Anal fissures and fistulas

Anal Anatomy

  • Surgical anal canal: the length between the anal verge  / intersphincteric groove to the anorectal ring
  • Anatomical anal canal: anal verge to the dentate line
  • Anal verge: anocutaneous line approximately 2 cm to the dentate line
  • Dentate line: Junction of ectoderm and endoderm of anal canal
  • Internal anal sphincter: Smooth muscle not under voluntary control; most distal part of the circular part of the tunica musuclaris of the gut
  • External anal sphincter: Voluntary muscle that merges with the puborectalis and levator ani

Anal fissure

  • Definition
    • Linear tear in the distal anal canal which involves the epithelium and variably, the full thickness of anal mucosa
  • Presentation
    • Severe pain during defecation >  not pooping > constipation > hard stools > more pain
    • Bright red blood on TP
    • Acute fissure: just a tear
    • Chronic fissure: fibres of internal anal sphincter visible, enlarged anal skin tag and proximal anal papillary hypertrophy commonly present
  • Medical Management
    • Stool softener + laxatives
    • Sitz bath post defecation > relives spasm > less pain, more healing
    • GTN/nifedipine pintment
    • Botulism toxin (=chemical sphincterotomy)
  • Surgical Management
    • Sphincter dilatation (not commonly used due to impaired continence)
    • Lateral internal sphincterotomy
      • Procedure of choice
      • Cut through hypertrophied internal sphincter to reduce tension

Fistula-in-ano

  • Definition – tract lined with granulation tissue that allows communication between the anal canal to the perianal skin
  • The Goodsall rule – fistuals with anterior openings will follow a staight radial line to the dentate; fistulas with posterior openings will follow a curved line
  • Typical follows anal abscess
  • Surgical options
    • Fistulotomy
    • Seton placement – cord/rubber band that runs through the fistula and joins up outside to prevent one end sealing up and forming an abscess
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Passing a Suturing OSCE Station

Suture Choice

  • Material choice
    • Deep: absorbable sutures
      • PDS (mono)
      • Vicryl (multi)
      • Monocryl
      • Caprosyn (monofilament)
    • Superficial: monofilament nonabsorbable sutures
      • Nylon
      • Prolene (polypropylene)
  • Suture size
    • Face – 6.0
    • Most places – 4.0 / 5.0
    • Back, foot, thick muscle – 3.0
  • Monofilament versus braided
    • Monofilament less infection risk, less inflammatory reaction
    • Multifilament easier to tie, less risk of slippage

Suture Removal

  1. Face: 3 days
  2. Ear, lip: 4 days
  3. Chest, abdomen, penis: 8 days
  4. Extremeties: 10 days
  5. Foot, back: 12 days
  6. Chronic steroid use, T2DM: 2-3 weeks

Anaesthetic

  • Lignocaine +/- adrenaline
  • Avoid adrenaline in end-arterial circulation sites
  • Handy tips
    • Inject through the wound edge
    • Use an insulin needle for minimal pain
    • Wait plz before stabbing people
    • A Biers block may be used if there are extensive lacerations on forearms
  • Maximum dosages
    • Lignocaine + adrenaline = 7mg/kg
    • Lignocaine without adrenaline = 3mg/kg
  • Local anaesthetic toxicity
    • Sentinel effects – tinnitus, dizziness, confusion, perioral numbness
    • CNS toxicity – seizures, coma
    • CVS toxicity – Na+ blockade effects (QRS prolongation, dysrhythymias, hypotension, bradycardia)
    • Sodium bicarb, benzos, fluid load, intralipid

Periprocedural considerations

  • Cleaning + sterile technique (but more like clean-contaminated)
  • Decontamination of wound
  • Tetanus vaccination
  • Consider flucloxacillin for wound infections

Pancreatitis Salient Points

Investigations

  • CT/MRI only indicated if
    • Diagnosis unclear from biochemistry or history
    • Failure to improve after 72 hours of admission
    • Suspicion of complications

Aetiology

  • GET SMASHED – gallstones, ethanol, trauma, salicylates, mumps, autoimmune, scorpion sting, hyperlipidemia, hypercalcemia and hypothermia, emboli, drugs
  • TA USS in all patients to look for gallstones
  • Lipids and calcium in the absence of a history suggestive of alcohol abuse and a normal TA USS
  • Unclear role for endoscopy

Risk stratification

  • Ranson and Glasgow scores. Ranson scores both at admission and 24 hours and is less useful for gallstone aetiologies
  • Glasgow score uses the mnemonic PANCREAS
    • P – PaO2 <8kPa
    • A – Age >55 years old
    • N – Neutrophilia – WCC >15×10(9)/L
    • C – Calcium <2 mmol/L
    • R – Renal function, Urea >16 mmol/L
    • E – Enzymes: LDH >600iu/L; AST >200iu/L
    • A – Albumin <32g/L (serum)
    • S – Sugar: blood glucose >10 mmol/L

ED management

  • Aggressive fluid resuscitation – up to 500ml/hour of CSL (third spacing)
  • Aim to normalize serum urea with fluid resuscitation

Inpatient management

  • Antibiotics
    • Not routinely indicated
    • Use for extra-pancreatic foci of infection or infected necrosis
  • Nutrition
    • Early low-fat feeding in mild pancreatitis as tolerated if N+V and abdominal pain have resolved
    • Enteric nutrition preferred over parenteral route in severe pancreatitis
    • No difference between NG and NJ tubes in severe pancreatitis
  • Surgery
    • Cholecystectomy if gallstones visualised in GB
    • If necrotising biliary pancretitis, defer until inflammation subsides
    • Surgery not indicated for asymptomatic pseudocysts and necrosis
    • In stable patients with infected necrosis, drainage should wait for 4/52 to allow for liquefaction and surrounding fibrosis
  • Infected necrosis
    • Difficult to distinguish sterile from infected necrosis
    • Reasonable strategy is to initiate empiric antibiotics while awaiting CT FNA
    • Inf patient stable, continue Abx, otherwise, send to theater for debridement
    • Tazocin or metronidazole + ceftriaxone are appropriate choices
  • ERCP
    • Acute cholangitis is an indication of urgent ERCP
    • Gallstone pancreatitis with no evidence of biliary obstruction should not receive ERCP
    • In the absence of cholangitis / obstruction, MRCP or endoscopic ultrasound (EUS) rather than diagnostic ERCP should be used to screen for
      choledocholithiasis
    • Pancreatic duct stents / postprocedure rectal SSAID suppositories should always be offered to prevent ERCP-induced pancreatitis

 

JMO Fracture Management – A Guide To Ticking OSCE Boxes

  1. ABCDs: resuscitate and stabilise if needed
  2. Admit
  3. Call the orthopod
  4. Analgesia and anti-emetics
  5. Rationalised regular medications
  6. DVT prophylaxis as indicated

Tests to order

  1. FBC
  2. UEC
  3. LFT
  4. Coags, consider group and hold
  5. Plain films, consider CT/MRI as follow up

Aims

  1. Reduction
  2. Fixation
  3. Immobilisation
  4. Soft tissue and neurovascular protection

Goals

  1. Anatomic reduction of fracture fragments
  2. Stable internal fixation to fulfil biomechanical demands
  3. Preservation of blood supply to the injured area of the extremity
  4. Active, pain-free mobilisation of adjacent muscles and joints to prevent fracture disease

Non-operative

  1. Casting
    1. Traction to long axis, reversal of mechanism of injury and immobilisation
    2. Contraindications:
      1. If reduction is impossible
      2. Severely comminuted fractures
      3. If fracture has been produced by traction forces
  2. Traction

Operative

  1. Open reduction and internal fixation
    1. K-wires – not useful for rotation, poor resistance to torque and bending forces
    2. Plates and screws
    3. Intramedullary nails
  2. External fixation
    1. Open fractures with significant soft-tissue disruption
    2. Soft tissue injury
    3. Pelvic fractures
    4. Limb-lengthening procedures

Surgical Admission Basics for the OSCE

Because surgeons like failing people who don’t list everything off

Bloods everyone gets

  1. FBP
  2. UEC
  3. CRP
  4. LFT – sepsis deranges LFTs and is a useful cover-all if asked to justify the test
  5. Coags – pre-operative standard, also if warfarin or liver pathology
  6. Group and hold +/- cross match – preoperative standard
  7. B-HCG – every female with an acute abdomen gets this
  8. Lipase and amylase

Other Ix everyone gets

  1. ECG – Pre-operative standard in anyone >50yo as per ASA guidelines. Everyone with epigastric pain scores this.
  2. CXR – Pre-operative standard in anyone >75yo as per ASA guidelines. Everyone with epigastric pain scores this. Every ? perforation gets this.
  3. CT abdomen – if oyung, don’t order unless they really need one
  4. U/S for biliary pathology
  5. AXR for obstruction

What You Need To Say You Would Do As A JMO

  1. Admit
  2. Resuscitate
  3. Call the surgeon
  4. IVC and fluids if needed
  5. Drugs
    1. Analgesia
    2. Antiemetics
    3. Antibiotics
  6. Anticoagulation
    1. Heparin and TEDS
  7. NPO + PPI
  8. Patient’s regular medication – ‘I would go through the patient’s regular medications and rationalise them’
  9. Adjuncts
    1. IDC
    2. NGT
  10. Discussion with surgeon about operation +/- consenting the patient
  11. Diabetic sliding scale if needed

Own the … Vascular Examination

Didn’t add videos because you don’t really need them to do this and all the ones on the net are a tad too brief anyway. Also, apparently there’s a few ways of doing the Trendelenburg test (seriously, how many things are named after this guy) so get your reg to show you.

  • History
    • Claudication
      • Factors in favour of neurogenic claudication are variabale caludication distance, aggravation with bending over, requiring sitting down or leaning on trolley to relieve pain and immediate relief once in a good posture
    • Rest pain – exacerbated by lying down or elevation of the foot, relieved by hanging the foot out of bed
    • Acute arterial occlusion – 6 Ps – pain, pallor, paraesthesia, ‘paralysis’, pulses absent, perishing cold
    • focal neurology, amaurosis fugax
  • Inspection
    • Inspect while erect for varicosities, scars (vein harvests) and changes indicative of diabetic foot (pes planus, clawing, hallux valgus etc.)
    • Skin changes
      • Lipodermatosclerosis – thickening, pigmentation, induration and inflammation of skin
      • Pigmentation may be a sequela of cellulitis – pigmentation without fibrosis is not venous disease. Pigmentation in the forefoot is also not typical of venous disease
    • Colour changes
      • Rubor is due to venous pooling
      • Hemosiderin deposition leads to brownish discolouration
      • Acute arterial occlusion leads to pallor
    • Ulceration – inspect between the webs of the toes
      • Venous ulcers – garter area, irregular margin, pale neo-epithelium, pink base of granulation, warm and oedematous surroundings
      • Arterial ulcers – regular margin, punched out appearance, cold surroundings, pain (pain very specific for arterial aetiology)
      • Diabetic ulcers –painless with reduced sensation in surrounding skin
    • Gangrene
  • Palpation
    • Capillary refill
    • Temperature
    • Tenderness
    • Tenseness
    • Pulses; if unsure if its a faint pulse of your own digital pulses, simultaneously palpate your own radial pulse and look for asynchrony
      • Radial, radial-radial delay
      • Brachials
      • Carotids
      • Abdominal aorta
      • Femorals
      • Popliteal
      • Posterior tibial
      • Dorsalis pedis
  • Auscultation
    • Subclavian
    • Carotids
    • Renal bruits
    • Aortic
    • Femoral
  • Special test
    • Buerger’s for arterial insufficiency – elevate the limb to 45 degrees for 30 seconds, then drop it into a dependent position. Poor arterial pressure is insufficient to overcome drainage to the heart causing pallor. Plethora on assuming the dependent position is due to reactive hyperaemia. Guttering of the veins when elevated is indicative of poor arterial driving pressure.
    • ABPI – use Doppler to measure pressures – remarkably difficult to auscultate DP or PT pulses. Severe arterial disease <0.5 < moderate <0.8 < mild < 0.9 <normal <1.2 < calcification
    •  Trendelenburg test
    • Neurological examination
  • Supplementary + random things noted down during registrar teaching
    • Sexual impotence +buttock claudication = Leriche’s syndrome
    • The 4 main categories of all PAD patients are caludicants (40%), critical limb ischaemics (rest pain +/- ulcers <5%), asymptomatics (40%) and atypical presentations (15%)
    • There is an equal risk of death of patients with PAD as those with CAD which is around 20% mortality in five years
    • There is no evidence showing benefit of dual antiplatelet therapy except for stent implantation
    • The 24 month mortality of critical limb ischaemia is 50%; 25% will lose one or both legs and 25% will live with both legs
    • Surgery for PAD is done to improve symptoms, not mortality as in all PAD patients, intervention has no significant effect on mortality
    • With patients, 1/3 get better, 1/3 stay the same, 1/3 get worse
    • Symptomatic patients with carotid stenosis >50% should be offered an operation within 3 weeks due to the high risk of recurrent strokes exceeding the risk of peri-operative stroking out (2-4%)
    • The evidence for operation in asymptomatic carotid stenosis is not great, but around 80-90% is a reasonable indication for intervention
    • In general endovascular techniques are inferior to carotid endarterectomy in terms of peri-operative complications
    • Women seem to do worse than men with carotid procedures