
    • Vomitting
    • Tympanic
  • Investigations:
    • Bloods: FBC, TFTs, Calcium, Magnesium etc…
    • CT abdo-pelvis with IV contrast (shows dilation and rules out mechanical obstruction)
66
Q

For volvulus, state:

  • What it is
  • Where it is most common
  • Risk factors
A
  • Twisting of loop of intestine around its’s mesenteric attachment resulting in closed loop obstruction
  • Sigmoid colon (has long mesentry and the length of mesentry increases with age)
  • Risk factors:
    • Age
    • Chronic constipation
    • Previous abdo operations/adhesions
    • High fibre diet
    • Neuropsychiatric disorders e.g. Parkingson’s
67
Q

Describe clinical features of sigmoid volvulus

A

Present with features of bowel obstruction:

  • Pain (colicky)
  • Abdo distension
  • Absolute constipation
  • Tympanic percussion
  • Signs of peritonism if perforated
68
Q

What investigations are required for suspected sigmoid volvulus?

A

Bloods

  • FBC
  • CRP
  • U&Es
  • TFTs: rule out pseudo-obstruction
  • Calcium: rule out pseudo-obstruction
  • Magnesium: rule out pseudo-obstruction

Imaging

  • CT abdo-pelvis: whirl sign (dilated colon has a whirl sign where mesentry is twisting around base)
  • AXR: coffee-bean sign, small bowel dilation if ileocaecal valve incompetent

Notes from passmed:

  • usually diagnosed on the abdominal film
  • sigmoid volvulus: large bowel obstruction (large, dilated loop of colon, often with air-fluid levels) + coffee bean sign
69
Q

Discuss the management of sigmoid volvulus

A

Most managed conservatively via decompression by sigmoidoscope and insertion of flatus tube.

  • Flexible sigmoidoscope inserted with pt in left lateral position and is manouevred to locate twisted bowel. Flatus tube then left in situ for ~24hrs to help decompression.

Indications for surgery include: colonic ischaemia or perforation, necrotic bowel. Surgical management is usually a lapartomy for Hartmann’s procedure

70
Q

State some potential complications of sigmoid volvulus

A
  • Bowel ischaemia
  • Bowel perforation
71
Q

Who does caecal volvulus usually affect?

What is the management of caecal volvulus?

A
  • Bimodal:
    • 10-30yrs
    • 60-70yrs
  • Management:
    • Lapartomy and ileocaecal resection or right hemicolectomy
72
Q

For colorectal cancer, state:

  • Most common type of cancer
  • What most colonic cancers start as
  • Genetic mutations associated with colorectal cancer
  • Risk factors
A
  • Adenocarcinoma
  • Polpys/colonic adenomas.
    • 10% of polyps progress to adenocarcinoma. May be present for years before become malignant.
  • APC (found in familial adenomatous polyposis) & HNPCC (also known as Lynch syndrome)
  • Often pts have no risk factors but they can include:
    • Age
    • FH
    • IBD
    • Low fibre diet
    • Smoking
    • Alcohol
    • High processed meat intake
73
Q

Describe clinical features of colorectal cancer; think about whic symptoms more likley with right and left sided

A

Common features:

  • Change in bowel habit
  • Weight loss (generally only if mets)
  • Abdo pain

Right sided:

  • Fe deficiency anaemia
  • Palpalbe mass RIF
  • Present late

Left sided:

  • Rectal bleeding
  • Tenesmus
  • Palpable mass in LIF
  • Palpalbe mass on DRE
74
Q

State the red flags that should make you consider colorectal cancer

A
  • Change in bowel habit
  • Unexplained weight loss
  • Rectal bleeding
  • Unexplained abdo pain
  • Fe deficiency anaemia
  • Abdo or rectal mass on examination
75
Q

Which pts do NICE reccommend you send for urgent bowel ca investigations?

A
76
Q

What investigations should you do if you suspect colorectal cancer?

A

Bedside

  • FIT test

Bloods

  • FBC: may show microcytic anaemia
  • LFTs:
  • Clotting
  • U&Es

Imaging

  • Colonscopy with biopsy- send biopsy to for histopatholgy * GOLD STANDARD

Other investigations for staging:

  • CT chest/abdo/pelvis
  • MRI rectum (rectal cancers only)
  • Endo-anal ultrasound (T1 or T2 rectal cancer to asses for resection)
77
Q

What is the FIT test?

A
  • Faecal immunochemical test
  • Looks for amount of human Hb in stool
  • Replaed faecal occult (gave false positives by detecting blood in food)
  • Used in the bowel cancer screening programme
    *
78
Q

Should CEA be routinely tested for when you suspect colorectal ca?

A

No, it has poor sensitivity & specificity.

May be used to monitor progression

Elevated CEA at start= worse prognosis

79
Q

What staging criteria is now most commonly used for colorectal ca?

Which staging criteria used to be used (and is still used in some centres)?

A
  • TNM
  • Duke’s
80
Q

Discuss the management of colorectal cancer (more detail next year cancer care)

A
  • Surgical resection with either end to end anastomosis or creating a stoma
  • Chemotherapy (pts with advanced disease)
  • Radiotherapy (pts with rectal cancer)
  • Palliative care
81
Q

Define each of the following resections:

  • Right hemicolectomy
  • Left hemicolectomy
  • Sigmoidcolectomy
  • High anterior resection
  • Low anterior resection
  • Abdominoperineal resection
  • Extended right hemicolectomy
A
  • Extended right hemicolectomy: caecum, ascending colon & up to distal transverse colon
  • Low anterior resection may remove upper or all of rectum
82
Q

Discuss bowel cancer screening in UK

A
  • Offer FIT test to people aged 60-74yrs to do every 2 years
  • If +ve result will have review and discuss for colonsocpy
83
Q

How are pts with bowel cancer followed up?

A

Follow up until 5 yrs post op with:

  • Regular appointments
  • CEA
  • Colonoscopy
84
Q

What does is the term bowel obstruction generally referring to?

A

Mechanical obstruction of bowel

If obstruction is because the bowel is not working properly but there is no mechanically obstruction this is called functional obstruction or paralytic ileus

85
Q

Why do pts with bowel obstruction need urgent fluid resuscitation and monitoring of fluid balance?

A
  • When bowel segment is blocked the segment proximal to it dilates
  • This results in increased peristalsis
  • This then leads to secretion of large volumes of electrolyte rich fluid into bowel (third spacing)
86
Q

What is meant by a closed loop obstruction?

State 2 examples of when it may occur

Why is it an emergency?

A
  • Obstruction both proximally and distally
  • E.g. in volvulus or large bowel obstruction with competent ileocaecal valve
  • Emergency as bowel will keep ditending until it becomes ischaemic or perforates
87
Q

State some examples of common causes of obstruction in:

  • Small bowel
  • Large bowel

Causes cana also be categories into intraluminal, mural and extramural; state some examples in each category

A
  • Small= adhesions, hernia
  • Large= malignancy, diverticular disease, volvuluste
88
Q

State the clinical features of bowel obstruction

A
  • Abdominal pain (colicky or crampy due to peristalsis)
  • Vomiting (intially gastric contents, then billious, then faeculent)
    • Late in distal
    • Early in proximal
  • Abdominal distension
  • Absolute constipation
    • Early in distal
    • Late in proximal
  • Foal tenderness
  • Tympanic sound on percussion
  • Tinkling bowel sounds on auscultation
89
Q

What investigations are required if you suspect bowel obstruction?

A

Bedside

  • VBG: signs of ischaemia e.g. high lactate & to quickly assess electrolytes

Bloods

  • FBC
  • U&Es
  • LFTs
  • CRP
  • G&S

Imaging

  • CT scan of abdomen and pelvis with IV contrast:look for signs of obstruction, identify where it is
  • AXR: Passmed says still commonly used as first line investigation
  • ?erect CXR: generally won’t need if done CT as this will show pneumoperitoneum
90
Q

Remind yourself how to differentiate between small and large bowel obstruction on AXR

A
91
Q

Discuss the initial management of someone with suspected bowel obstruction

A
  • Urgent fluid resuscitation
  • Urinary catheter
  • NG tube insertion
  • Analgesia & anti-emetic
  • NBM
92
Q

Discuss the management of bowel obstruction without closed loop obstruction or complications (e.g. ischaemia, perforation etc..)

A

Continue with conservative management: “Drip & suck”

  • Keep NBM
  • NG tube to decompress bowel
  • Continue IV fluids ensuring to correct any electrolyte imbalances (drip)
  • Monitor fluid balance (catheterised)
  • Continue analgesia & anti-emetics
93
Q

Discuss whether conservative management is usually sucessful for treating bowel obstruction

A
  • Stable pts with obstruction secondary to adhesions (from previous surgery) or volvulus= 80% sucess rate
  • Virgin abdomen (never had abdominal surgery before) rarely settles without surgery
94
Q

Discuss the management of closed loop bowel obstruction or obstruction with complications (e.g. perforation, ischaemia, strangulation)

A
  • Urgent fluid resuscitation
  • Catheter
  • NBM
  • Urgent surgery

Surgery is to treat underlying cause hence may be:

  • Adheiolysis
  • Hernia repair
  • Emergency resection
95
Q

Summarise which pts surgical intervention for bowel obstruction is indicated in

A
  • Complications e.g. ischaemia, perforation, strangulation= URGENT
  • Closed loop obstruction= URGENT
  • Cause that requires surgical intervention e.g. obstructing tumour
  • Failure to improve following conservative measures after 48hrs
96
Q

If a pt with small bowel obstruction has not responded to conservative management what test could you do?

What would you do following the results?

A
  • Water soluble contrast study
  • If contrast doesn’t reach colon by 6hrs it is unlikley that it will resolve on its’s own and pt should be taken to theatre
97
Q

State some potential complications of bowel obstruction

A
  • Bowel ischaemia
  • Bowel perforation
  • Dehydration
  • AKI
98
Q

What is the most common cause of GI perforations? (2)

A

Peptic uclers

Sigmoid diverticulum

99
Q

State some potential causes of GI perforation

A
  • Peptic ulcer
  • Foreign body
  • Diverticulitis
  • Cholecystitis
  • Meckel’s diverticulum
  • Mesenteric ischaemia
  • Obstructing lesions resulting in bowel distention and subsequent ischaemia and necrosis
  • Toxic megacolon
  • Iatrogen e.g. surgery, endoscopy
  • Trauma
  • Boerhaave syndrome
100
Q

State clinical features of bowel perforation

A
  • Pain
    • Rapid onset
    • Sharp
  • Vomiting
  • Lethargy/malaise
  • Look unwell
  • Abdo distension
  • Peritonism (localised or perforated)
101
Q

How may thoracic perforation present?

A
  • Pain
    • Chest or neck
    • Radiate to back
    • Worse on inspiration
  • Respiratory symptoms
  • Vomiting
  • Pleural effusion signs
102
Q

What investigations are required if you suspect a GI perforation?

A

Bedside

  • Urinalysis (rule out renal pathology)
  • Pregnancy test

Bloods

  • FBC
  • U&Es
  • LFTs
  • Coagulation
  • CRP
  • G&S or crossmatch

Imaging

  • eCXR: features of pneumoperitoneum
  • AXR: features of pneumoperitoneum
  • CT scan abdomen= GOLD STANDARD:features of pneumoperitoneum and show where and give better idea of underlying pathology
103
Q

State what you may see on AXR of pt with bowel perforation

A
  • Rigler’s sign: can clearly see edge of bowel due to free intra-abdominal air acting as additional contrast
  • Telltale triangle sign: appearance of a radiolucent triangle of gas formed between three loops of bowel or between two loops of bowel and the abdominal wall
  • Psoas sign: loss of sharp delineation of psoas muscle border secondary to fluid in retroperitoneum
104
Q

Discuss the initial management of GI perforation

A

MUST identiy & treat early:

  • NBM
  • NG tube (draining)
  • Broad spec abx
  • IV fluids
  • Analgesia
105
Q

Following the initial management, discuss the management of GI perforations

A

Management post-initial approach is highly specialised dependent on cause and pt. Most pts with perforated viscus require surgery. Key aspects of surgery:

  • Identification & managment of perforation
    • E.g. peptic ulcer with omental patch
    • E.g. sigmoid diverticulae with Hartmann’s
  • Thorough washout

Some pts may be managed conservatively if they are:

  • Physiologically well and only have localised perforation (<5cm)
  • Elderly pts who would not survive surgery
106
Q

State some potential complications of GI peforation

A
  • Infection/sepsis
  • Haemorrhage
107
Q

What is the sensitivity of AXRs for detecting GI perforations/pneumoperitoneum?

A

70%

108
Q

m

A
109
Q

What may you find on examination of someone with perforated viscus?

A
  • Tachycardia
  • Hypotension
  • Rigid abdomen
  • Guarding
  • Reduced or absent bowel signs
  • Peritonism
110
Q

For acute mesenteric ischaemia, discuss:

  • What it is
  • Common causes
A
  • Sudden decrease in blood supply to the bowel
  • Causes:
    • Thrombus in situ (AMAT)
    • Embolism (AMAE)
    • Non-occlusive (NOMI) e.g. shock
    • Venous occlusion & congestion (e.g. malignancy, coagulpathy)
111
Q

State some risk factors for acute mesenteric ischaemia

A

Thromvbus risk factors= atherosclerosis RF

  • Smoking
  • Hyperlipidaemia
  • Hypertension
  • Diabetes

Embolism risk factors

  • AF
  • Aortic aneuryseum
  • MI

Non-occlusive risk factors

  • Sepsis- shock
  • Haemorrahage- shock
112
Q

State clinical features of acute mesenteric ischaemia

A
  • Generalised abdo pain
    • Out of proportion to findings
    • Constant
  • Associated N&V
  • Non-specific tenderness (if not perforated)
  • Peritonism (if perforated)
  • Signs of cause e.g. AF
113
Q

What investigations are required if you suspect acute mesenteric ischemia?

A

Bedside

  • ABG: look for acidosis and lactate secondary to ischaemia +/-infarction

Bloods

  • FBC
  • U&Es
  • LFTs
  • CRP
  • Clotting
  • Amylase
  • Gropu & save or crossmatch

Imaging

  • CT scan abdomen & pelvis with IV contrast (triple phase scan)
114
Q

What may you find on CT of pt with acute mesenteric ischaemia?

A
  • Odematous bowel
  • Loss of bowel wall enhancement
  • Pneumatosis
115
Q

Discuss the initial management of acute mesenteric ischaemia

A
  • NBM
  • IV resuscitation fluids
  • Catheter & fluid balance
  • Broad spectrum IV abx (due to risk of feacal contamination in peforation)
  • Early support from surgical team & ITU
116
Q

Pts with acute mesenteric ischaemia require surgery; what are the two aims/objectives of surgery

A
  • Excise necrotic bowel
    • Managed on ITU after
    • May do re-look laparotmy in 48hrs
  • Revascularisation by removing thrombus or embolism (this can be done open or endovascularly)
117
Q

State some poetnetial complications of acute mesenteric ischaemia

A
  • Bowel necrosis
  • Perforation
  • Short gut syndrome following resection

*Mortality is 50-80%

118
Q

For chronic mesenteric ischaemia discuss:

  • What it is also called
  • Pathophysiology
  • Risk factors
    *
A
  • Intestinal angina
  • Atherosclerosis in mesenteric arteries impairing blood flow to viscera resuling in inadequete blood supply
  • Same as for any CVD disease:
    • Smoking
    • Hypertension
    • Diabetes
    • Hyperlipidaemia
    • FH
    • Age
119
Q

Discuss whether chronic mesenteric ischaemia is usually symptomatic

A

Pts often asymptomatic due to collaterisation. In order for pts to be symptomatic they usually need to have at least two vessels (coeliac trunk, SMA, IMA) affected and often one of these is fully occluded.

Even then, they are typicaly asymptomatic at rest and only get symptoms when there is increased demand (e.g. after eating) or reduction in overall blood volume (e.g. severe haemorrhage)

120
Q

If a pt with chronic mesenteric ischaemia is symptomatic, what symptoms may they have?

*HINT: classic triad

A

Classic triad of:

  • Post-prandial central colicky abdo pain (about 30 mins after eating & lasts 1-2hrs)
  • Weight loss (due to food avoidance as causes pain)
  • Concurrent vascular abnormalities e.g. previous MI, stroke, PVD, signs of vascular disease on examination

Other symptoms & signs may include change in bowel habit, N&V, generalised abdo tenderness, abdominal bruits

121
Q

What investigations would you do if you suspect chronic mesenteric ischaemia?

A

Bedside

  • ABG: lactate can be sign of ischaemia

Bloods

  • FBC
  • U&Es
  • LFTs
  • Coagulation
  • Lipids
  • HbA1c
  • Magnesium: may be low due to manutrition
  • Calcium: may be low due to malnutrition

Imaging

  • CT angiography *DIAGNOSTIC TEST
  • ?CXR: if suspect perforation
122
Q

Discuss the management of chronic mesenteric ischaemia

A

Conservative

  • Stop smoking
  • Lose weight
  • Healthy diet

Medical

  • Antiplatelet therapy e.g. aspirin 75mg
  • Statin e.g. atorvastatin 80mg??? CHECK

Surgical

Revascularistion may be required in severe, progressive and or debilitating disease e.g. weight loss malabsorption:

  • Endovascular (more common): angioplasty with stenting
  • Open: emdartectomy or bypass
123
Q

State some potential complications of chronic meseneric ischaemia

A
  • Bowel infarction
  • Malabsorption

Yr3 Surgery: General (13 decks)

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