Acute Colorectal and Anoproctology Flashcards

1
Q

Define “Massive Lower Gastrointestinal Bleeding”

What proportion of massive LGIB is actually UGI in aetiology?

A

Massive LGIB is defined as bleeding distal to the ligament of Treitz associated with haemodynamic abnormality.

Between 15-20% of massive LGIBs are UGIBs.

This has lead to a recent proposal to reserve the term LGIB for bleeding occuring distal to the ICV.

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2
Q

What is the mortality rate associated with LGIB?

What factors affect this?

A

A recent UK audit showed a 3-4% mortality associated with LGIB.

This was higher in inpatients who develop LGIB compared with outpatients who present with LBIG, which reflects the underlying comorbidities associated with inpatients who bleed.

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3
Q

Provide an overview of the causes of lower GI bleeding

A

LGIB is most common in elderly patients with multiple comorbidities; however, causes vary by age. In adolescents, common causes are Meckel’s diverticula, IBD, and benign polyps. LGIB in adults is most often caused by colonic diverticula, cancer, and angiodysplasia.

In a recent audit of UK data:

  • Diverticulosis 20-65%
    • Self-limiting 80% of the time
    • Often not a formal diagnosis (25% of audit diagnoses)
  • Colitis 15%
    • Ischaemic​
    • Inflammatory bowel disease
    • Infectious
  • Haemorrhoids 3-15%
    • Rarely cause massive LGIB
  • Angiodysplastic lesions 3-15%
    • Over-represented in massive LGIB 20-30%!
    • Over two thirds are >70 years old
    • More commonly in the right colon (54%)
  • Iatrogenic bleeding 5-10%
    • Post-polypectomy; immediate and delayed
    • Post-colorectal surgery
    • Post radiotherapy
  • Malignancy
    • Often occult, rarely massive LGIB
  • Miscellaneous:
    • Varices, Rectal ulceration, Dieulafoy lesions, NSAIDS, Meckel’s
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4
Q

What are the key principles in managing LGIB?

Which index should be used in the assessment of potentially massive LGIB? What is its utility?

A
  • Simultaneously assess and resuscitate
  • Determine the severity of bleeding
  • Determine the location of the bleeding
  • Determine the cause of the bleeding.

The British guidelines advocate the use of the shock index (HR/SBP) with a value greater than 1 as an indicator of ongoing bleeding.

Increasing shock index is associated with increasing risk of mortality and it is widely used in the trauma literature.

A shock index >1 is also a predictor of detecting a contrast blush on CT angiography and therefore may be useful in identifying patients who would benefit from CTA and likely need therapeutic intervention.

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5
Q

Describe the key features of a focussed history when assessing a patient with lower GI bleeding.

A
  • HPC:
    • Timing, frequency, and volume of the bleeding
    • Associated symptoms
  • PMHx:
    • Anticoagulant / anti-platelet use
    • Previous colonoscopy
    • History of bleeding diathesis
    • History of IBD
    • History of irradiation
    • History of liver disease
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6
Q

What are the guidelines for NG placement in lower GI bleeding?

A

The American guidelines recommend placement of a nasogastric tube and lavage to assess for an UGIB source; however, the British guideline advise against this practice as it does not reliably aid diagnosis, affect outcomes and maybe associated with complications in up to a third of patients.

Reliance on a negative nasogastric tube aspirate to exclude an UGIB has poor sensitivity and low negative predictive value (64%).

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7
Q

Describe the principles of blood transfusion in lower GI bleeding.

Cite Hb thresholds and targets in your answer.

A
  • All the guidelines recommend a restrictive approach to blood product transfusion with a threshold haemoglobin of 70g/L in haemodynamically stable patients with a target haemoglobin of 70-90 g/L.
  • In patients with ischaemic heart disease or significant comorbidity this threshold can be increased to 80g/L with a target haemoglobin of 80-100g/L.
  • Haemodynamically unstable patients should be actively resusciated with a massive transfusion protocol in consultation with a haemotologist to target a haemoglobin of 90g/L.
  • There is no randomised data from patients with LGIB to support these recommendations. They are derived from UGIB data where a recent meta-analysis has demonstrated increased survival when a restrictive blood transfusion strategy is adopted.
  • A separate systematic review has shown that a restrictive transfusion strategy in patients with ischaemic heart disease, previous stroke and vascular disease have an increased risk of myocardial infarction and death.
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8
Q

What is the evidence for TXA use in lower GI bleeding?

A

The HALT-IT trial, published in 2020, demonstrated that patients administered 4g TXA after acute GI bleeding experienced more venous thromboembolic events than controls (0.8% vs 0.4%, RR 2.11) without a concomitant reduction in death or rebleeding at 24hrs, 5 days, or 28 days.

Use of TXA is not recommended in the setting of acute LGIB.

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9
Q

How can patients with lower GI bleeding be risk-stratified?

A
  1. The Oakland Score
    • Recommended by British Guidelines
    • Clinical and demographic data with various weighting
    • Safe discharge with OP scope if score is less than 8
  2. The NOBLADS score
    • Developed in Japan, validated internationally
    • 8 parameters, all easily assessed on admission
    • Score ≥5 = ~80% severe bleeding risk (≥2URBC)
    • Score <4 = ~2% severe bleeding risk
    • Safe discharge and OP scope if score less than 2
  3. The Strate score
    • Derived from multivariate analysis
    • Provides OR for severe bleeding
    • Similar to NOBLADS parameters.
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10
Q

What proportion of patients presenting with lower GI bleeding are on anticoagulation?

A

30% are on either anti-platelets or anti-coagulants

5% are on dual antiplatelet therapy or antiplatelets + anti-coagulants.

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11
Q

In the setting of lower GI bleeding, how do you address:

Warfarin?

Dabigatran?

Rivaroxiban / Apixaban?

Aspirin?

DAPT?

Heparin?

A
  • Warfarin
    • Cease and reverse with PTX + FFP if INR >2.0
    • Recommence 7 days later where feasible
    • Bridge with Heparin in high risk patients
  • Dabigatran
    • Cease and reverse with Idarucizumab
  • Rivaroxiban / Apixaban
    • Cease and reverse with Adexanet alfa (both direct and indirect Factor Xa inhibitors)
  • Aspirin
    • Cease in primary prevention
    • Continue in secondary prevention
  • DAPT
    • DAPT for cardiac stents should be discussed with cardio
    • In massive LGIB, P2Y12 inhibitors (e.g Cloipidogrel) should be ceased while Aspirin continues
    • Patients on DAPT have a 5-fold risk of re-bleeding
  • Heparin
    • Reverse with Protamine sulfate
    • Ciraparantag is a small molecule drug which binds UFH and LMWH - not widely in use
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12
Q

For elective colonoscopy, when should Warfarin, DOACS, and antiplatelets be withheld from and when should they be resumed?

A
  • Warfarin
    • withhold from 5 days
    • resume same day
  • DOACS
    • withhold from 2 days
    • resume next day
  • Aspirin
    • do not stop
  • P2Y12 agents
    • withhold for 7 days
    • resume within 24 hours
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13
Q

What is the role of colonoscopy in lower GI bleeding?

A
  • Colonoscopy should be the first-line diagnostic investigation in haemodynamically stable patients to investigate a major LGIB.
    • If the bleed is major (Oakland score >8) = inpatient
    • If the bleed is minor (Oakland ≤8 points) = outpatient
  • A major advantage of colonoscopy is that it can be used simultaneously to provide definitive therapy in up to 60% of cases
  • Inpatient colonoscopy requires prep as caecal intubation rates are ~60% without prep. This adds complexity to the case and the risks of inpatient prep following bleeding should be balanced with the expediency of diagnosis.
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14
Q

What colonoscopic therapeutic modalities exist for control of lower GI bleeding?

A
  • Clipping via through the scope clips
    • Can be applied to post-polypectomy site
    • Can be applied to the base of a bleeding divertic for tamponade
  • Adrenaline injection
    • 20% re-bleed rate if used as monotherapy!
  • Endoscopic band ligation
    • Technically more challenging but lower re-bleed rates cf clips
  • Argon Plasma Coagulation
    • Angioectatic lesions
    • 20-60W, 1-2L flow, 1-2 sec pulses, 1-3mm from lesion
  • Haemostatic powders
    • Hemospray
    • Caution with liberal use in heavy bleeding - embolises
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15
Q

Describe the role of interventional radiology in lower GI bleeding.

Overall success rates?

Strengths and weaknesses of the various approaches?

A

IR can be used to both localise and treat lower GI bleeding, with an overall success rate of 85% with regard to haemostasis.

In the haemodynamically unstable patient experiencing a massive LGIB, CTA is recommended before any therapy is instigated. CTA can detect bleeding as slow as 0.3ml/min. Expedited transfer to angioembolization is required, and some consider this to be a KPI in IR units.

Catheter angiography requires a faster rate of bleeding (1ml/min) for diagnostic purposes. Super selective angioembolization involves the embolization with absorbable gelatin sponges, cyanoacrylate glue, ethylene, or polyvinyl alcohol, and microcoils to control haemorrhage.

A systematic review reported that this technique can be successful in achieving immediate haemostasis in between 40-100% of cases with re-bleeding rates reported between 0-50%

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16
Q

Describe the risks of IR-angioembolization

A
  • Contrast nephropathy
  • Bleeding
  • Pseudoaneurysm formation
  • Thromboembolic events
  • Colonic ischaemia
    • Can occur if angioembolization is not super-selective.
    • This can result in a spectrum of clinical presentation from self-limiting ischaemic colitis to perforation and associated peritonitis
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17
Q

Describe the management algorithm for lower GI bleeding put forward by the British Society of Gastroenterology

A
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18
Q

What is the cryptoglandular theory and why is it incomplete?

A

The cryptoglandular theory can be summarised in three steps;

  1. Cystic dilatation of an anal gland (obstructive or congenital)
  2. Infection of the anal gland leading to abscess formation
  3. Surgical or spontaneous drainage in the perianal skin leads to tract formation and epithelisation

Critical points against the cryptoglandular theory include;

  • It is unlikely for an abscess to traverse intact skeletal muscle preferentially to an unimpeded path
  • Most peri-anal abscesses do not result in fistula
  • The theory doesn’t explain why fistula-in-ano is more common in males (12.3/100,000 versus 5.6/100,000)
  • A scarcity of bowel derived bacteria in fistula tracts
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19
Q

Describe the pathophysiology of perianal fistulae in Crohn’s

A
  • Based on the Epithelial to Mesenchymal Transition
  • EMT is a normal physiological process in embryology and healing
  • Indices of EMT include upregulated TGF-1, TGF-2, and β6-integrin with decreased expression of E-cadherin and β-catenin
    • This pattern is observed in Crohn’s disease.
    • EMT results in activation of matrix remodelling enzymes and induces expression of molecules involved with cellular invasion, creating a fistulating phenotype.
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20
Q

Is there a unifying theory of perianal fistula formation?

A
  1. The host’s innate immunity is unable to fully resolve an acute infection of an anal gland
  2. Persistence of bacterial remnants triggers EMT
  3. Activation of EMT leads to release of pro-inflammatory cytokines such as IL-1beta and TGFbeta as well as release of MMPs
  4. This leads to degradation of the extracellular matrix as well as migration of epithelial cells, facilitating fistula formation
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21
Q

What is the evidence for antibiotics in perianal fistula treatment?

A
  • Randomised evidence to show reduced fistula rates after I+D of perianal abscess (14% versus 31%)
    • 7-day course of Cipro and Metronidazole
  • There is evidence from small trials in patients with Crohn’s disease that the use of antibiotics alone can lead to fistula closure
  • Of note, the original description of the LIFT procedure includes 2 weeks of Ciprofloxacin and Metronidazole post op.
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22
Q

What modifiable factors promote or facilitate perianal fistulisation?

A

FRIENDS again…

Foreign body (therapeutic Seton!)

Radiation or tissue damage causing chronic inflammatory change

Inflammation around the fistula

Epithelialisation (reflects chronicity)

Neoplasia

Distal obstruction; in this setting the high pressure zone

Sepsis or bacterial load

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23
Q

Classify fistula-in-ano in terms of management categories

A

Simple (laying open fistula)

  • Intersphincteric
  • Transphincteric <30% of the sphincter complex involved

Complex (draining Seton for at least 6 weeks…)

  • Transphincteric >30%
  • Suprasphincteric (cannot have have L.I.F.T)
  • Extrasphincteric
  • Any fistula with
    • Concomittant anorectal disease
      • Crohn’s
      • TB/HIV
      • Radiotherapy
      • Cancer
    • Multiple tracts
    • Recurrent fistula
    • Anterior fistula in a woman
    • Faecal incontinence
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24
Q

What factors need to be considered when estimating liklihood of incontinence following fistulotomy?

A
  • Current degree of continence
  • Age
  • Presence of IBS
  • Previous childbirth
  • Previous anorectal surgery
  • Anoreceptive intercourse
  • Previous irradiation
  • Underlying neurological disorders.
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25
Q

Describe the most well established “sphincter-preserving” procedures for fistula in ano, their original and subsequently analysed success rates, as well as their main advantages and disadvantages.

A
  1. Ligation of the Inter-sphincteric Tract
    • Original series 94%
    • Meta-analyses 76%
      • Pros:
        • Down stages the fistula if it fails
        • Requires no special equipment
      • Cons:
        • Technically difficult for high fistulas with success rates from the OG of 60%
  2. Endoanal advancement flap
    • Success proportional to thickness of flap
    • 70% for MAF, 81% for PAF, 92% for FAF
      • Pros:
        • High pressure zone repaired
      • Cons:
        • Is not actually sphincter preserving with PAF and FAF
        • Potential for mucosal ectropion
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26
Q

What are the less well established methods of perianal fistula repair?

What are the approximate success rates?

A
  • Anal fistula plug
    • Simple but expensive
    • 54%
  • Fibrin glue
    • Success rate reportedly 0-87%!
  • Video-assissted anal fistula treatment
    • Requires fistuloscope and cautery
    • Reported success rate 82% but little take up
  • Fistula laser closure
    • Laser wire destroys the fistula tract epithelium and obliterates the remaining fistula tract through shrinkage
    • Success rates of 65%
  • Over the scope clip
    • Theorised to more securely close the internal opening
    • Success rates of 63%
  • Stem cell treatment
    • In evolution, improved cf placebo at 4 weeks but no difference at one year…
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27
Q

Is there a role for anal fistula plugs in the treatment of fistula in ano?

A

The lack of efficacy in long-term fistula healing when compared to other techniques might be tempered by a lack of detriment to continence, and the conclusion of the position paper by the Association of Coloproctologists of Great Britain and Ireland is that anal fistula plugs may have a niche role in the patient who has some pre-existing incontinence

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28
Q

What are the complications of the LIFT procedure for fistula in ano?

What are the risk factors for failure?

A

Complications include:

  • Wound breakdown and bleeding ~13%
  • Failure ~30%; often converts to inter-sphincteric fistula

Risk-factors for failure include:

  • Crohn’s disease
  • Horseshoe fistulas
  • Tracts longer than 3cm
  • Diabetes
  • Obesity
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29
Q

Describe modifications to the traditional LIFT procedure and state whether these have any evidence.

A
  1. Omission of tract excision
    • Variable reported outcomes
  2. Coring out the tract via the external opening
    • Small series seem to suggest improved rates of healing
  3. Placing a Seton to drain the external component
    • Small series seem to suggest improved rates of healing
  4. Addition of a trans-anal advancement flap
    • Results disappointing
  5. Addition of an anal plug
    • Single study showed promise but success rates very high in both arms…
  6. Insertion of a bio-prosthetic mesh between divided tract
    • “Biolift” small series, mixed results.
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30
Q

What are the rates of bleeding detectable by:

Catheter angiography?

CTA?

Radionucleotide Scintigraphy?

A

Catheter angiography = 0.5-1.0ml/min

CTA = 0.3ml/min

Radionucleotide Scintigraphy = 0.1ml/min

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31
Q

Describe the suspensory ligaments of the anal cushions.

A

Treitz’s muscle maintains the anal cushions in their normal position. It consists of submucosal muscle, which fixes the haemorrhoids to the internal anal sphincter. These muscles will be encountered during haemorrhoidectomy and traverse the plane of dissection.

Park’s ligament is a mucosal suspensory ligament that penetrates the internal sphincter and fixes the sinusoids to the conjoined longitudinal muscle. This ligament is orientated longitudinally and is thought to be pathologically elongated in haemorrhoidal prolapse.

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32
Q

Describe the pathophysiology of haemorrhoidal disease.

A
  • Sliding of the anal cushions
  • Loss of the connective anal cushion tissue
  • Reduced venous return to the superior and middle rectal veins during defaecation
  • Dilated haemorrhoidal plexus with stagnant sinusoidal blood
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33
Q

What is the success rate of rubber band ligation for symptomatic haemorrhoidal disease?

What are the complications?

A

80% success rate where success is defined as permanent relief of symptoms for follow-up period; marked improvement in symptomatology with rare manifestation of bleeding; symptom relief for a limited period of time.

Complications:

  • bleeding (2.8%), secondary bleeding occurs between 5-15 days
  • thrombosed external haemorrhoids (1.5%)
  • bacteraemia (0.09%)
  • Mild bleeding, pain, slippage of bands, and difficulty urination are more common complications and normally minor
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34
Q

What is the role of injection sclerotherapy for haemorrhoids?

How does it work?

What are the complications?

A
  • Limited role given reported complication rate of ~30%
    • Theoretical advantage in anti-coagulated patients
  • Injection of 5% almond phenol into the submucosal space causes inflammation, apoptosis, and scarring.
  • Potential complications include
    • urological (prostatitis, haematuria, urinary retention, epididymitis)
    • bacteraemia
    • haemorrhage
    • mucosal necrosis
    • injection site ulcer
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35
Q

Describe the complications of surgical haemorrhoidectomy and any interventions/modifications used to mitigate these.

A
  • Pain (opiate use in 40%)
    • Reduced pain with regional blockade
    • Reduced pain with oral metronidazole (unclear mechanism)
    • Multi-modality post operative regimen recommended
  • Urinary retention (15%)
    • Multifactorial
    • May be due to pudendal block
    • Assess risk pre-operatively
  • Bleeding (2%)
    • Primary or secondary
  • Infection (<1%)
    • Higher rates in immunocompromised patients
  • Change in continence (<1% incontinence)
    • Even without sphincter damage loss of cushions associated with reduced passive continence
  • Anal stenosis (<5%)
    • Mitigated by leaving 1cm anodermal/mucosal bridges.
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36
Q

What is the rate of incontinence with lateral spincterotomy?

A

The rate of long-term faecal incontinence has been reported between 6 and 30%, with a meta-analysis of 22 studies with 4512 patients (prospective + retrospective) identifying that 14% had incontinence of some degree at greater than 2 years.

This is overwhelmingly flatus incontinence only (9/14%), with less than 1% having solid stool incontinence.

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37
Q

What is the mechanism of action of Botox in the treatment of fissure-in-ano?

A

Botox inhibts contraction of somatic striated muscle by inhibiting the release of Acetylcholine from pre-synaptic motor neurons.

But, in the treatment of fissure in ano, the injection is either into the IAS or into the inter-sphincteric space (IAS = smooth muscle), with proven efficacy; injecting Botox into the inter-sphincteric space is known to reduce both squeeze pressure and resting tone.

Pharmacological studies on porcine IAS concluded that Botox directly inhibits release of NA from sympathetic nerves, abolishing the normal sympathetic action of contracting the IAS.

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38
Q

How can faecal incontinence be classified?

Note any associated aetiology.

A

Three clinical sub-types

  • Passive incontinence: involuntary leakage of faecal material or gas without awareness.
    • Loss of percetion, altered neurology, +/- sphincter injury
  • Urge incontinence: leakage of faecal material or gas in spite of active attempts to retain them.
    • Disruption of the sphincter or in compliance/capacity
  • Faecal seepage: undesired leakage of faecal material after normal bowel movement without abnormal continence or evacuation.
    • Incomplete evacuation and/or altered rectal sensation.
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39
Q

Define faecal incontinence.

How prevalent is it?

A

Faecal incontinence is generally defined as either the involuntary passage or inability to control the discharge of faecal material through the anus in individual older than the age of four.

It is a common problem, and likely underreported in the general population due to embarrassment and the associated social stigma. It has an estimated prevalence of 7.7% (IQR 2.0 - 20.7%) in an adult population and is typically seen more commonly with increasing age and in the female patient.

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40
Q

Provide an overview of the causes of faecal incontinence

A

Anatomical

  • Sphincter injury
    • Obstetric injury
    • Iatrogenic
  • Previous rectal surgery (LARS after ULAR)
  • Pelvic fractures

Neurological

  • Pudendal neuropathy
  • Diabetes mellitus
  • MS
  • Spinal cord lesions
  • Central nervous ssytem disorders; CVA, dementia etc

Functional

  • IBD
  • Faecal impaction with overflow
  • Diarrhoea
  • Radiation proctitis
  • Rectal prolapse
  • Fistula in ano
  • Hypersecretory rectal tumours.
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41
Q

Describe the Wexner incontinence score

A
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42
Q

What is the Recto-Anal Inhibitory Reflex?

In what conditions is it pathologically affected?

A

The rectoanal inhibitory reflex (RAIR) (also known as the anal sampling mechanism, anal sampling reflex, rectosphincteric reflex, or anorectal sampling reflex) is a reflex characterized by a transient involuntary relaxation of the internal anal sphincter in response to distention of the rectum.

This reflex is absent in Hirschsprungs disease, and may be absent in patients following low resection, or those with rectal prolapse.

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43
Q

What parameters are assessed during anorectal manometry?

A
  • Resting and squeeze pressures along the length of the anal canal and sphincter complex (if using station pull-through technique)
    • Functional sphincter length can be calculated from this
  • RAIR using a 10ml puff of air via catheter-tip syringe
  • First sensation of fullness/flatus
  • Urge to defaecate
  • Maximum tolerance
  • Maximum squeeze pressure
  • Maximum duration of squeeze
  • Cough pressure.
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44
Q

What is the utility of Pudendal Nerve Latency Testing?

A

The validity of PNTML remains unclear, as this test measures the conduction in the fastest remaining fibres and therefore significant nerve damage may be overlooked.

A normal test does not exclude pudendal neuropathy. The test is also uncomfortable and in many cases the readings are unrecordable or not able to be reproduced.

Most studies have shown a poor correlation between PNTML and clinical symptoms and treatment/surgical outcomes. The routine use of PNTML in the assessment of patients with FI is therefore questionable.

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45
Q

Provide an overview of biofeedback and its utility in treating faecal incontinence

A
  • Biofeedback is performed by inserting a pressure-sensitive EMG probe into the anal canal, and the pressure or muscle activity of the anal sphincter contracting around this device is measured with feedback of activity given audibly or visually.
  • Biofeedback works by “operant conditioning” to correct dyssynergia and improve coordination of the abdominal muscles and pelvic floor during defecation, and to improve perception of rectal filling in patients with impaired rectal sensation.
  • Success from biofeedback ranges from 38 – 100%. The exact mechanism for symptom improvement is unclear; no consistent changes in sphincter pressures, rectal distension, or duration of contractions have been demonstrated.
  • A recent systematic review of 13 randomised trials concluded that twice the number of patients regained continence with biofeedback when compared to pelvic floor exercises, and that a combination biofeedback and electrical stimulation was superior to any monotherapy.
46
Q

What are the phases of a DPG?

What is being assessed?

A

A DPG is measured in 3 stages: rest, evacuation and recovery.

  • In the resting phase, the anorectal angle is acute and the anal canal is closed.
  • Evacuation is characterized by an initiation of pelvic floor descent and widening of the anorectal angle.
  • Following evacuation, the anal canal closes and the anorectal angle becomes acute again. The pelvic floor and anorectal junction elevate to their resting position.

DPG involves administering ~100mls of contrast via a rectal catheter, followed by thickened barium paste to simulate faeces. Rectal dimensions (length, diameter, anorectal angles, capacity, rectal wall morphology, perineal descent and evacuatory efficacy rate) are measured.

47
Q

What is the rationale for endoanal-US?

What are the indications for EAUS?

How does the test influence management?

What are the limitations?

A
  • Rationale:
    • Relatively cheap, low morbidity
    • Gold-standard for assessment of the sphincter complex
  • Indications:
    • Sphincter injury
    • Fistula in ano assessment
    • Incontinence
  • Influence on management:
    • Diagnosis of sphincter injury for operative planning
    • Path of fistulas and degree of sphincters traversed
    • Able to identify the presence of other anorectal pathology such as fistulae, tumours and abscesses
  • Limitations
    • User-dependant
    • Invasive
    • Anatomical information only
48
Q

What is the rationale for Defaecating Proctogram?

What are the indications for DPG?

How does the test influence management?

What are the limitations?

A
  • Rationale
    • DPG is a dynamic fluoroscopic or MRI-based study of the function of defaecation
    • Proctography is invaluable in distinguishing the three main pathophysiological causes for obstructed defecation
      • Anismus
      • Rectocele
      • Intrarectal intussusception.
  • Indications
    • Incontinence
    • Obstructed defaecation
    • Prolapse, rectocele, intussusception
    • Pelvic floor disorders; dyssynergia
  • Influence on management
    • Diagnosis and exclusion of the above
    • Concurrent pathology identified pre-operatively
    • May lead to change in management e.g biofeedback for dyssynergia.
  • Limitations
    • Resource intensive (Barium porridge, spec. radiologist)
    • MRI-DPG costly and limited access
    • Invasive
49
Q

What is the rationale for Anorectal Manometry?

What are the indications for this?

How does the test influence management?

What are the limitations?

A
  • Rationale:
    • Physiological testing of the anorectal complex
    • Provides objective data
  • Indications:
    • Incontinence
    • Constipation
    • Anismus/pain - assuming pain controlled pre-procedure
    • IBS
  • Influence on management:
    • Lack of RAIR suggestive of Hirschsprung’s
    • Sphincter function pre-fistula repair
    • Provides baseline function pre-intervention
  • Limitations:
    • Expensive and limited access
    • Invasive
    • Evidence base for interpretation guiding management is lacking.
50
Q

What is the utility of a Balloon Expulsion test?

How is it performed?

A

A balloon expulsion test is a useful adjunct in the investigation of ODS or an evacuation disorder.

A balloon expulsion test is performed by instilling a rectal balloon catheter with 50ml of warmed water. The patient is then asked to expel the balloon; a rise in intrarectal pressure of <40mmHg indicates inadequate rectal pressure or impaired anal relaxation. Failure to expel the balloon after 5 attempts is suggestive of an outlet obstruction.

51
Q

Describe the rationale and role Anorectal Electromyography.

A

EMG records spontaneous and voluntary electrical muscle activity when needles are placed near or in the external anal sphincter (EAS) which allows mapping of myopathic or neuropathic processes.

The EMG reading can be obtained from surface or needle electrodes, with the data from concentric needle electrodes the most robust.

This technique is used to identify sphincter injury as well as denervation–reinnervation potentials that can indicate neuropathy.

52
Q

What are the physiological phases of defaecation?

What reflexes/actions typify each phase?

A
  1. Basal phase
    • Quiescent activity
    • Motility affected by gastro/duodenocolic reflexes
    • Non-propagating contractions
      • “Mixing movements”
      • Slowly mixes chyme from small bowel into faces
    • Propagating contractions
      • “Mass movements”
      • Antegrade propagation predominantly right sided
      • Retrograde propagation in the rectum to keep empty
      • HAPS 5-6 times per day; assoc. with flatus or urgency
  2. Pre-defaecatory phase
    • Increase in HAPS which fill the rectum; RAIR detects solid motion and urge to defaecate forms
  3. Expulsive phase
    • Voluntary straining increases IAP
    • Parasympathetic defaecation reflex triggered initiates further peristalsis and relaxes IAS
    • Somatic relaxation of the pelvic floor and puborectalis sling releases the angle and expulsion occurs
  4. Termination of defaecation
    • The sense of complete rectal emptying, with involuntary contraction of EAS (closing reflex) and pelvic floor, closes the anal canal and reverses the pressure gradient towards the rectum.
    • The anal canal also elongates with distension of the vascular anal cushions to the basal state.
53
Q

What is Obstructed Defecation?

A

OD is a symptom, not a diagnosis;

Obstructed defecation (OD) refers to “difficulty passing stool when there is a preserved urge to defecate.”

54
Q

How is obstructed defecation diagnosed?

A

To be diagnosed with OD, patients must first meet the Rome IV criteria for Functional Constipation, and then the subset of criteria for Functional Defecation Disorders.

This means that patients with OD are first identified as having “Functional Constipation” on historical/interview grounds, then they are classified as having a “Functional Defecation Disorder” on formal assessment with testing.

55
Q

Describe the Rome IV criteria for Functional Constipation

A

Must include 2 or more of the following:

  • Straining during >25% of defecations
  • Lumpy or hard stools >25% of defecations
  • Sensation of incomplete evacuation >25% of defecations
  • Sensation of anorectal obstruction/blockage >25% of defecations
  • Manual manoeuvres to facilitate >25% of defecations
    • (eg digital evacuation, support of the pelvic floor)
  • Fewer than 3 spontaneous bowel movements per week

Loose stools are rarely present without the use of laxatives

Insufficient criteria for irritable bowel syndrome

**Criteria fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis.

56
Q

Describe the Rome IV Criteria for Functional Defectation Disorders

A

The patient must satisfy diagnostic criteria for functional constipation

  • During repeated attempts to defecate, there must be features of impaired evacuation as demonstrated by 2 of the following 3 tests:
    • Abnormal balloon expulsion test
    • Abnormal anorectal evacuation pattern with manometry or anal surface EMG
    • Impaired rectal evacuation by imaging

**Criteria fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis.

57
Q

How can Obstructed Defecation be further categorised?

A

The Oxford group divides OD causes into 3 pathophysiological groups:

  1. Functional OD
    • eg Anismus/pelvic floor dyssynergia
  2. Mechanical OD
    • eg High-grade rectal intussusception or external rectal prolapse
  3. Inefficient force vector
    • eg Rectocele
58
Q

What are the most commonly used and validated scoring systems for ODS and functional constipation?

A
  • The Cleveland Clinic Constipation Score is widely adopted
    • Easy to administer with only 8 questions
  • The Constipation Severity Index is comprehensive but long
    • 78 variables, distinguishes between OD, STC, and IBS-C
  • The Obstructed Defectation Score is specific to ODS
    • Prospectively validated
59
Q

Describe a pelvic floor examination.

A
  • Position
    • Usually left lateral in Australasia
    • Sitting or knees-to-elbows higher yield
  • Inspection
    • Deformities, scars, descended perineum
    • Presence of coexisting haemorrhoids, tags, fissures, etc.
    • Anal gape
    • Have the patient bear-down and assess descent
  • DRE
    • Bulk, length, symmetry, tone of sphincter complex
    • Masses, mucosal abnormalities, rectocoele.
    • PR sling, repeated examination for relaxation of this
  • Proctoscopy
    • Assessment of mucosa
    • Prolapse or intussusception better detected on DPG.
60
Q

What are the three sub-groups within primary or “functional” constipation?

A
  1. Constipation predominant irritable bowel syndrome (IBS)
    • Constipation without prolonged colonic transit often associated with abdominal pain and bloating.
  2. Slow-transit constipation (STC)
    • Associated with prolonged colonic transit time.
  3. Obstructed defecation
61
Q

Provide an overview of the investigation of constipation.

A
  • Biochemistry
    • Exclusion of organic causes
    • Anaemia, IDA are red-flags
  • Colonoscopy
    • Arranged if the mucosa requires exoneration (e.g IDA)\
  • Examination under anaesthesia
    • May be valuable when clincal exam is limited
  • Colonic transit studies
    • Radio-opaque markers ingested
    • <20% persistent at day-5 = normal
    • Persistent throughout colon = slow transit
    • Persistent in rectum = possible ODS
  • DPG
    • Visualization of anatomical and functional components of the pelvic floor and its associated dysfunction
  • Anorectal Manometry
    • Physiological data regarding anorectal sphincter function and rectal capacity and compliance.
  • Conduction studies
    • Objective data on regional nerve function.
62
Q

Provide an overview of treatment of ODS

A
  • Lifestyle and behavioural modification
    • Physical activity reduces colonic transit time
    • Improved toileting habits
    • Fibre supplementation and judicious laxative use
    • Safe digitation may be a temporising measure
  • Pelvic floor rehabilitation
    • Biofeedback
    • Pelvic floor physiotherapy
    • Includes rectal irrigation
  • Operative
    • Botox has been used for “anismus” but relapse rates high
    • Aimed at correcting anatomical defects contributing to symptoms
      • Repair of rectocele
      • Repair of internal intussusception
      • Repair of rectal prolapse
    • Careful selection required given mismatch of anatomical defects, patient’s subjective symptoms, and operative approaches available.
63
Q

Describe the Oxford Grading of Rectal Prolapse

How does this pertain to surgery?

A

Recto-rectal Intussusception

  • Grade I
    • Descends no lower than proximal limit of the rectocele
  • Grade II
    • Descends into the level of the rectocele, not to the sphincter

Recto-anal intussusception

  • Grade III
    • Descends onto sphincter / anal canal
  • Grade IV
    • Descends into sphincter / anal canal
  • Grade V
    • External rectal prolapse

In general, repair of external rectal prolapse is not controversial. However, repair of IRP has generated controversy both within the surgical literature and tabloid media. Surgery for IRP with isolated OD remains controversial. Most surgeons would advocate an extensive trial of conservative measures and biofeedback for OD with IRP.

64
Q

What is your approach to management of rectocoeles?

Any points regarding case selection?

A

Rectoceles frequently present as part of the pelvic floor pathology and it is unusual to find them in isolation. However, they also occur asymptomatically with rectocoeles of <2cm present in up to 80% of asymptomatic female volunteers.

If anismus or pelvic dyssynergia is present, this should be addressed first with lifestyle and behavioural modification as well as pelvic floor physiotherapy and biofeedback.

Generally, if prolapse is also present (co-exist in ~80%) then the prolapse takes priority, and some approaches (e.g. LVMR) may address both pathologies.

In those in whom surgery is in-fact indicated; anterior Delorme’s.

Outcomes from surgery may still be improved be improved by further case selection:

• Patients who digitate on most defecations AND
• Rectoceles that do not empty on proctography

65
Q

Describe the classification of perineal tears in obtetric injury

A
  • 1st degree
    • Laceration of the vaginal mucosa or perineal skin only
  • 2nd degree
    • Involvement of the perineal muscles
  • 3rd degree
    • a) <50% of EAS is torn
    • b) >50% of EAS is torn
    • c) EAS and IAS are torn
  • 4th degree
    • Laceration/tear of the perineum involving the entire anal sphincter complex and the anorectal epithelium.
66
Q

Describe the risk factors for obsteric anal sphincter injury

How common is it?

A

Obstetric anal sphincter injury complicates ~11% of births

  • Maternal
    • Primiparity
    • Asian/Indian ethnicity
    • Age <20 years
    • Shortened perineum (<20mm)
  • Fetal
    • Large birth weight (>4kg)
    • Shoulder dystocia
    • Occipito-posterior position
  • Delivery
    • Instrumental (forceps, vaccum assisted)
    • Prolonged second stage labour (>60min)
    • Gestational age >41 weeks
    • Epidural use
    • Oxycontin use
    • Episiotomy
    • Innapropriate maternal position (lithotomy and squatting)
67
Q

Is it safe to delay repair of obstetric anal sphincter injury?

A
  • While a first or second-degree tear can be repaired in the birthing suite, an OASI should be repaired in an operating theatre under spinal or general anaesthesia, with appropriate lighting, availability of equipment and aseptic operating conditions.
  • If surgical expertise is not available, then delay by 8-12 hours is acceptable based on a Swedish RCT showing that this delay is not associated with worse outcomes at one year.
68
Q

What is the evidence for the different types of surgical repair of Obstetric Anal Sphincter Injury?

Should a defunctioning stoma be utilised?

A
  • The two recognised methods of repair are end-to-end and overlap.
  • 2nd, 3rdA, and 3rdB degree tears should be repaired end-to-end
  • A recent Cochrane systematic review of six trials reported that primary overlap repair was associated with significantly lower rates of faecal urgency and anal incontinence at 12 months.
  • However, at 36 months follow up, there was no difference in quality of life, flatus incontinence or faecal incontinence between the two techniques.
  • There is no consensus on which OASI patients require defunctioning
    • No routine use
    • Most surgeons would support the use of a stoma in someone with a 4th degree injury extending above the levator, or where significant risk of fistula exists.
69
Q

What adjuncts to surgical repair can be used in the setting of an obstetric anal sphincter injury?

A
  • Analgesia
    • Regular ice packs or frozen nappies for cold-compress
  • Antibiotic
    • Antibiotics administered at time of repair can help reduce wound infections from OASI, especially as approximately 25% of women suffer a wound breakdown after OASI repair.
    • Wound sepsis is a significant post-partum problem
  • Pelvic floor training
    • Shown in a Norwegian RCT to reduce post partum anal incontinence symptoms in women who underwent primary repair of an OASI
  • Avoidance of constipation
    • Bulking fibre laxatives
  • Counselling
    • Significant psychosocial issues arise from OASI
70
Q

Describe your work-up of a patient with suspected obstetric anal sphincter injury.

A
  • **Consider re-referring to obstetric team for a de-brief
    • Significant mental anguish around traumatic delivery
    • Can be helped by de-briefing with specialists
  • Complete history and exam with particular attention to risk factors such as large birth weight, instrumental delivery, and episiotomy.
  • Complete exam
  • Validated incontinence scores e.g. Wexner
  • Endo-anal USS
  • Anorectal manometry
  • Pudendal nerve testing for neuropathy
71
Q

List preventative strategies with regard to obstetric anal sphincter injury.

A
  • Perineal massage during labour
    • Cochrane review showing that a warm compress between contractions reduces 3rd and 4th degree tears
  • Caecarean delivery
    • Considered in those with pre-existing OASI or known large birth weights and other risk factors (Asian/Indian ethnicity)
  • Maternal birth position
    • Avoid prolonged lithotomy or squatting
    • Kneeling and on-all-fours thought to be protective.
72
Q

What is the evidence for the use of SNS in faecal incontinence?

What are the measurable outcomes?

What is the big caveat here?

A

Systematic reviews have shown:

  • Mean reduction in FI episodes per week of 7-8
  • Reduction in Wexner score of 8-9
  • Median trial phase success rate was 81%
  • Full continence achieved in 43% in those who went on to a permanent implant.

For such an expensive and invasive therapy, there is yet to be a randomized controlled trial comparing SNS and sham and the mechanism of action of SNS has yet to be fully explained.

73
Q

What are the indications for Sacral Nerve Stimulation?

A
  • Faecal incontinence where organic causes have been excluded
  • Low anterior resection syndrome (LARS) patients
  • Patients with congenital faecal incontinence
  • Patients with an anal sphincter defect
  • *Small RCT showing benefit in IBS
  • **Low level trials showing benefit in IPAA and Radiation FI

In fact, in patients with a sphincter defect, the paradigm has shifted to using SNS as the primary intervention instead of an anal sphincter repair.

74
Q

What are the complications associated with Sacral Nerve Stimulation?

What is the cost-efficacy data locally?

A
  • Failure of SNS efficacy
    • ~40% achieve complete continence
  • Pain or dysthesia
    • Complaints to FDA suggest about 30%
  • Re-operation
    • ~20% reoperation rate
    • ~10% removal rate

A recent study in New Zealand found that SNS cost >NZ$30,000 for implantation and >NZ$46,000 if reintervention was required and in their study, reintervention was required in 41.5%.

75
Q

What are the available alternative therapies, other than SNS, for patients with faecal incontinence?

A
  • “Traditional alternatives”
    • Dietary and behavioural change
    • Pelvic floor physiotherapy and biofeedback
    • Anal sphincter repair
  • “Experimental or novel alternatives”
    • Bulking agents (i.e. injectable polymers into sphincter)
    • Gatekeeper®
    • SphinKeeper©
    • Magnetic sphincters
    • Secca-system - RFA scarring to induce sphincter contraction
76
Q

Describe the landmark for the S3 foramina

A

Use of the ‘H’ technique can accurately identify the S3 foramen, therefore increasing the chances for a successful outcome of SNS therapy.

This is done by marking the medial edges of the sacral foramina under fluoroscopic guidance, and horizontally marking at the lowermost point of the sacroiliac joint.

The meeting points of the ‘H’ are the landmark for S3.

77
Q

What does Sacral Nerve Stimulation / Modulation entail?

How does it work?

A
  • SNM entails surgical placement of stimulating electrodes adjacent to the sacral nerve root, typically S3.
  • Despite its clinical success, the mechanism of action has not been clearly elucidated.
  • Sacral neuromodulation has been hypothesised to modulate afferent, central, autonomic, and somatic neural pathways
    • It may act through somatic afferents to reduce inhibition of sphincter function via ascending central pathways.
    • Locally, external sphincter hypertrophy secondary to stimulation have also been implicated
  • There is little evidence that SNM affects sphincter activation, anal squeeze pressures, anal reflexes, or internal sphincter slow wave amplitudes
78
Q

What is the role of the STARR procedure in patients with obstructed defectation?

A
  • The Stapled Trans-Anal Rectal Resection procedure has had cyclical popularity, and may have a renewed role is established pelvic floor MDT services.
  • In selected patients it may offer acceptable resolution rates ~70%
  • Patients should have an intact rectum (Endo-USS + Manometry)
  • Exclusion criteria
    • Enterocoele
    • Solitary Rectal Ulcer
    • Significant gynaecological pathology
    • Foreign bodies in the pelvis
    • Incontinence
79
Q

Describe the pathophysiology of pilonidal sinus disease

A

The contemporary belief is that of local trauma with the passage of hair into the subcutaneous tissues of the natal cleft.

Karydakis proposed that hair, with its chisel-like roots, inserts into the natal cleft, leading to a foreign body tissue reaction and subsequent infection. Bascom reported that the vacuum effect of the movement of muscles within the gluteal region allows hair to enter through pre-formed pits within the natal cleft.

Although the specific mechanisms whereby pilonidal disease and the development of sinuses form are unclear, and professional opinions are conflicting, a chronic inflammatory process secondary to the presence of hair within the natal cleft is an established contributing factor.

80
Q

What are the risk factors for pilonidal disease?

Which triple-hit is particularly risky?

A
  • Hirsutism
  • Obesity (BMI >24)
  • Sedentary work (seated for > 6 hours per day)
  • Male gender
  • Poor sacrococcygeal hygeine
  • Deep natal cleft
  • Excessive sweating

A person who is hirsute, with a sedentary occupation, who bathes less than twice a week is 291 times more likely to develop PNA than a person without thosew risk factors.

81
Q

What are the presentations of symptomatic pilonidal sinus disease?

A
  1. Acute pilonidal abscess
  2. Sub-acute recurrent pilonidal abscess
  3. Chronic pilonidal disease
  4. Complicated pilonidal disease
82
Q

Describe the prinicples of management in pilonidal sinus disease

A
  • Due to the morbidity of surgery, it should only be considered in the symptomatic patient or those with chronic disease.
  • Removal of diseased tissue, including hair and granulation tissue, with minimisation of healthy tissue excised.
  • Off midline wound
  • Natal cleft flattening
83
Q

List the differential diagnoses for Pilonidal Sinus Disease

A
  • Acute PNA
    • Perianal fistula or abscess
    • Acute hydradenitits-suppurativa
    • Infected sebaceous cyst
  • Recurrent pilonidal cysts or pits
    • Sacrococcygeal sinus (vestigial remnant medullary canal)
    • Presacral sinus or dimple (traction dermoid)
    • Inclusion dermoid cyst
  • Complex pilonidal disease
    • SCC or BCC
    • Atypical infections; actinomycoses, TB, syphilis
    • Chronic hydradenitis suppurativa
    • Pyoderma gangrenosum
    • Sacral osteomyelitis
84
Q

Provide an overview of treatment for pilonidal sinus disease

A

In acute disease; drain the pus off the midline and curette the cavity.

For chronic disease:

  • Non-operative measures
    • Improve sacrococcygeal hygeine - known RF
    • Depilation - recommended by ASCRS guidelines
  • Non-excisional, non-operative interventions
    • Phenol injection
      • 80% phenol solution into tract for several minutes
      • Associated with cellulitis and dermal injury
      • Limited evidence, poor outcomes in sepsis
    • Fibrin glue
      • Very limited evidence
    • Antibiotics
      • Often used in primary care for abscesses
      • No established role for chronic / complex disease
  • Non-excisional, operative interventions
    • Pit-picking / Gip’s procedure
      • Comparable outcomes with excisional operations
      • Ambulatory surgery under local
    • LOCULA procedure
      • Similarly promising outcomes
    • Video-assisted ablation
      • Small series, resource intensive, no better cf Gip’s
  • Excisional operations
    • Karydakis
      • Down to sacro-coccygeal fascia
      • Low recurrence 1% reported by Karydakis
    • Bascombe
      • “Smear” flap w/o fat excision
      • Low recurrence rates 4% reported by Bascombe
    • Rhomoid / Limberg flap
    • V-Y advancement flap / Z-plasty flap
85
Q

What is the proposed pathophysiology of acute colonic pseudo-obstruction?

A

Altered autonomic regulation of the large intestine is the most commonly suggested mechanism for ACPO.

An increase in sympathetic modulation leads to decrease in colonic motility and dilatation, especially in the proximal colon.

A decrease in sacral parasympathetic modulation leads to relative atonicity of the distal colon causing functional obstruction at the level of splenic flexure.

The role of the autonomic nervous system is supported by the use of neostigmine in the treatment of ACPO.

86
Q

How does neostigmine work in the context of pseudo-obstruction?

What dose is given for ACPO?

How is it administered and what needs to be considered?

Is there a safer way to administer it?

A

Neostigmine is a parasympathomimetic that works by reversibly inhibiting cholinesterase; it increases the activation of muscarinic receptors by inhibiting the breakdown of acetylcholine.

In pseudo-obstruction, this is though to stimulate colonic motor activity and decrease intestinal transit time via enhancement of the parasympathetic activity in the gut.

Given IV as a 2mg bolus.

Neostigmine has pro-cholinergic effects, so can cause bradycardia/bradyarrhythmias. Cardaic monitoring should be considered.

A recent Australian retrospective study showed treatment success with subcutaneous administration of neostigmine (0.5mg upto four times daily) in 93% of patients. This study showed no incidences of bradycardia with subcutaneous neostigmine.

87
Q

List the predictors of poor repsonse to Neostigmine in the context of ACPO

A
  • Younger age
  • Electrolyte abnormalities
  • Being on anti-motility agents
  • Opiate usage
  • Post-operative setting
88
Q

Define acute colonic pseudo-obstruction.

A

Acute colonic pseudo-obstruction is a clinical disorder characterised by severe colonic distension in the absence of mechanical obstruction.

89
Q

Categorise and name some of the conditions associated with colonic pseudo-obstruction

A
  • Surgical (head to toe)
    • Neurosurgery
    • Spinal asurgery
    • Thoracic surgery
    • Cardiac surgery
    • Solid organ transplant
    • Pelvic surgery / Pelvic trauma
    • C-section / Vaginal delivery
    • Long bone / hip surgery
  • Medical (head to toe)
    • Neurological d/o; CVA, dementia, severe CI
    • Cardiac; MI, CHF, Cardiogenic shock
    • Infectious; Varicella zoster, CMV
    • Haematological malignancies
    • Medications; neuroleptics, immuno-suppressive meds
90
Q

Define ileus.

How can it be sub-categorised?

A

Paralytic ileus refers to abnormal pattern of gastrointestinal motility following an abdominal operation, that leads to obstipation and intolerance in oral intake.

  • Post-operative ileus
    • Resolution within 4 days
    • 10-30%
  • Prolonged post-operative ileus
    • Persistence beyond 4 days
    • 10%
  • Recurrent ileus
    • Recurrs after resolution
91
Q

Describe the pathophysiology of ileus

A

The pathophysiology of POI is a complex interplay between the neurogenic, humoral and pharmacological components.

  • Initial sympathetic phase
    • Mediated by adrenergic activity inhibiting perstalsis
  • Subsequent inflammatory phase
    • Pro-inflammatory cytokines increase NO and PG within the gut wall inhibiting peristalsis.
92
Q

Describe the various mechanisms of traumatic injury to the colon and rectum.

Cite pathophysiological processes accompanying each type.

A
  1. Direct penetrating injury
    • Firearms and knives
    • Colon second only to small bowel in visceral injury rates
    • Direct local injury to the organ with mechanical loss of barrier and resultant peritonitis
      • GSW usually require segemental resection
      • Stab wounds can often be repaired primarily
  2. Pneumatic blow-out of the colonic or rectal wall
    • 0.5% of all blunt trauma injuries
    • 10% of blunt trauma injuries taken to theatre
    • Mostly MVAs
    • Often large segement of colonic wall ruptured neccesitating segmental resection
  3. Mesenteric/vascular injury affecting associated colon / rectum
    • Associated with deceleration injuries
    • May present later when devitalised colon perforates
      • Associated with ischaemia/reperfusion injury
      • Significant inflammatory mediators
93
Q

How can colonic injury be classified?

A
  • Destructive
    • Wound >50% circumference of colon
    • Complete transection
    • Significant tissue loss
    • Devascularised segment
  • Non-destructive
    • Wound <50% circumference of colon
    • No devascularisation

In blunt trauma:

  • Destructive
    • Serosal tear >50% of circumference
    • Full thickness perforation from blunt injury
    • Mesenteric devascularisation
94
Q

Describe the AAST grading of rectal trauma

A
95
Q

How can peritonitis be classified?

How is this relevant in terms of treatment?

A
  • Primary peritonitis
    • Occurs most commonly in setting of acsites
      • CAPD and cirrhosis
    • Monomicrobial e.g. Enterobacteriaceae, Streptococcus
    • Rarely requires surgical intervention
  • Secondary peritonitis
    • Occurs most commonly due to disruption of GI tract
    • Polymicrobial e.g Bacteroides and E. coli
    • Underlying cause requires surgical intervention
  • Tertiary peritonitis
    • Recurrent or progessive infection after source control of secondary peritonitis
    • Usually in immunocompromised or critically ill
    • Often MDR-organisms e.g. ESBL, Fungi, VRE
96
Q

Define sepsis

Define septic shock

A

Sepsis is a “life threatening organ dysfunction caused by a dysregulated host response to infection”.

Septic shock is a subset of sepsis and is present when there are profound circulatory, cellular, and metabolic abnormalities resulting in inadequate tissue oxygenation and perfusion.

Septic shock may be clinically determined by:

  • Vasopressor requirement to maintain MAP of 65mmHg or greater
  • Serum lactate >2mmol/L
  • Above in absence of hypovolaemia
97
Q

What are the SOFA and qSOFA scores?

What is their utility?

A

The SOFA and q(uick)SOFA scores are used to identify septic patients likely to require ICU support.

Bedside qSOFA:

  • SBP <100mmHg
  • RR >22
  • GCS <15

The SOFA score uses seven measures of organ dysfunction

  • Platelet count, bilirubin, mean arterial pressure, GCS, serum creatinine and urine output per day.
  • Each measure is assigned a maximum score of 4, with higher scores indicating increased mortality.

Organ dysfunction is potentially life threatening if the Sequential Organ Failure Assessment score (SOFA) increases by two points or greater, or the bedside qSOFA score is two or more.

98
Q

Define Intra-Abdominal Hypertension

What is normal IAP?

Define Compartment Syndrome

A

Intra-abdominal hypertension (IAH) is a “sustained or repeated pathological elevation in intra-abdominal pressure greater than or equal to 12mmHg”.

IAP is typically 2-7mmHg in healthy individuals and 5-7mmHg in those who are critically unwell.

Abdominal compartment syndrome (ACS) is defined as a “sustained IAP greater than 20mmHg with associated new organ dysfunction”.

99
Q

How can Abdominal Compartment Syndrome be classified?

A

Primary ACS

  • Primary ACS results from injury or pathology within the abdomen or pelvis eg. Pancreatitis, ascites, haemoperitoneum. This usually requires early intervention which may be in the form of surgery or interventional radiology.

Secondary ACS

  • Secondary ACS results from pathology outside the abdomen or pelvis eg. Burns, sepsis, overzealous fluid resuscitation

Recurrent ACS

  • Recurrent ACS occurs when ACS re-develops after treatment of either primary or secondary ACS.
100
Q

Provide an overview of ACS treatment

A

Non-operative measures:

  1. Evacuate intraluminal contents
    • Cathartic laxatives, NG tubes, IDC, rectal tube
    • Endoscopic decompression
  2. Evacuate intra-abdominal space occupying lesions
    • Drain collections, drain ascites, remove packs
  3. Improve abdominal wall compliance
    • Muscular paralysis or relaxation
  4. Optimise fluid administration
    • Diuresis
    • Goal directed fluid therapy
    • Consider haemodialysis
  5. Optimise regional and systemic perfusion
    • Judicious vasopressors

Operative measures:

  1. Midline laparotomy with temporising VAC laparostomy
101
Q

Describe clinical prediction tools used in appendicitis.

Are any of them useful?

A

The most well known is the Alvarado score, which incorporates clinical, symptomatic, and laboratory indices into its calculation of low/medium/high risk.

The APPEND (Anorexia, migratory Pain, Peritonism, Elevated CRP, Neutrophilia, and Dude) score is locally validated; a score of 1 has a NPV of 95.6% and as score of 5 has a PPV of 95.5%.

102
Q

What is the current state of evidence regarding non-operative, antibiotic-based, management of uncomplicated appendicitis?

A

Recently assessed in a 2019 meta-analysis in Annals of Surgery:

  • Surgery has a higher total success rate
    • Treatment failure rate of 30% with antibiotics
    • This is sustained at one year
  • Equivalent length of stay
  • Lower cost with antibiotic treamtent
  • No increase in perforation rate in those treated with antibiotics
103
Q

What is the rationale for interval appendicectomy?

A

Interval appendicectomy is recommended for patients managed non-operatively for complicated appendicitis, because this cohort has been found (on meta-analysis) to have higher rates of neoplastic pathology upon resection.

The overall rate of neoplasm is about 10-20% and is much higher in patients over 30 years of age. The most common neoplasm is a mucinous neoplasm.

There is no evidence for interval appendicectomy in patients with non-operatively managed uncomplicated appendicitis.

104
Q

Describe the classification of appendiceal neoplasms.

A
  1. Mucinous
    • Simple mucocoeles
    • Appendiceal mucinous neoplasms
      • Low grade appendiceal mucinous neoplasms
      • High grade appendiceal mucinous neoplasms
    • Appendiceal mucinous adenocarcinomas
  2. Non-mucinous
    • Epithelial tumours
      • Non-mucinious adenocarcinomas
      • Goblet cell adenocarcinomas
    • Neuroendocrine tumours
105
Q

What distinguishes a simple mucocoele from a LAMN/HAMN?

What distiunguishes a LAMN from a HAMN, and what distinguishes them from adenocarcinoma?

How is it possible that LAMNs and HAMNs can cause PMP?

A
  • A simple mucocoele has no cellular dysplasia and is simply the result of obstructive build up of mucin within the appendiceal lumen.
  • LAMNs and HAMNs have some degree of cellular atypia, the grade of this (based on mitotic activty and nuclear atypica) is what distinguishes from one another.
  • The defining feature of adenocarcinomas of the appendix is their infiltrative invasion pattern, typically with a marked desmoplastic stromal reaction.
  • Although by definition LAMNs and HAMNs do not invade, their expansile growth may push and thin the appendiceal wall until the appendix ruptures, and the resultant spillage of cellular or acellular mucin may lead to pseudomyxoma peritonei (PMP).
106
Q

Describe your follow-up protocol of a completely excised LAMN/HAMN.

What about colonoscopy?

A
  • There is lack of data regarding appropriate intervals for imaging surveillance in these patients.
  • In patients with completely resected LAMN/HAMN, one strategy is to obtain MRI (more sensitivity for detecting extracellular mucin) or CT every 6 months for 2 years.
  • Following that, HAMN should have annnual follow up with MRI/CT.
  • Tumour markers CEA, CA 19.9 and CA 125 should also be obtained at baseline and for surveillance.
  • Follow‐up colonoscopy is also recommended with an increased incidence of synchronous colorectal lesions seen
    • 42% in one study
107
Q

Which NETs of the appendix require further treatment?

A
  • NETs >2cm should undergo right hemicolectomy due to risk of lymph node metastases.
  • NETs between 1‐2cm have an intermediate risk; right hemicolectomy is indicated if the following are present:
    • mesoappendiceal invasion >3mm
    • mitotic index >2
    • Ki 67 >3%
    • LVI
    • involved margins
108
Q

How can anorectal-vaginal fistula be classified?

A
109
Q

What are the components of the Oakland Score for Lower GI Bleeding?

A
  • Age
  • Gender
  • Previous lower GI bleed
  • DRE findings
  • Heart rate
  • Blood pressure
  • Haemoglobin

Different weighting to each component, with the heaviest on Hb.

Safe discharge if score is 8 or less.

110
Q

Describe the treatment of ACPO.

A

All patients diagnosed with uncomplicated ACPO and without biochemical and radiological signs of ischemia, perforation or peritonism, can be treated supportively.

Medical intervention:

  • Neostigmine
    • 0.5 mg submit QID
    • 2mg IVI (requires cardiac monitoring)

Endoscopic intervention:

  • Colonoscopic decompression in ACPO can be technically challenging and it is recommended that it should be undertaken by an experienced endoscopist. The perforation rate is quoted to be between 1-3%.
111
Q

Describe the Pilonidal Sinus Disease “Equation” proposed by Karydakis

A

Pilonidal Disease = H x F x V2

H = Hair, local or distant

F = Force, applied by hair (root down)

V = Vulnerability, predisposing pores, splits, erosions at the natal cleft.

Bascombe’s theory of negative pressure “drawing-in” the hair may modify the F component.