Surgery 2012 PDF

Surgery
Alasdair Scott
BSc (Hons) MBBS PhD
2012
dr.aj.scott@gmail.com
Table of Contents
1. Perioperative Management .................................................................................... 1
2. Fluids and Nutrition .............................................................................................. 11
3. Trauma ................................................................................................................. 17
4. Upper GI Surgery ................................................................................................. 25
5. Hepatobiliary Surgery ........................................................................................... 35
6. Lower GI Surgery ................................................................................................. 43
7. Perianal Surgery................................................................................................... 58
8. Hernias ................................................................................................................. 64
9. Superficial Lesions ............................................................................................... 69
10. Breast Surgery ................................................................................................... 80
11. Vascular Surgery ................................................................................................ 85
12. Urology ............................................................................................................... 94
13. Orthopaedics .................................................................................................... 109
14. Ear, Nose and Throat ....................................................................................... 131
15. Ophthalmology ................................................................................................. 144

Perioperative Management
Contents
Pre-Operative Assessment and Planning ..................................................................................................................................... 2
Specific Pre-operative Complications............................................................................................................................................ 3
Anaesthesia ................................................................................................................................................................................... 4
Analgesia ....................................................................................................................................................................................... 4
Enhanced Recovery After Surgery ................................................................................................................................................ 5
Surgical Complications .................................................................................................................................................................. 5
Post-op Complications: General.................................................................................................................................................... 6
Post-op Complications: Specific .................................................................................................................................................... 7
Post-op Pyrexia ............................................................................................................................................................................. 8
DVT................................................................................................................................................................................................ 9
Other Common Post-Operative Presentations ............................................................................................................................ 10
© Alasdair Scott, 2012 1

Pre-Operative Assessment and Planning
Aims Preparation
 Informed consent
 Assess risk vs. benefits NBM
 Optimise fitness of patient  ≥2h for clear fluids, ≥6h for solids
 Check anaesthesia / analgesia type c̄ anaesthetist
Bowel Prep
Pre-op Checks: OP CHECS  May be needed in left-sided ops
 Picolax: picosulfate and Mg citrate
 Operative fitness: cardiorespiratory comorbidities
 Klean-Prep: macrogol
 Pills
 Not usually needed in right-sided procedures
 Consent
 Necessity is controversial as benefit of minimising post-
 History
op infection might not outweigh risks
 MI, asthma, HTN, jaundice
 Liquid bowel contents spilled during surgery
 Complications of anaesthesia: DVT, anaphylaxis
 Electrolyte disturbance
 Ease of intubation: neck arthritis, dentures, loose teeth  Dehydration
 Clexane: DVT prophylaxis  ↑ rate of post-op anastomotic leak
 Site: correct and marked
Prophylactic Abx
Drugs  Use
 GI surgery (20% post-op infection if elective)
Anti-coagulants  Joint replacement
 Balance risk of haemorrhage c̄ risk of thrombosis  Give 15-60min before surgery
 Avoid epidural, spinal and regional blocks  Regimens: (see local guidelines)
 Biliary: Cef 1.5g + Met 500mg IV
AED  CR or appendicetomy: Cef+Met TDS
 Give as usual  Vascular: co-amoxiclav 1.2g IV TDS
 Post-op give IV or via NGT if unable to tolerate orally  MRSA+ve: vancomycin
OCP / HRT
 Stop 4wks before major / leg surgery DVT Prophylaxis
 Restart 2wks post-op if mobile  Stratify pts according to patient factors and type of
surgery.
β-Blockers  Low risk: early mobilisation
 Continue as usual  Med: early mobilisation + TEDS + 20mg enoxaparin
 High: early mobilisation + TEDS + 40mg enoxaparin +
intermittent compression boots perioperatively.
 Prophylaxis started @ 1800 post-op
Pre-op Investigations  May continue medical prophylaxis at home (up to 1mo)
Bloods
 Routine: FBC, U+E, G+S, clotting, glucose ASA Grades
 Specific 1. Normally healthy
 LFTs: liver disease, EtOH, jaundice 2. Mild systemic disease
 TFT: thyroid disease 3. Severe systemic disease that limits activity
 Se electrophoresis: Africa, West Indies, Med 4. Systemic disease which is a constant threat to life
 Cross-match 5. Moribund: not expected to survive 24h even c̄ op
 Gastrectomy: 4u
 AAA: 6u
Cardiopulmonary Function
 CXR: cardiorespiratory disease/symptoms, >65yrs
 Echo: poor LV function, Ix murmurs
 ECG: HTN, Hx of cardiac disease, >55yrs
 Cardiopulmonary Exercise Testing
 PFT: known pulmonary disease or obesity
Other
 Lat C-spine flexion and extension views: RA, AS
 MRSA swabs

Specific Pre-operative Complications
Diabetes Jaundice
 Best to avoid operating in jaundiced pts.
↑ Risk of post-operative complications  Use ERCP instead
 Surgery → stress hormones → antagonise insulin
 Pts. are NBM Risks
 ↑ risk of infection  Pts. c̄ obstructive jaundice have ↑ risk of post-op renal
 IHD and PVD failure  need to maintain good UO.
 Coagulopathy
Pre-op  ↑ infection risk: may → cholangitis
 Dipstick: proteinuria
 Venous glucose Pre-op
 U+E: K
+
 Avoid morphine in pre-med
 Check clotting and consider pre-op vitamin K
IDDM  Give 1L NS pre-op (unless CCF) → moderate diuresis
 Urinary catheter to monitor UPO
Practical Points  Abx prophylaxis: e.g. cef+met
 Put pt. first on list and inform surgeon and anaesthetist
 Some centres prefer to use GKI infusions Intra-op
 Sliding scale may not be necessary for minor ops  Hrly UO monitoring
 If in doubt, liaise c̄ diabetes specialist nurse  NS titrated to output
Insulin Post-op
 ± stop long-acting insulin the night before  Intensive monitoring of fluid status
 Omit AM insulin if surgery is in the morning  Consider CVP + frusemide if poor output despite NS
 Start sliding scale
 5% Dex c̄ 20mmol KCl 125ml/hr
 Infusion pump c̄ 50u actrapid Anticoagulated Patients
 Check CPG hrly and adjust insulin rate  Balance risk of haemorrhage c̄ risk of thrombosis
 Check glucose hrly: aim for 7-11mM  Consult surgeon, anaesthetist and haematologist
 Post-op  Very minor surgery may be undertaken w/o stopping
 Continue sliding-scale until tolerating food warfarin if INR <3.5.
 Switch to SC regimen around a meal  Avoid epidural, spinal and regional blocks if
anticoagulated,
NIDDM  In general, continue aspirin/clopidogrel unless risk of
 If glucose control poor (fasting >10mM): treat as IDDM bleeding is high – then stop 7d before surgery
 Omit oral hypoglycaemics on the AM of surgery
 Eating post-op: resume oral hypoglycaemics c̄ meal Low thromboembolic risk: e.g. AF
 Stop warfarin 5d pre-op: need INR <1.5
 No eating post-op
 Check fasting glucose on AM of surgery  Restart next day
 Start insulin sliding scale
 Consult specialist team ore. restarting PO Rx High thromboembolic risk: valves, recurrent VTE
 Need bridging c̄ LMWH
Diet Controlled  Stop warfarin 5d pre-op and start LMWH
 Usually no problem  Stop LMWH 12-18h pre-op
 Pt. may be briefly insulin-dependent post-op  Restart LMWH 6h post-op
 Monitor CPG  Restart warfarin next day
 Stop LMWH when INR >2
Emergency Surgery
Steroids  Discontinue warfarin
 Vit K .5mg slow IV
Risks  Request FFP or PCC to cover surgery
 Poor wound healing
 Infection
COPD and Smoking
 Adrenal crisis
Risks
Mx
 Basal atelectasis
 Need to ↑ steroid to cope c̄ stress
 Aspiration
 Consider cover if high-dose steroids w/i last yr  Chest infection
 Major surgery: hydrocortisone 50-100mg IV c̄ pre-med
then 6-8hrly for 3d. Pre-op
 Minor: as for major but hydrocortisone only for 24h  CXR
 PFTs
 Physio for breathing exercises
 Quit smoking (at least 4wks prior to surgery)
Anaesthesia Analgesia
Principals and Practical Conduct Necessity
 Aims: hypnosis, analgesia, muscle relaxation  Pain → autonomic activation → arteriolar constriction →
 Induction: e.g. IV propofol ↓ wound perfusion → impaired wound healing
 Muscle Relaxation  Pain → ↓ mobilisation → ↑ VTE and ↓ function
 Depolarising: suxamethonium  Pain → ↓ respiratory excursion and ↓ cough →
 Non-depolarising: vecuronium, atracurium atelectasis and pneumonia
 Airway Control: ET tube, LMA  Humanitarian considerations
 Maintenance
 Usually volatile agent added to N2O/O2 mix General Guidance
 E.g. halothane, enflurane  Give regular doses at fixed intervals
 End of Anaesthesia  Consider best route: oral when possible
 Change inspired gas to 100% O2  PCA should be considered: morphine, fentanyl
 Reverse paralysis: neostigmine + atropine (prevent  Follow stepwise approach
muscarinic side effects)  Liaise c̄ Acute Pain Service
Pre-Op
Pre-medication: 7As
 Epidural anaesthesia: e.g. c̄ bupivacaine
 Anxiolytics and Amnesia: e.g. temazepam
 Analgesics: e.g. opioids, paracetamol, NSAIDs
 Anti-emetics: e.g. ondansetron 4mg / metoclop 10mg End-Op
 Antacids: e.g. lansoprazole  Infiltrate wound edge c̄ LA
 Anti-sialogue e.g. glycopyrolate (↓ secretions)  Infiltrate major regional nerves c̄ LA
 Antibiotics
Post-Op: stepwise approach
Regional Anaesthesia 1. Non-opioid ± adjuvants

 May be used for minor procedures or if unsuitable for GA  Paracetamol
 Nerve or spinal blocks  NSAIDs
 CI: local infection, clotting abnormality  Ibuprofen: 400mg/6h PO max
 Use long-acting agents: e.g. bupivacaine  Diclofenac: 50mg PO / 75mg IM
2. Weak opioid + non-opioid ± adjuvants

 Codeine
Complications of Anaesthesia
 Dihydrocodeine
 Tramadol
Propofol Induction
 Cardiorespiratory depression
3. Strong opioid + non-opioid ± adjuvants
 Morphine: 5-10mg/2h max
Intubation  Oxycodone
 Oro-pharyngeal injury c̄ laryngoscope  Fentanyl
 Oesophageal intubation
Spinal or Epidural Anaesthesia
Loss of pain sensation
 ↓ SE as drugs more localised
 Urinary retention
 1st line for major bowel resection
 Pressure necrosis
 Caution
 Nerve palsies  Respiratory depression
 Neurogenic shock → ↓BP
Loss of muscle power
 Corneal abrasion
 No cough → atelectasis + pneumonia
Malignant Hyperpyrexia
 Rare complication ppted by halothane or suxamethonium
 AD inheritance
 Rapid rise in temperature + masseter spasm
 Rx: dantrolene + cooling
Anaphylaxis
 Rare
 Possible triggers
 Antibiotics
 Colloid
 NM blockers: e.g. vecuronium

Enhanced Recovery After Surgery Surgical Complications
ERAS Immediate (<24h)
 Commonly employed in colorectal and orthopaedic surgery  Intubation → oropharyngeal trauma
 Surgical trauma to local structures
Aims  Primary or reactive haemorrhage
 Optimise pre-op preparation for surgery
 Avoid iatrogenic problems (e.g. ileus) Early (1d-1mo)
 Minimise adverse physiological / immunological responses  Secondary haemorrhage
to surgery  VTE
 ↑ cortisol and ↓ insulin (absolute or relative)  Urinary retention
 Hypercoagulability  Atelectasis and pneumonia
 Immunosuppression  Wound infection and dehiscence
 ↑ speeded of recovery and return to function  Antibiotic association colitis (AAC)
 Recognise abnormal recovery and allow early intervention
Late (>1mo)
 Scarring
Pre-op: optimisation  Neuropathy
 Aggressive physiological optimisation  Failure or recurrence
 Hydration
 BP (↑ / ↓)
 Anaemia
 DM
 Co-morbidities
 Smoking cessation: ≥4wks before surgery
 Admission on day of surgery, avoidance of prolonged fast
 Carb loading prior to surgery: e.g. carb drinks
 Fully informed pt., encouraged to participate in recovery
Intra-op: ↓ physical stress

 Short-acting anaesthetic agents
 Epidural use
 Minimally invasive techniques
 Avoid drains and NGTs where possible
Post-op: early return to function and mobilisation

 Aggressive Rx of pain and nausea
 Early mobilisation and physiotherapy
 Early resumption of oral intake (inc. carb drinks)
 Early discontinuation of IV fluids
 Remove drains and urinary catheters ASAP

Post-op Complications: General
Haemorrhage Classification Wound Infection

 Primary: continuous bleeding starting during surgery  5-7d post-op
 Reactive  Organisms: S. aureus and Coliforms
 Bleeding at the end of surgery or early post-op
 2O to ↑ CO and BP Operative Classification
 Secondary  Clean: incise uninfected skin w/o opening viscus
 Bleeding >24h post-op  Clean/Cont: intra-op breach of viscus (not colon)
 Usually due to infection  Contaminated: breach of viscus + spillage or opening of
colon
 Dirty: site already contaminated – faeces, pus, trauma
Post-op Urinary Retention Risk Factors
 Pre-operative
Causes
 ↑ Age
 Drugs: opioids, epidural/spinal, anti-AChM
 Comorbidities: e.g. DM
 Pain: sympathetic activation → sphincter contraction  Pre-existing infection: e.g. appendix perforation
 Psychogenic: hospital environment  Pt. colonisation: e.g. nasal MRSA
 Operative
Risk Factors  Op classification and wound infection risk
 Male  Duration
 ↑ age  Technical: pre-op Abx, asepsis
 Neuropathy: e.g. DM, EtOH  Post-operative
 BPH  Contamination of wound from staff
 Surgery type: hernia and anorectal
Mx
Mx  Regular wound dressing
 Conservative  Abx
 Privacy  Abscess drainage
 Ambulation
 Void to running taps or in hot bath
 Analgesia
 Catheterise ± gent 2.5mg/kg IV stat Wound Dehiscence
 TWOC = Trial w/o Catheter
 If failed, may be sent home c̄ silicone catheter Presentation
and urology outpt. f/up.  Occurs ~10d post-op
 Preceded by serosanguinous discharge from wound
Pulmonary Atelectasis Risk Factors

 Occurs after every nearly every GA  Pre-Operative Factors
 ↑ age
 Mucus plugging + absorption of distal air → collapse
 Smoking
 Obesity, malnutrition, cachexia
Causes
 Comorbs: e.g. BM, uraemia, chronic cough, Ca
 Pre-op smoking
 Drugs: steroids, chemo, radio
 Anaesthetics ↑ mucus production ↓ mucociliary
 Operative Factors
clearance
 Length and orientation of incision
 Pain inhibits respiratory excursion and cough
 Closure technique: follow Jenkin’s Rule
 Suture material
Presentation
 Post-operative Factors
 w/i first 48hrs
 ↑ IAP: e.g. prolonged ileus → distension
 Mild pyrexia  Infection
 Dyspnoea  Haematoma / seroma formation
 Dull bases c̄ ↓AE
Mx
Mx  Replace abdo contents and cover c̄ sterile soaked gauze
 Good analgesia to aid coughing  IV Abx: cef+met
 Chest physiotherapy  Opioid analgesia
 Call senior and arrange theatre
 Repair in theatre
 Wash bowel
 Debride wound edges
 Close c̄ deep non-absorbable sutures (e.g. nylon)
 May require VAC dressing or grafting

Post-op Complications: Specific
General Surgery Vascular
Cholecystectomy Arterial Surgery

 Conversion to open: 5%  Thrombosis and embolization
 CBD injury: 0.3%  Anastomotic leak
 Bile leak  Graft infection
 Retained stones (needing ERCP)
 Fat intolerance / loose stools Aortic Surgery
 Gut ischaemia
Inguinal Hernia Repair  Renal failure
 Early  Aorto-enteric fistula
 Haematoma / seroma formation: 10%  Anterior spinal syndrome (paraplegia)
 Intra-abdominal injury (lap)  Emboli → distal ischaemia (trash foot)
 Infection: 1%
 Urinary retention Breast
 Late  Arm lymphoedema
 Recurrence (<2%)  Skin necrosis
 Ischaemic orchitis: 0l5%  Seroma
 Chronic groin pain / paraesthesia: 5%
Urological
Appendicectomy  Sepsis (instrumentation c̄ infected urine)
 Abscess formation  Uroma: extravasation of urine
 Fallopian tube trauma
 Right hemicolectomy (e.g. for carcinoid, caecal Prostatectomy
necrosis)  Urinary incontinence
 Erectile dysfunction
Colonic Surgery  Retrograde ejaculation
 Early  Prostatitis
 Ileus
 AAC
 Anastomotic leak ENT
 Enterocutaneous fistulae
 Abdominal or pelvic abscess Thyroidectomy
 Late  Wound haematoma → tracheal obstruction
 Adhesions → obstruction  Recurrent laryngeal N. trauma → hoarse voice
 Incisional hernia  Transient in 1.5%
 Permanent in 0.5%
Post-op Ileus  R commonest (more medial)
 Causes  Hypoparathyroidism → hypocalcaemia
 Bowel handling  Thyroid storm
 Anaesthesia  Hypothyroidism
 Electrolyte imbalance
 Presentation Tracheostomy
 Distension  Stenosis
 Constipation ± vomiting  Mediastinitis
 Absent bowel sounds  Surgical emphysema
 Rx
 IV fluids + NGT Orthopaedic Surgery
 TPN if prolonged
Fracture Repair
Anorectal Surgery  Mal-/non-union
 Anal incontinence  Osteomyelitis
 Stenosis  AVN
 Anal fissure  Compartment syndrome
Small Bowel Surgery Hip Replacement

 Short gut syndrome (≤250cm)  Deep infection
 VTE
Splenectomy  Dislocation
O
 Gastric dilatation (2 gastric ileus)  Nerve injury: sciatic, SGN
 Prevent c̄ NGT  Leg length discrepancy
 Thrombocytosis → VTE
 Infection: encapsulated organisms Cardiothoracic Surgery
 Pneumo-/haemo-thorax
 Infection: mediastinitis, empyema
Post-op Pyrexia
Causes Pneumonia
Early: 0-5d post-op Cause

 Blood transfusion  Anaesthesia → atelectasis
 Physiological: SIRS from trauma: 0-1d  Pain → ↓ cough
 Pulmonary atelectasis:24-48hr  Surgery → immunosuppression
 Infection: UTI, superficial thrombophlebitis, cellulitis
 Drug reaction Rx
 Chest physio: encouraging coughing
Delayed: >5d post-op  Good analgesia
 Pneumonia  Abx
 VTE: 5-10d
 Wound infection: 5-7d
 Anastomotic leak: 7d Collection
 Collection: 5-20d
Presentation
 Malaise
 Swinging fever, rigors
Examination of Post-Op Febrile Pt.
 Localised peritonitis
 Observation chart, notes and drug chart
 Shoulder tip pain (if subphrenic)
 Wound
 Abdo + DRE Locations
 Legs  Pelvic: present @ 4-10d post-op
 Chest  Subphrenic: present @ 7-21d post-op
 Lines  Paracolic gutters
 Urine  Lesser sac
 Stool  Hepatorenal recess (Morrison’s space)
 Small bowel (interloop spaces)
Ix Ix
 Urine: dip + MCS  FBC, CRP, cultures
 Blood: FBC, CRP, cultures ± LFTs  US, CT
 Cultures: wound swabs, CVP tip for culture  Diagnostic lap
 CXR
Rx
 Abx
 Drainage / washout
Cellulitis
 Acute infection of the subcutaneous connective tissue
Cause: β-haemolytic Streps + staph. aureus
Presentation
 Pain, swelling, erythema and warmth
 Systemic upset
 ± lymphadenopathy
Rx
 Benpen IV
 Pen V and fluclox PO

DVT
Epidemiology Preventing DVT
 DVTs occur in 25-50% of surgical patients
Pre-Op
Risk Factors: Virchow’s Triad  Pre-op VTE risk assessment
 Blood Contents  TED stockings
 Surgery → ↑ plats and ↑ fibrinogen  Aggressive optimisation: esp. hydration
 Dehydration  Stop OCP 4wks pre-op
 Malignancy
 Age: ↑ Intra-Op
 Blood Flow  Minimise length of surgery
 Surgery  Use minimal access surgery where possible
 Immobility  Intermittent pneumatic compression boots
 Obesity
 Vessel Wall Post-Op
 Damage to veins: esp. pelvic veins  LMWH
 Previous VTE  Early mobilisation
 Good analgesia
Signs  Physio
 Peak incidence @ 5-10d post-op  Adequate hydration
 65% of below knee DVTs are asymptomatic
 Calf warmth, tenderness, erythema, swelling
 Mild pyrexia
 Pitting oedema
Differential
 Cellulitis
 Ruptured Baker’s cyst
Ix
 D-Dimers: sensitive but not specific
 Compression US (clot will be incompressible)
 Thrombophilia screen if:
 No precipitating factors
 Recurrent DVT
 Family Hx
Dx
1. Assess probability using Wells’ Score
2. Low-probability → perform D-dimers
 Negative → excludes DVT
 Positive → Compression US
3. Med / High probability → Compression US
Rx
Anticoagulate
 Therapeutic LMWH: enoxaparin 1.5mg/kg/24h SC
 Start warfarin using Tait model: 5mg OD for first 4d
 Stop LMWH when INR 2.5
 Duration
 Below knee: 6-12wks
 Above knee: 3-6mo
 On-going cause: indefinite
Graduated Compression Stockings

 Consider for prevention of post-phlebitic syndrome

Other Common Post-Operative Presentations
Dyspnoea / Hypoxia Hypotension
Causes Immediate Mx
 Previous lung disease  Tilt bed head down, give O2
 Atelectasis, aspiration, pneumonia  Assess fluid status
 LVF
 PE Causes: CHOD
 Pneumothorax (e.g. due to CVP line insertion)  Cardiogenic
 Pain → hypoventilation  MI
 Fluid overload
Ix  Hypovolaemia
 FBC, ABG  Inadequate replacement of fluid losses
 CXR  Haemorrhage
 ECG  Obstructive
 PE
Rx  Distributive
 Sit up, give O2, monitor SpO2  Sepsis
 Rx cause  Neurogenic shock
Mx
 Hypovolaemia → fluid challenge
Reduced Urine Output  250-500ml colloid over 15-30min
 Haemorrhage → return to theatre
Causes  Sepsis → fluid challenge, start Abx
 Post-renal  Overload → frusemide
 Commonest cause  Neurogenic → NA infusion
 Blocked / malsited catheter
 Acute urinary retention
 Pre-renal: hypovolaemia
Hypertension
 Renal: NSAIDs, gentamicin
 Continue anti-hypertensives during peri-operative period
 Anuria usually = blocked or malsited catheter
 Oliguria usually = inadequate fluid replacement Causes
 Pain
Mx
 Urinary retention
 Information
 Previous HTN
 Op Hx
 Obs chart: UO
Rx
 Drug chart: nephrotoxins
 Rx cause
 Examination
 May use labetalol 50mg IV every 5min (200mg max)
 Assess fluid status
 Examine for palpable bladder
 Inspect drips, drains, stomas, CVP
 Action Acute Confusional State
 Flush c̄ 50ml NS and aspirate back  Agitation, disorientation, attempts to leave hospital
 Fluid challenge
Common Causes: DELIRIUM
 Drugs: opiates, sedatives, L-DOPA
Nausea and Vomiting  Eyes, ears and other sensory deficits
 Causes  Low O2 states: MI, stroke, PE
 Obstruction  Infection
 Ileus  Retention: stool or urine
 Emetic drugs: e.g. opioids  Ictal
 Consider NGT, AXR and ondansetron 4mg IV TDS  Under- hydration / -nutrition
 Metabolic: Na, AKI, glucose, EtOH withdrawal
Mx
↓ Na  May need sedation: midazolam / haldol
 What was pre-op level?
 Nurse in well-lit environment
 Common Causes:
 Rx cause
 S(I)ADH: pain, nausea, opioids, stress
 Over administration of IV fluids
 Correct slowly
 Acute: 1mM/h
 Chronic:15mM/d

Fluids and Nutrition
Contents
Fluid Homeostasis ....................................................................................................................................................................... 12
Crystalloid .................................................................................................................................................................................... 13
Colloid .......................................................................................................................................................................................... 13
Fluid Problems............................................................................................................................................................................. 14
Nutrition ....................................................................................................................................................................................... 15
Refeeding Syndrome ................................................................................................................................................................... 16

Fluid Homeostasis
Body Composition Fluid Balance
 Total water: 60% of 70kg = 42L
 2/3 intracellular = 28L Input Output
 1/3 extracellular = 14L Water 1500 Urine 1500
 Plasma = 3L (21% of ECF) Food 1000 Stool 300
 Interstitial = 10L Metabolism 300 Insensible 1000
 Transcellular = 1L - lungs
- sweating
Total 2800ml Total 2800ml
Starling’s Forces = 40ml/kg/d = 40ml/kg/d
Other Values
Osmotic Pressure
 Minimum UO = 0.5ml/kg/h = ~30ml/h
 Pressure which needs to be applied to prevent the inflow
 Na requirement = 1.5-2mmol/kg/d = 100mmol/d
of water across a semipermeable membrane.
 K requirement = 1mmol/kg/d = 60mM/d
 i.e. the ability of a solute to attract water.
 Oncotic pressure: form of osmotic pressure exerted by
proteins. Fluid Regimens
Hydrostatic Pressure Daily Requirements

 Pressure exerted by a fluid at equilibrium due to the force  3L dex-saline c̄ 20mM K+ in each bag
of gravity.  1L NS + 2L dex c̄ 20mM K+ in each bag
 Each bag over 8h = 125ml/h
Replace other losses

Distribution  Vomiting and Diarrhoea
 Distribution between the ECF and ICF is driven by
 NGT
differences in osmotic pressure only.
 Drains
 Distribution w/i the ECF is determined by Starling’s
 Fever (+500ml for each OC)
forces.
 Tachypnoea
 Capillary and interstitial oncotic pressure.
 Capillary and interstitial hydrostatic pressure.  High-output stomas
 Filtration coefficient (capillary permeability)
CVP Monitoring
rd  Indicates RV preload and depends on
3 Space Losses → ↓ ECF  Venous return
rd
 Bowel obstruction → ↓ fluid reabsorption → 3 space  Cardiac output
loss
 ↑ CVP
 Sudden diuresis on day 2-3 post op = recovery of ileus  ↑ circulating volume
 Peritonitis → ascites → 3rd space loss  ↓CO: i.e. pump failure
 ↓ CVP
 ↓ circulating volume
 Normal value: ~5-10cmH2O
 Single reading is not as useful as serial
measurements before and after fluid challenge.
 Unchanged: hypovolaemic
 ↑ that reverses after 30min: euvolaemic
 Sustained ↑ >5cmH2O: overload / failure
 Passive leg raising may be more useful than fluid
challenge in determining response to fluids.
 Sustained ↑ in CVP suggests heart failure.

Crystalloid Colloid
NS Physiology
 Contain large molecular wt. molecules
Contents  Gelatin
 0.9% NaCl = 9g/L  Dextrans
 154mM NaCl  Preserves oncotic pressure  remains intravascular
→ preferential ↑ in intravascular volume
pH: 5-6
Synthetic
Use  Gelofusin
 Normal daily fluid requirements + replace losses  Volplex
 Haemaccel
 Voluven
5% Dextrose
Natural
Contents  Albumin
 50g dextrose /L  Blood
Use Use
 Normal daily fluid requirements
 Fluid challenge: 250-500ml over 15-30min
 Hypovolaemic shock
 Mount Vernon Formula
Dextrose-Saline  (wt. x %burn)/2 = ml colloid per unit time
Contents Problems
 4% dextrose = 40g/L  Anaphylaxis
 0.18% NaCl = 31mM NaCl  Volume overload
 Can interfere c̄ cross-matching therefore take blood
Use
for x-match before using.
 Normal daily fluid requirements
Hartmann’s / Ringer’s Lactate

Contents
 Na: 131mM
 Cl: 111mM
 K: 5mM
 Ca: 2.2mM
 Lactate / HCO3: 29mM
Use
 Resuscitation in trauma pts.
 Parkland’s formula: 4 x wt x %burn = mL in 1st 24hrs
pH
 pH = 6.5 but Hartmann’s is an alkalinising solution
 Lactate is not an acid in itself: it’s a conjugate base
 Given exogenously as sodium lactate
 Lactate metabolised in liver → HCO3 production
 The Cori Cycle
Daily Requirements
 3L dex-saline c̄ 20mM K+ in each bag
 1L NS + 2L dex c̄ 20mM K+ in each bag
 Each bag over 8h = 125ml/h
Problems
 Give 1L NS → ~210ml remaining IV
 Give 1L D5W → ~70ml remaining IV
 Acidosis or electrolyte disturbances
 Fluid overload

Fluid Problems
Assessing Fluid Status Ileostomy
 Hx: balance chart, surgery, other losses, thirsty  Ileal fluid composition
 Impression: drowsy, alert  Na: 130mM
 Inspection: drips, drains, stomas, catheters, CVP  Cl: 110mM
 K: 10mM
Examination  HCO3: 30mM
 IV volume  Normal output: 10-15mL/Kg/d = ~700ml/d
 CRT  High output = >1000ml/d
 HR  Ileum will adapt to limit fluid and electrolyte losses
 BP lying and standing  Fluids
 JVP  0.9% NS +KCl
 Tissue perfusion  Daily requirements + replaces losses, titrated to
 Skin turgor UO
 Oedema: ankle, pulmonary, ascites  Serial U+Es guide electrolyte replacement
 Mucus membranes  High Output
 End-organ  Loperamide
 UO, ↑U+Cr  Codeine
 Consciousness
 Lactate
Reduced Urine Output Post-op
Other Tests
 PCWP: indirect measure of left atrial pressure Causes
 CVP  Post-renal
 Commonest cause
Post-operative Fluids  Blocked / malsited catheter
 Acute urinary retention
Problems  Pre-renal: hypovolaemia
 ↑ADH, ↑aldosterone, ↑cortisol → Na +H2O conservation  Renal: NSAIDs, gentamicin
 ↑ K+: tissue damage, transfusion, stress hormones  Anuria usually = blocked or malsited catheter
 Oliguria usually = inadequate fluid replacement
Solutions
 Use UO (aim>30ml/h) to guide fluid replacement but may Mx
need to ↓ maintenance fluids to 2L first 24h post-op  Information
 Avoid K+ supplementation for first 24h post-op  Op Hx
 Obs chart: UO
 Drug chart: nephrotoxins
Cardiac or Renal Failure  Examination
 Assess fluid status
Problem  Examine for palpable bladder
 RAS activation → Na and H2O retention  Inspect drips, drains, stomas, CVP
 Action
Solution  Flush c̄ 50ml NS and aspirate back
 Avoid fluids c̄ Na → give 5% dextrose  Fluid challenge
Suspect Catheter Problem

 Flush c̄ 50ml NS and aspirate back
Bowel Obstruction
 Pts. have significant third space losses c̄ loss of both water Suspect Pre-renal Problem
and electrolytes.  Fluid challenge
 Likely to need significantly more than standard daily  250-500ml colloid bolus over 15-30min
requirements.  Look for CVP or UO response w/i minutes
 Regimen
 0.9% NS c̄ 20-40mm KCl added to each bag
 Titrate rate of fluid therapy to clinical findings on
serial examination.
 Serial U+Es guide electrolyte replacement
Pancreatitis
 Inflammation → significant fluid shift into the abdomen.
 Pts require aggressive fluid resuscitation and maintenance
 Insert urinary catheter and consider CVP monitoring
 0.9% NS c̄ 20-40mm KCl added to each bag
 Keep UO >30ml/h
 Serial U+Es guide electrolyte replacement
Nutrition
Assessment Parenteral Nutrition
 May be “Total” or used to supplement enteral feeding
Clinical  Combined c̄ H2O to deliver total daily requirements
 Hx
 Wt. loss
 Diet Indications
 Examination  Prolonged obstruction or ileus (>7d)
 Skin fat  High output fistula
 Dry hair  Short bowel syndrome
 Pressure sores  Severe Crohn’s
 Cheilitis  Severe malnutrition
2
 Wt. and BMI (<20kg/m )
 Severe pancreatitis
 Unable to swallow: e.g. oesophageal Ca
Anthropometric
 Skin-fold thickness
 Arm circumference Delivery
 Delivered centrally as high osmolality is toxic to veins
Ix  Short-term: CV catheter
 Albumin  Long-term: Hickman or PICC line
 Transthyretin (prealbumin)  Sterility is essential: use line only for PN
 Phosphate
Monitoring
Requirements (/kg/24h)  Standard
 Calories: 20-40 Kcal  Wt., fluid balance and urine glucose daily
 Carb: 2g  Zn, Mg weekly
 Fat: 3g  Initially
 Protein: 0.5-1  Blood glucose, FBC, U+E + PO4 3x /wk
 Nitrogen:0.2-0.4g  LFTs 3x /wk
 Once stable
Enteral Nutrition  Blood glucose, FBC, U+E + PO4 daily
 LFTs weekly
Delivery
 PO is best
 Consider semi-solid diet if risk of aspiration Contents
 Fine bore NGT (9 Fr)  2000Kcal: 50% fat, 50% carb
 Percutaneous Endoscopic Gastrostomy  10-14g nitrogen
 Jejunostomy  Vitamins, minerals and trace elements
 Build up feeds gradually to prevent diarrhoea
Feeds Complications
 Oral supplements  Line-related
 Polymeric: e.g. osmolite, jevity  Pneumothorax / haemothorax
 Intact proteins, starches and long-chain FAs  Cardiac arrhythmia
 Disease Specific  Line sepsis
 e.g. ↓ branched chain AAs in hepatic  Central venous thrombosis → PE or SVCO
encephalopathy  Feed-related
 Elemental  Villous atrophy of GIT
 Simple AAs and oligo/monosaccharides  Electrolyte disturbances
 Require minimal digestion and used if abnormal  Refeeding syndrome
GIT: e.g. in Crohn’s  Hypercapnoea from excessive CO2
production
Indications  Hyperglycaemia and reactive hypoglycaemia
 Catabolic: sepsis, burns, major surgery  Line sepsis: ↑ risk c̄ TPN
 Coma/ITU  Vitamin and mineral deficiencies
 Malnutrition
 Dysphagia: stricture, stroke
Complications
 NGT
 Nasal trauma
 Malposition or tube blockage
 Feeding
 Feed intolerance → diarrhoea
 Electrolyte imbalance
 Aspiration
 Refeeding
© Alasdair Scott, 2012 syndrome 15
Refeeding Syndrome
Definition
 Life-threatening metabolic complication of refeeding via
any route after a prolonged period of starvation.
Pathophysiology
 ↓ carbs → catabolic state c̄ ↓insulin, fat and protein
catabolism and depletion of intracellular PO4
 Refeeding → ↑ insulin in response to carbs and ↑
cellular PO4 uptake.
 → hypophosphataemia
 Rhabdomyolysis
 Respiratory insufficiency
 Arrhythmias
 Shock
 Seizures
Chemistry
 ↓K, ↓Mg, ↓PO4
At-Risk Patients
 Malignancy
 Anorexia nervosa
 Alcoholism
 GI surgery
 Starvation
Prevention
 Identify and monitor at-risk patients
 Liaise c̄ dietician
Rx
 Identify at-risk pts in advance and liaise c̄ dietician
 Parenteral and oral PO4 supplementation
 Rx complications

Trauma
Contents
Primary Survey ............................................................................................................................................................................ 18
Secondary Survey ....................................................................................................................................................................... 19
Shock ........................................................................................................................................................................................... 19
Life-Threatening Chest Injuries ................................................................................................................................................... 20
2O Survey Chest Injuries ............................................................................................................................................................. 20
Abdominal Trauma ...................................................................................................................................................................... 21
Head Injury .................................................................................................................................................................................. 22
Burns ........................................................................................................................................................................................... 23
Hypothermia ................................................................................................................................................................................ 24

Primary Survey
ADDRESS PROBLEMS IN 1O SURVEY IN THE Circulation
ABCDE ORDER.  Two-large bore cannulae (14/16G) in each ACF
 FBC, U+E, x-match (6U), clotting, VBG
Airway and C-Spine
Assessment
Airway  Inspection: pale, sweaty, active bleeding
 Check for airway compromise  Vascular status: BP, HR, JVP, heart sounds, cardiac
 Ask pt. a question mon
 Stridor  End-organ: consciousness, UO
 Orofacial injury or burns
 Visualise airway and use suction if necessary Sites of Haemorrhage
 Manoeuvres to open airway  Chest
 Jaw thrust  Abdomen
 Adjuncts if compromise / potential compromised  Pelvis: use pelvic binder
 NPA: gag reflex present  Floor
 OPA: no gag reflex (stop tongue swallowing)
 Emergency Airways Mx
 Needle cricothyroidotomy or surgical cric  If haemodynamic compromise give 2L warmed
 Definitive Airways (no risk of aspiration) Hartmann’s stat.
 Endotracheal tube  Consider further colloid / blood
 Tracheostomy  Insert CVP and catheter (after PR) to guide resus
C-Spine Response
 Maintain in-line cervical support to keep neck stable  Assess response to fluids using UO, lactate, BP
 Place pt. in hard-collar and sandbags c̄ tape
Rapid
 Usually <20% loss
Breathing  Slow fluid to maintenance if haemodynamically
stable
 Start 15L O2 via non-rebreathe mask (Hudson)
Transient
Assessment
 20-40% loss
 SpO2
 On-going losses or inadequate resuscitation
 Inspection of chest
 Position of trachea
None
 RR and chest expansion
 Exsanguinating haemorrhage → theatre
 Breath sounds, vocal resonance
 Consider non-haemorrhagic shock
 Percussion  Tamponade
 ABG  Pneumothorax
Tension Pneumothorax
 Signs
Disability
 Respiratory distress
 ↑JVP and ↓BP
Assessment
 Tracheal deviation + displaced apex
 Assess consciousness using AVPU or GCS
 ↓ air entry and ↓ VR
 Hyperresonant percussion  Pupil responses
 Rx: immediate decompression
nd
 Insert large-bore venflon into 2 ICS, mid-
clavicular line. Exposure
 Insert ICD later
Assessment
Open Sucking Chest Wounds  Completely undress pt.
 Convert to closed wounds by covering with damp  Perform log-role and PR
occlusive dressing stuck down on 3 sides.  Feel for high riding prostate (urethral rupture)
 Look for bleeding
 Prevent hypothermia
REPEAT 1O SURVEY AGAIN!

Secondary Survey Shock
History Haemorrhagic Shock
 Allergies
 Circulating blood volume = 7% body mass
 Medication
 PMH
 Last ate / drunk % ml RR HR BP UO Mental
1 0-15 750 ↔ ↔ ↔ ↔ Normal
 Events 2 15-30 750-1500 >20 >100 ↔ <30 Anxious++
3 30-40 1500-2000 >30 >120 ↓ 5-20 Confused
Examination 4 >40 >2000 >35 >140 ↓↓ <5 Lethargic
 Head-to-toe examination
 Examine every system
Neurogenic Shock
Ix  Disruption of sympathetic nervous system
 Trauma series
 C-spine: lat + peg Causes
 CXR
 Spinal anaesthesia
 Pelvis
 Hypoglycaemia
 FAST scan (Focussed Assessment c̄ Sonography in
 Cord injury above T5
Trauma)
 Closed head injuries
 CT: when pt. is stable.
Presentation
 Hypotension
Assessing C-spine Radiographs
 Bradycardia
 Views
 Warm extremities
 Lateral
 AP
Mx
 Open-mouth Peg view
 Vasopressors: vasopressin and norad
 Adequacy
 Must see C7-T1 junction  Atropine: reverse the bradycardia
 May need swimmer’s view c̄ abducted arm
 Alignment: 4 lines
 Ant. vertebral bodies Spinal Shock
 Ant. vertebral canal  Acute spinal cord transection
 Post. vertebral canal  Loss of all voluntary and reflex activity below the level
 Tips of spinous processes of injury
 Bones: shapes of bodies, laminae, processes
 Cartilage: IV discs should be equal height Presentation
 Soft tissue  Hypotonic paralysis
 Width of soft tissue shadow anterior to upper  Areflexia
vertebrae should be 50% of vertebral width.  Loss of sensation
 Bladder retention
Clearing the C-Spine
Clinical Clearance
 Indication: NEXUS Criteria
 Fully alert and orientated
 No head injury
 No drugs or alcohol
 No neck pain
 No abnormal neurology
 No distracting injury
 Method
 Examine for bruising or deformity
 Palpate for deformity and tenderness
 Ensure pain-free active movement
Radiological Clearance
 Indications
 Pt. doesn’t meet criteria for clinical clearance
 Modalities
 Radiograph initially
 Clear if normal radiograph and clinical exam
 CT C-spine if abnormal radiograph or clinical exam

Life-Threatening Chest Injuries 2O Survey Chest Injuries
Differential: ATOMIC Rib #
 Airway obstruction  Usually 5th-9th ribs
 Tension Pneumothorax  # of upper 4 ribs = high energy trauma
 Open pneumothorax (sucking)  Complications
 Massive haemothorax  Pneumothorax
 Intercostal disruption and pulmonary contusion  Lacerate thoracic or abdominal viscera
 Cardiac Tamponade  Rx: good analgesia
 NSAIDs + opioids
 Intrapleural analgesia
Massive Haemothorax  Intercostal block
 Accumulation of >1.5L of blood in chest cavity
 Usually caused by disruption of hilar vessels
Sternal #
Presentation  Usually MVA driver vs. steering wheel
 Signs of chest wall trauma  Risk of mediastinal injury
 ↓BP  Rx
 ↓ expansion  Analgesia, admit, observe
 Cardiac monitor
 ↓ breath sounds and ↓VR
 Troponin: rule out myocardial contusion
 Stony dull percussion
Mx Pulmonary Contusion
 X-match 6u  Usually due to rapid deceleration injury or shock waves
 Large-bore chest drain c̄ hep saline for autotransfusion  May → ARDS
 Pres: dyspnoea, haemoptysis, respiratory failure
 Thoracotomy if >1.5L or >200ml/h
 Ix
 CXR: opacification
Flail Chest  Serial ABGs: ↓ PaO2:FiO2 ratio
 Ant. or lat. # of ≥2 adjacent ribs in ≥2 places  Rx: O2, ventilate if necessary
 Flail segment moves paradoxically c̄ respiration
 ↓ Oxygenation Myocardial Contusion
 Underlying pulmonary contusion  Direct blunt trauma over precordium
 ↓ Ventilation of affected segment  Ix
 ECG: abnormal, arrhythmias
Ix  ↑ troponin
 CXR / CT chest: pulmonary contusion (white)  Rx: bed rest, cardiac monitoring, Rx arrhythmias
 Serial ABGs: ↓PaO2:FiO2 ratio
Contained Aortic Disruption
Rx
 Rapid deceleration injury (80% immediately fatal)
 O2
 Pres: initially stable but → hypotensive
 Good analgesia: PCA, epidural
 Ix
 Persistent respiratory failure: PPV
 CXR: wide mediastinum, deviation of NGT
 CT
Cardiac Tamponade  Rx: cardiothoracic consult
 Disruption of myocardium or great vessels → blood in the
pericardium → ↓ filling and contraction → shock
Diaphragmatic Injury
 Usually results from penetrating trauma
 Consider in penetrating injuries below 5th rib or high
energy compression.
Presentation
 Ix: CXR (visceral herniation), CT
 Beck’s Triad
 ↑ JVP / distended neck veins
 ↓ BP Oesophageal Disruption
 Muffled heart sounds  Usually penetrating trauma
 Pulsus paradoxus: SBP fall of >10mmHg on inspiration  → mediastinitis
 Kussmaul’s sign: ↑ JVP on inspiration  Ix
 Intensely restless pt.  CXR: pneumomediastinum, surgical emphysema
 CT
Ix
 US: FAST or transthoracic echo Tracheobronchial Disruption
 CXR: enlarged pericardium  Presentation
 ↑CVP >12mmHg  Persistent pneumothorax
 ECG: low voltage QRS ± electrical alternans  Pneumomediastinum
 Rx: thoracotomy
Mx
 Pericardiocentesis: spinal needle in R subxiphoid space
O
aiming at 45 towards the R tip of left scapula
 Thoracotomy may be needed
Abdominal Trauma
Mechanisms Damage Control Surgery
 Penetrating
 All require exploration as tract may be deeper Aim
than it appears.  Early Mx of abdominal trauma should focus on “damage
 Blunt control” to limit physiological stress.
 Have a high index of suspicion for taking to  Control haemorrhage: ligation and packing
theatre.  Control contamination
 Stabilise in ITU
Specific Ix
Spleen
Urine Dip  Kehr’s Sign
O
 Shoulder tip pain 2 to blood in the peritoneal
 Haematuria suggests injury to renal tract
cavity.
 Left Kehr sign is classic symptom of ruptured
FAST Scan
spleen
 Replacing DPL in most centres
 Classification
 Check for fluid in the abdomen, pelvis and pericardium.
 1: capsular tear
 90% sensitive for free fluid
 2: Tear + parenchymal injury
 Can be extended to look for pneumothoraces  3: Tear up to the hilum
 4: Complete fracture
Diagnostic Peritoneal Lavage
 Mx
 Advantages and Disadvantages  Haemodynamically unstable: laparotomy
 98% sensitive for intra-abdominal haemorrhage  Stable 1-3: observation in HDU
 Useful if FAST unavailable  Stable 4: consider laparotomy
 May be better for identifying injury to hollow viscus
 Suture lac or partial / complete splenectomy
 Unable to identify retroperitoneal injury
 Insert urinary catheter and NGT Liver
 Decompression to minimise risk of injury
 Conservative if capsule is intact
 Midline incision through skin and fascia @ 1/3 distance
 Suture laceration
form umbilicus to pubic symphysis (arcuate line).
 Partial hepatectomy
 Carefully dissect to the peritoneum and insert a urinary
 Packing
catheter.
 Instil 10ml/kg warmed Hartmann’s
Bowel
 Drain fluid back into bag and send sample to lab.
3  Resection may be required
 +ve = >100,000 RBCs/mm , bile/intestinal contents
Bladder (often assoc. c̄ pelvic injury)
Indications for Laparatomy  Intraperitoneal rupture requires laparoscopic repair c̄
 Unexplained shock urethral and suprapubic drainage
 Peritonism: rigid silent abdomen  Extraperitoneal rupture can be treated conservatively c̄
 Evisceration: bowel or omentum urethral drainage.
 Radiological evidence of intraperitoneal gas  Give prophylactic Abx
 Radiological evidence of ruptured diaphragm
 Gunshot wounds Urethra
 +ve DPL or CT  Classification
 Anterior
 Spongy urethra (penile + bulbar)
 Occur following straddling injuries or
instrumentation
 Posterior
 Membranous urethra
 Occur following pelvic #s
 Presentation
 Often assoc. c̄ pelvic fracture
 Blood in the urethral meatus or scrotum
 Perineal bruising
 High-riding prostate
 Inability to micturate + palpable bladder
 Ix
 Retrograde urethrogram
 Mx
 Suprapubic catheter
 Surgical repair

Head Injury
Epidemiology History
 Head injury, alone or in combination c̄ other injuries, is  LOC
the commonest cause of trauma death (50%)  Amnesia: anterograde worse
 Nausea / vomiting
Primary Brain Injury  Fits
 Occurs @ time of injury and is a result of direct or  Focal neurology
indirect injury to brain tissue.  Mechanism
 Drugs: e.g. antiplats, warfarin
Diffuse
 Concussion / Mild Traumatic Brain Injury Examination
 Temporary ↓ in brain function  GCS: E4, V5, M6
 Headache, confusion, visual symptoms, amnesia,  3-8 = coma
nausea  9-12 = moderate head injury
 Diffuse Axonal Injury  13-15 = mild head injury
 Shearing forces disrupt axons  Scalp lacerations
 May → coma and persistent vegetative state
 Autonomic dysfunction → fever, HTN, sweating Basal Skull #
 CSF rhinorrhoea or otorrhoea (Test: halo sign)
Focal  Battle sign: bruised mastoid
 Contusion  Pando sign: bilateral orbital bruising
 E.g. coup and contra-coup  Haemotypmanum
 May have focal neurological deficit
Ix
 Intracranial Haemorrhage  C-spine
 Extradural
 CT Head
 Subdural  Basal or other skull #
 Subarachnoid  Amnesia: > 30min retrograde (before event)
 Parenchymal haemorrhage and laceration
 Neurological deficit: e.g. seizures
 GCS: <13 @ scene, <15 2h later
Secondary Brain Injury  Sick: vomiting > 1
 Occurs after primary injury.  Bloods: FBC, U+E, glucose, clotting, EtOH level, ABG
Causes Mx
 Hypoxia
 Neurosurgical consult if +ve CT
 Hypercapnoea
 Admit if
 Hypotension  LOC >5min
 ↑ ICP  Abnormalities on imaging
 Infection  Difficult to assess: EtOH, post-ictal
 Not returned to GCS 15 after imaging
Monroe-Kelly Doctrine  CNS signs: persistent vomiting, severe headache
 Cranium is rigid box  total volume of intracranial  Neuro obs: half hrly until GCS 15/15
contents must remain constant if ICP is not to change.  GCS, pupils, TPR, BP
 ↑ in volume of one constituent → compensatory ↓ in  Analgesia: codeine phosphate 30-60mg PO/IM QDS
another:  Suture scalp lacs
 CSF  Abx: if open / base of skull #
 Blood (esp. venous)
 These mechanisms can compensate for a volume Intubate if
change of ~100ml before ICP ↑.  GCS ≤ 8
 As autoregulation fails, ICP ↑ rapidly → herniation.  PaO2 <9KPa on air / <13KPa on O2 or PCO2 >6KPa
 Spontaneous hyperventilation: PCO2 <4KPa
Cerebral Blood Flow  Respiratory irregularity
 CBF  CPP x radius of vessels
 CPP = MABP – ICP Rx ↑ ICP
 ↑ ICP → ↓CPP → ↓CBF  Elevate bed
 Autoreg → vasodilatation → ↑ volume → ↑ICP…  Good sedation, analgesia ± NM block
 Prevent or attenuate this vicious circle by  Neuroprotective ventilation
 Ventilate to normocapnoea: 4.5KPa  Mannitol or hypertonic saline
 IV fluid to normovolaemia
 Mannitol bolus acutely
Discharge Advice
Cushing Reflex: imminent herniation  Stay with someone for first 48hrs
 Hypertension  Give advice card advising return on:
 Confusion, drowsiness, unconsciousness, fits
 Bradycardia
 Visual problems
 Irregular breathing
 V. painful headache that won’t go away
© Alasdair Scott, 2012  Vomiting 22
Burns
Risk Factors Mx
 Age: children and elderly  Based on ATLS principals
 Co-morbidities: epilepsy, CVA, dementia, mental illness  Specific concerns c̄ burns
 Occupation  Secure airway
 Manage fluid loss
Classification  Prevent infection
Superficial Airway
 Erythema  Examine for respiratory burns
 Painful  Soot in oral or nasal cavity
 E.g. sunburn  Burnt nasal hairs
 Hoarse voice, stridor
Partial Thickness  Flexible laryngoscopy can be helpful
 Heal w/i 2-3wks if not complicated  Consider early intubation + dexamethasone (↓ inflam)
 Superficial
 No loss of dermis Breathing
 Painful  100% O2
 Blisters  Exclude constricting burns
 Deep  Signs of CO poisoning
 Loss of dermis but adnexae remain  Headache
 Healing from adnexae: e.g. follicles  n/v
 V. painful  Confusion
 Cherry red appearance
Full Thickness  ABG
 Complete loss of dermis  COHb level
 Charred, waxy, white, skin  SpO2 unreliable if CO poisoning
 Anaesthetic
 Heal from the edges → scar Circulation
 Fluid losses may be huge
 2x large-bore cannulae in each ACF
 Bloods: FBC, U+E, G+S/XM
Complications
 Start 2L warmed Hartmann’s immediately
 Formula guide additional fluid requirements in burns pts.
Early
 Infection: loss of barrier function, necrotic tissue, SIRS st
Parkland Formula to guide replacement in 1 24hrs
 Hypovolaemia: loss of fluid in skin + ↑ cap permeability
 4 x wt. (kg) x % burn = mL of Hartmann’s in 24h
 Metabolic disturbance: ↑↑K, ↑↑myoglobin, ↑Hb → AKI
 Replace fluid from time of burn
 Compartment syndrome: circumferential burns
 Give half in 1st 8h
 Peptic ulcers: Curling’s ulcers
 Best guide is UO: 30-50mL/h
 Pulmonary: laryngeal oedema, CO poisoning, ARDS
 Renal and hepatic impairment Muir and Barclay Formula to guide fluid replacement
 (wt. x % burn)/2 = mL of Colloid per unit time
Intermediate
 Time units: 4, 4, 4, 6, 6, 12 = 36hrs total
 VTE
 May need to use blood
 Pressure sores
Burn Treatments
Late
 Analgesia: morphine
 Scarring
 Dress partial thickness burns
 Contractures  Biological: e.g. cadaveric skin
 Psychological problems  Synthetic
 Cream: e.g. Flamazine (silver sulfadiazine) +
sterile film
Assessment  Full thickness burns
 Tangential excision debridement
Wallace Rule of 9s: % BSA burnt  Split-thickness skin grafts
 Head and neck: 9%  Circumferential burns may require escharotomy to
 Arms: 9% each prevent compartment syndrome.
 Torso: 18% front and back  Anti-tetanus toxoid (0.5ml ATT)
 Legs: 18% each  Consider prophylactic Abx: esp. anti-pseudommonal
 Perineum: 1%
 (Palm: 1%)
NB. may also use Lund and Browder charts

Hypothermia
Definition Ix
 Core (rectal) temperature <35OC  Rectal / ear temperature
 FBC, U+E, glucose
 TFTs, blood gas
Pathophysiology  ECG
 Body heat is lost via 4 mechanisms  J waves: between QRS and T wave
 Arrhythmias
1. Radiation: 60%
 Infra-red emissions Mx
 Cardiac monitor
2. Conduction: 15%  Warm IVI 0.9% NS
 Direct contact  Urinary catheter
 1O means in cold water immersion  Consider Abx for prevention of pneumonia
 Routine if temp <32 and >65yrs
3. Convection: 15%
 Removes warmed air from around the body Slowly Rewarm
 ↑d in windy environments  Reheating too quickly → peripheral vasodilatation and
shock.
4. Evaporation: 10% O
 Aim for 0.5 C /hr
 Removal of warmed water  Passive external: blankets, warm drinks
 ↑ in dry, windy environments  Active external: warm water or warmed air
 Active internal: mediastinal lavage and CPB
 Severe hypothermia only
Aetiological Classification
 Primary: environmental exposure
 Secondary: change in temperature set-point Complications
 E.g.: age-related, hypothyroidism, autonomic  Arrhythmias
neuropathy  Pneumonia
 Coagulopathy
 Acute renal failure
Presentation
Mild: 32 – 35OC
 Shivering
 Tachycardia
 Vasoconstriction
 Apathy
Moderate: 28 – 32OC
 Dysrhythmia, bradycardia, hypotension
 J waves
 ↓ reflexes, dilated pupils, ↓ GCS
Severe: <28OC
 VT → VF → Cardiogenic shock
 Apnoea
 Non-reactive pupils
 Coagulopathy
 Oliguria
 Pulmonary oedema

Upper GI Surgery
Contents
Dysphagia.................................................................................................................................................................................... 26
Oesophageal Cancer .................................................................................................................................................................. 27
GORD .......................................................................................................................................................................................... 28
Hiatus Hernia ............................................................................................................................................................................... 28
Peptic Ulcer Disease ................................................................................................................................................................... 29
Upper GI Bleeding ....................................................................................................................................................................... 30
Perforated Peptic Ulcer ............................................................................................................................................................... 31
Gastric Outlet Obstruction ........................................................................................................................................................... 31
Gastric Cancer............................................................................................................................................................................. 32
Other Gastric Neoplasms ............................................................................................................................................................ 33
Zollinger-Ellison Syndrome ......................................................................................................................................................... 33
Bariatric Surgery .......................................................................................................................................................................... 34

Dysphagia
Oesophageal Anatomy Achalasia

 25cm long muscular tube (40cm from GOJ → lips)  Pathophysiology
 Starts at level of cricoid cartilage (C6)  Degeneration of myenteric plexus (Auerbach’s)
 In the neck lies in the visceral column  ↓ peristalsis
 LOS fails to relax
 Runs in posterior mediastinum and passes through right
crus of diaphragm @ T10.  Cause
 1O / idiopathic: commonest
 Continues for 2-3cm before entering the cardia
 2O: Chagas’ disease (T. cruzii)
 3 locations of narrowing
 Presentation
 Level of cricoid
 Dysphagia: liquids then solids
 Posterior to left main bronchus and aortic arch
 Regurgitation (esp. @ night)
 LOS
rds  Substernal cramps
 Divided into 3 : reflects change in musculature from
 Wt. loss
striated → mixed → smooth.
 Comps: Chronic → oesophageal SCC in 3-5%
 Lined by non-keratinising squamous epithelium.
 Ix
 Z-line: transition from squamous → gastric columnar
 Ba swallow: dilated tapering oesophagus
 Bird’s beak
 Manometry: failure of relaxation + ↓ peristalsis
Causes  CXR: widened mediastinum, double RH border
 OGD: exclude malignancy
Inflammatory  Rx:
 Tonsillitis, pharyngitis  Med: CCBs, nitrates
 Oesophagitis: GORD, candida  Int: botox injection, endoscopic balloon dilatation
 Oral candidiasis  Surg: Heller’s cardiomyotomy (open or lap)
 Aphthous ulcers
Pharyngeal Pouch: Zenker’s Diverticulum
Neurological / Motility Disorders  Outpouching between crico- and thyro-pharyngeal
 Local components of the inf. pharyngeal constrictor.
 Achalasia  Area of weakness = Killian’s dehiscence.
 Diffuse oesophageal spasm  Defect usually occurs posteriorly but swelling usually
 Nutcracker oesophagus bulges to left side of neck.
 Bulbar / pseudobulbar palsy (CVA, MND)  Food debris → pouch expansion → oesophageal
 Systemic compression → dysphagia.
 Systemic sclerosis / CREST  Pres: Regurgitation, halitosis, gurgling sounds
 MG  Rx: excision, endoscopic stapling
Mechanical Obstruction
Diffuse Oesophageal Spasm
 Luminal
 Intermittent severe chest pain ± dysphagia
 FB
 Large food bolus  Ba swallow shows corkscrew oesophagus
 Mural
 Benign stricture Nutcracker Oesophagus
 Web (e.g. Plummer-Vinson)  Intermittent dysphagia ± chest pain
 Oesophagitis  ↑ contraction pressure c̄ normal peristalsis
 Trauma (e.g. OGD)
 Malignant stricture Plummer-Vinson Syndrome
 Pharynx, oesophagus, gastric  Severe IDA → hyperkeratinisation of upper 3rd of
 Pharyngeal pouch oesophagus → web formation
 Extra-Mural  Pre-malignant: 20% risk of SCC
 Retrosternal goitre
 Rolling hiatus hernia Oesophageal Rupture
 Lung Ca  Iatrogenic (85-90%): endoscopy, biopsy, dilatation
 Mediastinal LNs (e.g. lymphoma)  Violent emesis: Boerhaave’s syndrome
 Thoracic aortic aneurysm  Carcinoma
 Caustic ingestion
 Trauma: surgical emphysema ± pneumothorax
Ix
 Upper GI endoscopy Features
 Ba swallow  Odonophagia
 Manometry  Mediastinitis: tachypnoea, dyspnoea, fever, shock
 Surgical emphysema
Mx
 Iatrogenic: PPI, NGT, Abx
 Other: resus, PPI, Abx, antifungals, debridement +
© Alasdair Scott, 2012 formation of oesophago-cutaneous fistula c̄ T-tube
26
Oesophageal Cancer
Epidemiology Staging: TNM
 Incidence: 12/100,000, increasing (↑ Barrett’s)  Tis: carcinoma in situ
 Age: 50-70 yrs  T1: submucosa
 Sex: M>F = 5:1  T2: muscularis propria (circ / long)
 Geo: ↑ Iran, Transkei, China  T3 adventicia
 T4: adjacent structures
Risk Factors  N1: regional nodes
 EtOH  M1: distant mets
 Smoking
 Achalasia Rx
 GORD → Barrett’s  Discuss in an MDT
 Plummer-Vinson  Upper GI surgeon + gastroenterologist
 Fatty diet  Radiologist
 ↓ vit A+C  Pathologist
 Nitrosamine exposure  Oncologist
 Specialist nurses
Pathophysiology  Macmillan nurses
 65% adenocarcinoma  Palliative care
 Lower 3rd
 GORD → Barrett’s → dysplasia → Ca Surgical: oesophagectomy
 35% SCC  Only 25-30% have resectable tumours
 Upper and middle 3rds  May be offered neo-adjuvant chemo before surgery to
 Assoc. c̄ EtOH and smoking downstage tumour: e.g. cisplatin + 5FU
 Commonest type worldwide  Approaches
 Ivor-Lewis (2 stage): abdominal + R thoracotomy
Presentation  McKeown (3 stage): abdominal + R thoracotomy
+ left neck incision
 Progressive dysphagia: solids → liquids (esp. bread)
 Trans-hiatal: abdominal incision
 Often alter dietary habit → soft food →
 Prognosis
exacerbation of wt. loss.
 Stage dependent
 Wt. loss
 ~15% 5ys
 Retrosternal chest pain
 Lymphadenopathy Palliative
 Upper 3rd:  Majority of pts.
 Hoarseness: recurrent laryngeal N. invasion  Laser coagulation
 Cough ± aspiration pneumonia
 Alcohol injection + ↓ Ascites (spiro)
 Stenting and Secretion reduction (e.g. hyoscine patch)
Spread  Analgesia: e.g. fentanyl patches
 Direct extension, lymphatics and blood  Radiotherapy: external or brachytherapy
 75% of pts have mets @ Dx  Referral
 Palliative care team
Ix  Macmillan nurses
 Bloods  Prognosis
 FBC: anaemia  5ys <5%
 LFTs: hepatic mets, albumin  Median: 4mo
 Diagnosis
 Upper GI endoscopy: allows biopsy
 Ba swallow: not often used, apple-core stricture
Benign Tumours
 Staging: TNM
 Leiomyoma
 CT
 EUS  Lipomas
 Laparoscopy / mediastinoscopy: mets  Haemangiomas
 Benign polyps

GORD
Pathophysiology Rx
 LOS dysfunction → reflux of gastric contents →
oesophagitis. Conservative
 Lose wt.
Risk Factors  Raise head of bed
 Hiatus hernia  Small regular meals ≥ 3h before bed
 Smoking  Stop smoking and ↓ EtOH
 EtOH  Avoid hot drinks and spicy food
 Obesity  Stop drugs: NSAIDs, anti-AChM, nitrates, CCB, TCAs
 Pregnancy
 Drugs: anti-AChM, nitrates, CCB, TCAs Medical
 Iatrogenic: Heller’s myotomy  OTC antacids: Gaviscon, Mg trisilicate
 1: Full-dose PPI for 1-2mo
Symptoms  Lansoprazole 30mg OD
 2: No response → double dose PPI BD
Oesophageal  3: No response: add an H2RA
 Retrosternal pain: heartburn  Ranitidine 300mg nocte
 Related to meals  Control: low-dose acid suppression PRN
 Worse lying down (e.g. @ night) / stooping
 Relieved by antacids Surgical: Nissen Fundoplication
 Belching  Indications: all 3 of:
 Regurgitation  Severe symptoms
 Acid brash, water brash  Refractory to medical therapy
 Confirmed reflux (pH monitoring)
 Odonophagia
Extra-oesophageal Nissen Fundoplication

 Nocturnal asthma  Aim: prevent reflux, repair diaphragm
 Chronic cough  Usually laparoscopic approach
 Laryngitis, sinusits  Mobilise gastric fundus and wrap around lower
oesophagus
Complications  Close any diaphragmatic hiatus
 Oesophagitis  Complications
 Ulceration: rarely → haematemesis, melaena, ↓Fe  Gas-bloat syn.: inability to belch / vomit
 Benign stricture: dysphagia  Dysphagia if wrap too tight
 Barrett’s oesophagus
 Intestinal metaplasia of squamous epithelium Hiatus Hernia
 Metaplasia → dysplasia → adenocarcinoma
 Oesophageal adenocarcinoma Classification
Differential Dx Sliding (80%)
 Oesophagitis  Gastro-oesophageal junction slides up into chest
 Infection: CMV, candida  Often assoc. c̄ GORD
 IBD
 Caustic substances / burns Rolling (15%)
 PUD  Gastro-oesophageal junction remains in abdomen but a
 Oesophageal Ca bulge of stomach rolls into chest alongside the
oesophagus
Ix  LOS remains intact so GORD uncommon
 Isolated symptoms don’t need Ix  Can → strangulation
 Bloods: FBC
 CXR: hiatus hernia may be seen Mixed (5%)
 OGD if:
 >55yrs Ix
 Persistent symptoms despite Rx  CXR: gas bubble and fluid level in chest
 Anaemia  Ba swallow: diagnostic
 Loss of wt.  OGD: assess for oesophagitis
 Anorexia
 24h pH + manometry: exclude dysmotility or achalasia
 Recent onset progressive symptoms
 Melaena
 Swallowing difficulty Rx
 OGD allows grading by Los Angeles  Lose wt.
Classification  Rx reflux
 Ba swallow: hiatus hernia, dysmotility  Surgery if intractable symptoms despite medical Rx.
 24h pH testing ± manometry  Should repair rolling hernia (even if asympto)
 pH <4 for >4hrs as it may strangulate.
Peptic Ulcer Disease
Presentation Surgery for PUD
 Epigastric pain
 DU Concepts
 Before meals and at night  No acid → no ulcer
 Relieved by eating  Acid secretion stimulated by gastrin (from antral G cells)
 GU and vagus N.
 Worse on eating (→ ↓ wt.)
 Relieved by anatacids Vagotomy
 Truncal
Risk Factors  ↓ acid secretion directly and via ↓ gastrin
 H. pylori  Prevents pyloric sphincter relaxation
 NSAIDs, steroids   must be combined c̄ pyloroplasty (widening of
 Smoking, EtOH pylorus) or gastroenterostomy
 Stress (GU)  Selective
 Cushing’s ulcers: head injury  Vagus nerve only denervated where it supplies
 Curling’s: ulcers: burns lower oesophagus and stomach
 Nerves of Laterjet (supply pylorus) left intact
Pathology Antrectomy c̄ Vagotomy
 Punched out ulcers
 Distal half of stomach removed.
 Usually background of chronic inflammation
 Anastomosis:
 DU
 Billroth 1: directly to duodenum
 4x commoner cf. GU
 Billroth 2 /Polya: to small bowel loop c̄ duodenal
 1st part of duodenum (cap)
stump oversewn
 GU
 Lesser curvature of gastric antrum
Subtotal Gastrectomy c̄ Roux-en-Y
 Occasionally performed for Zollinger-Ellison
Complications
 Haemorrhage
 Haematemesis or melaena Physical Complications
 Fe deficiency anaemia
 Ca: ↑ risk of gastric Ca
 Perforation: peritonitis
 Reflux or bilious vomiting (improves c̄ time)
 Gastric Outflow Obstruction
 Abdominal fullness
 Vomiting
 Colic  Stricture
 Distension  Stump leakage
 Malignancy
 ↑ risk c̄ H. pylori infection Metabolic Complications
 Actual malignant transformation probably doesn’t  Dumping syndrome
occur  Abdo distension, flushing, n/v, fainting, sweating
 Early: osmotic hypovolaemia
 Late: reactive hypoglycaemia
Ix  Blind loop syndrome → malabsorption, diarrhoea
 Bloods: FBC, urea (↑ in haemorrhage)  Overgrowth of bacteria in duodenal stump
 C13 breath test  Vitamin deficiency
 OGD (stop PPIs >2wks before)  ↓ parietal cells → B12 deficiency
 CLO / urease test for H. pylori  Bypassing proximal SB → Fe + folate deficiency
 Biopsy all ulcers to check for malignancy  Osteoporosis
 Gastrin levels if Zollinger-Ellison suspected  Wt. loss: malabsorption of ↓ calories intake
Mx
Conservative
 Lose wt.
 Stop smoking and ↓ EtOH
 Avoid hot drinks and spicy food
 Stop drugs: NSAIDs, steroids
 OTC antacids
Medical
 OTC antacids: Gaviscon, Mg trisilicate
 H. pylori eradication: PAC 500 / PMC 250
 Acid suppression
 PPIs: lansoprazole 30mg/d
 H2RAs: ranitidine 300mg nocte

Upper GI Bleeding
Hx Management
 Previous bleeds
 Dyspepsia, known ulcers Resuscitate
 Liver disease or oesophageal varices  Head-down.
 Dysphagia, wt. loss  100% O2, protect airway
 Drugs and EtOH  2 x 14G cannulae + IV crystalloid infusion up to 1L.
 Co-morbidities  Bloods: FBC, U+E (↑ urea), LFTs, clotting, x-match
6u, ABG, glucose
o/e
 Signs of CLD
 PR: melaena Blood if remains shocked
 Shock?  Group specific or O- until x-matched
 Cool, clammy, CRT>2s
 ↓BP (<100) or postural hypotension (>20 drop)
 ↓ urine output (<30ml/h)
 Tachycardia Variceal Bleed
 ↓GCS  Terlipressin IV (splanchnic vasopressor)
 Prophylactic Abx: e.g. ciprofloxacin 1g/24h
Common Causes
 PUD: 40% (DU commonly)
 Acute erosions / gastritis:20% Maintenance
 Mallory-Weiss tear: 10%  Crystalloid IVI, transfuse if necessary (keep Hb≥10)
 Varices: 5%  Catheter + consider CVP (aim for >5cm H2O)
 Oesophagitis: 5%  Correct coagulopathy: vit K, FFP, platelets
 Ca stomach / oesophagus:<3%  Thiamine if EtOH
 Notify surgeons of severe bleeds
Rockall Score: (Prof T Rockall, St. Mary’s)
 Prediction of re-bleeding and mortality
 40% of re-bleeders die
Urgent Endoscopy
 Initial score pre-endoscopy
Haemostasis of vessel or ulcer
 Age
 Adrenaline injection
 Shock: BP, pulse
 Comorbidities  Thermal / laser coagulation
 Final score post-endoscopy  Fibrin glue
 Final Dx + evidence of recent haemorrhage  Endoclips
 Active bleeding
Variceal bleeding:
 Visible vessel
 2 of: banding, sclerotherapy, adrenaline,
 Adherent clot
coagulation
 Initial score ≥3 or final >6 are indications for surgery
 Balloon tamponade c̄ Sengstaken-Blakemore tube
 Only used if exsanguinating haemorrhage or
Oesophageal Varices failure of endoscopic therapy
 Portal HTN → dilated veins @ sites of porto-systemic
 TIPSS if bleeding can’t be stopped endoscopically
anastomosis: L. gastric and inferior oesophageal veins
 30-50% c̄ portal HTN will bleed from varices
 Overall mortality 25%: ↑ c̄ severity of liver disease.
After endoscopy
Causes of portal HTN  Omeprazole IV + continuation PO (↓s re-bleeding)
 Pre-hepatic: portal vein thrombosis  Keep NBM for 24h → clear fluids → light diet @ 48h
 Hepatic: cirrhosis (80% in UK), schisto (commonest  Daily bloods: FBC, U+E, LFT, clotting
worldwide), sarcoidosis.  H. pylori testing and eradication
 Post-hepatic: Budd-Chiari, RHF, constrict pericarditis  Stop NSAIDs, steroids et.c.
Bleed Prevention
O
 1 : β-B, repeat endoscopic banding Indications for Surgery
 2O: β-B, repeat banding, TIPSS  Re-bleeding
 Bleeding despite transfusing 6u
Transjuglar Intrahepatic Porto-Systemic Shunt (TIPSS)
 Uncontrollable bleeding at endoscopy
 IR creates artificial channel between hepatic vein and
 Initial Rockall score ≥3, or final >6.
portal vein → ↓ portal pressure.
Open stomach, find bleeder and underrun vessel.
 Colapinto needle creates tract through liver
parenchyma which is expand using a balloon and
maintained by placement of a stent. NB. Avoid 0.9% NS in uncompensated liver disease (worsens
 Used prophylactically or acutely if endoscopic therapy ascites). Use blood or albumin for resus and 5% dex for
fails to control variceal bleeding. maintenance.
Perforated Peptic Ulcer Gastric Outlet Obstruction
Pathophysiology Cause
 Perforated duodenal ulcer is commonest  Late complication of PUD → fibrotic stricturing
 1st part of the duodenum: highest acid conc  Gastric Ca
 Ant. perforation → air under diaphragm
 Post. perforation can erode into GDA → bleed Presentation
 ¾ of duodenum retroperitoneal  no air under  Hx of bloating, early satiety and nausea
diaphragm if perforated.  Outlet obstruction
 Perforated GU  Copious projectile, non-bilious vomiting a few hrs
 Perforated gastric Ca after meals.
 Contains stale food.
Presentation  Epigastric distension + succussion splash
 Sudden onset severe pain, beginning in the epigastrium
and then becoming generalised. Ix
 Vomiting  ABG: Hypochloraemic hypokalaemic met alkalosis
 Peritonitis  AXR
 Dilated gastric air bubble, air fluid level
Differential  Collapsed distal bowel
 OGD
 Pancreatitis
 Contrast meal
 Acute cholecystitis
 AAA
 MI Rx
 Correct metabolic abnormality: 0.9% NS + KCl
Ix  Benign
 Endoscopic balloon dilatation
 Bloods
 Pyloroplasty or gastroenterostomy
 FBC, U+E, amylase, CRP, G+S, clotting
 Malignant
 ABG: ? mesenteric ischaemia
 Stenting
 Urine dipstick
 Resection
 Imaging
 Erect CXR
 Must be erect for ~15min first
Hypertrophic Pyloric Stenosis
 Air under the diaphragm seen in 70%
 False +ve in Chailaditi’s sign
Epidemiology
 AXR
 Sex: M>F=4:1
 Rigler’s: air on both sides of bowel wall
 Race: ↑ in Caucasians
Mx Presentation
 6-8wks
Resuscitation  Projectile vomiting minutes after feeding
 NBM  RUQ mass: olive
 Aggressive fluid resuscitation  Visible peristalsis
 Urinary Catheter ± CVP line
 Analgesia: morphine 5-10mg/2h max Dx
 ± cyclizine  Test feed: palpate mass + see peristalsis
 Abx: cef and met  Hypochloraemic hypokalaemic metabolic alkalosis
 NGT  US
Conservative Mx
 May be considered if pt. isn’t peritonitic  Resuscitate and correct metabolic abnormality
 Careful monitoring, fluids + Abx  NGT
 Omentum may seal perforation spontaneously  Ramstedt pyloromyotomy: divide muscularis propria
preventing operation in ~50%
Surgical: Laparotomy
 DU: abdominal washout + omental patch repair
 GU: excise ulcer and repair defect
 Partial / gastrectomy may rarely be required
 Send specimen for histo: exclude Ca
Test and Treat

 90% of perforated PU assoc. c̄ H. pylori

Gastric Cancer
Epidemiology Spread
 Incidence: 23/100,000  w/i stomach: linitis plastica
 Age: 50s  Direct invasion: pancreas
 Sex: M>F=2:1  Lymphatic: Virchow’s node
 Geo: ↑ in Japan, Eastern Europe, China, S. America  Blood: liver and lung
 Transcoelomic
Risk Factors  Ovaries: Krukenberg tumour (Signet ring morph)
 Atrophic gastritis (→ intestinal metaplasia)  Sister Mary Joseph nodule: umbilical mets
 Pernicious anaemia / AI gastritis
 H. pylori Ix
 Diet: ↑ nitrates – smoked, pickled, salted (↑ Japan)  Bloods
 Nitrates → carcinogenic nitrosamines in GIT  FBC: anaemia
 Smoking  LFTs and clotting
 Blood group A  Imaging
 Low SEC  CXR: mets
 Familial: E. cadherin abnormality  USS: liver mets
 Partial gastrectomy  Gastroscopy + biopsy
 Ba meal
Pathology  Staging
 Mainly adenocarcinomas  Endoluminal US
 CT/MRI
 Usually located on gastric antrum
 Diagnostic laparoscopy
 H. pylori may → MALToma
Mx
Classification
Medical Palliation
Depth of Invasion
 Analgesia: e.g. fentanyl patch
 Early gastric Ca: mucosa or submucosa
 PPI
 Late gastric Ca: muscularis propria breached
 Secretion control
 Chemo: epirubicin, 5FU, cisplatin
Microscopic Appearance
 Intestinal: bulky, glandular tumours, heaped ulceration  Palliative care team package
 Diffuse: infiltrative c̄ signet ring cell morphology
Surgical Palliation
 Pyloric stenting
Borrmann Classification
 Bypass procedures
1. Polypoid / fungating
2. Excavating
Curative Surgery
3. Ulcerating and raised
4. Linitis plastica: leather-bottle like thickening c̄ flat rugae  EGC may be resected endoscopically
 Partial or total gastrectomy c̄ roux-en-Y to prevent bile
reflux.
Symptoms  Spleen and part of pancreas may be removed
 Usually present late
 Wt. loss + anorexia
Prognosis
 Dyspepsia: epigastric or retrosternal pain/discomfort
 Overall: 5ys <10%
 Dysphagia
 Surgery: 20-50% 5ys
 n/v
Signs
 Anaemia
 Epigastric mass
 Jaundice
 Ascites
 Hepatomegaly
 Virchow’s node (= Troisier’s sign)
 Acanthosis nigricans
Complications
 Perforation
 Upper GI bleed: haematemesis, melaena
 Gastric outlet obstruction → succession splash

Other Gastric Neoplasms Zollinger-Ellison Syndrome
Benign Pathophysiology
 Benign polyps: adenomas  Gastrin-secreting tumour (gastrinoma) most commonly
 Leiomyoma found in the small intestine or pancreas.
 Lipomas  ↑ Gastrin → ↑HCL→ PUD + chronic diarrhoea
 Haemangiomas  Diarrhoea due to inactivation of panc enzymes
 Schwannomas  ECL proliferation can → carcinoid tumours
 60-90% of gastrinomas are malignant
Malignant  25% assoc. c̄ MEN1
 Lymphoma
 Carcinoid Presentation
 GIST  Abdominal pain and dyspepsia
 Chronic diarrhoea / Steatorrhoea
 Refractory PUD
Gastrointestinal Stromal Tumour
 Commonest mesenchymal tumour of the GIT Ix
 >50% occur in the stomach.  ↑ gastrin c̄ ↑↑ HCl (pH<2)
Epidemiology  MRI/CT
 M=F  Somatostatin receptor scintigraphy
 ~60yrs
 ↑ c̄ NF1 Rx
 High dose PPI
Pathology  Surgery
 Arise from intestinal cells of Cajal  Tumour resection
 Located in muscularis propria  May do subtotal gastrectomy c̄ Roux en Y
 Pacemaker cells
 OGD: well-demarcated spherical mass c̄ central
punctum
Presentation
 Mass effects: abdo pain, obstruction
 Ulceration: → bleeding
Poor Prognosticators
 ↑ size
 Extra-gastric location
 ↑ mitotic index
Mx
 Medical
 Unresectable, recurrent or metastatic disease
 Imatinib: kit selective tyrosine kinase inhibitor
 Surgical
 Resection
Carcinoid Tumours
 Diverse group of neuroendocrine tumours of
enterochromaffin cell origin
 May secrete multiple hormones
 10% occur in the stomach
Gastric Carcinoids
 Atrophic gastritis → ↓ acid production → ↑ gastrin →
ECL hyperplasia → carcinoid tumour
 Gastrinomas may also → carcinoid
Gastric Lymphoma
 Commonest site for extranodal lymphoma
 Most commonly MALToma due to chronic H. pylori
gastritis
 H. pylori eradication can be curative

Bariatric Surgery
Benefits
 Sustained wt. ↓
 Symptom improvement
 Sleep apnoea
 Mobility
 HTN
 DM
Indications
 All the criteria must be met
 BMI ≥40 or ≥35 c̄ significant co-morbidities that
could improve c̄ ↓ wt.
 Failure of non-surgical Mx to achieve and
maintain clinically beneficial wt. loss for 6mo.
 Fit for surgery and anaesthesia
 Integrated program providing guidance on diet,
physical activity, psychosocial concerns and
lifelong medical monitoring
 Well-informed and motivated pt.
 If BMI >50, surgery is 1st-line Rx
Laparoscopic Gastric Banding

 Inflatable silicone band around proximal stomach →
small pre-stomach pouch.
 Limits food intake
 Slows digestion
 At 1yr 46% mean excess wt. loss
Roux-en-Y Gastric Bypass

 Oesophagojejunostomy allows bypass of stomach,
duodenum and proximal jejunum.
 Alters secretion of hormones influencing glucose
regulation and perception of hunger / satiety.
 Greater wt. loss and lower reoperation rates.
 Complications
 Dumping syndrome
 Wound infection
 Hernias
 Malabsorption
 Diarrhoea
 Mortality 0.5%

Hepatobiliary Surgery
Contents
Gallstones .................................................................................................................................................................................... 36
Biliary Colic .................................................................................................................................................................................. 36
Acute Cholecystitis ...................................................................................................................................................................... 37
Chronic Cholecystitis ................................................................................................................................................................... 37
Rarer Gallstone Disease ............................................................................................................................................................. 37
Obstructive Jaundice ................................................................................................................................................................... 38
Pancreatic Carcinoma ................................................................................................................................................................. 38
Acute Pancreatitis........................................................................................................................................................................ 39
Complications of Acute Pancreatitis ............................................................................................................................................ 40
Chronic Pancreatitis .................................................................................................................................................................... 40
Pancreatic Endocrine Neoplasia ................................................................................................................................................. 41
Pancreatic Malformations ............................................................................................................................................................ 41
Cholangiocarcinoma .................................................................................................................................................................... 42
Hydatid Cyst ................................................................................................................................................................................ 42

Gallstones Biliary Colic
Epidemiology Pathogenesis
 ~8% of the population >40yrs  Gallbladder spasm against a stone impacted in the neck of
 Incidence ↑ over last 20yrs: western diet the gallbladder – Hartmann’s Pouch.
 Slightly ↑ incidence in females  Less commonly, the stone may be in the CBD
 90% of gallstones remain asymptomatic
Presentation
Formation  Biliary colic
 RUQ pain radiating → back (scapular region)
General Composition  Assoc. c̄ sweating, pallor, n/v
 Phospholipids: lecithin  Attacks may be ppted. by fatty food and last <6h
 Bile pigments (broken down Hb)  o/e may be tenderness in right hypochondrium
 Cholesterol  ± jaundice if stones passes in to CBD
Aetiology Differential
 Lithogenic bile: Admirand’s Triangle  Cholecystitis / other gallstone disease
 Biliary sepsis  Pancreatitis
 GB hypomotility → stasis  Bowel perforation
 Pregnancy, OCP
 TPN, fasting Ix
 Same work up as cholecystitis as may be difficult to
Cholesterol Stones: 20% differentiate clinically.
 Large  Urine: bilirubin, urobilinogen, Hb
 Often solitary  Bloods: FBC, U+E, amylase, LFTs, G+S, clotting, CRP
 Formation ↑ according to Admirand’s Trangle  Imaging
 ↓ bile salts  AXR: 10% of gallstones are radio-opaque
 ↓ lecithin  Erect CXR: look for perforation
 ↑ cholesterol  US:
 Risk factors  Stones: acoustic shadow
 Female
 Dilated ducts: >6mm
 OCP, pregnancy
 Inflamed GB: wall oedema
 ↑ age
 High fat diet and obesity  If Dx uncertain after US
 Racial: e.g. American Indian tribes  HIDA cholescintigraphy: shows failure of GB filling
 Loss of terminal ileum (↓ bile salts) (requires functioning liver)
 If dilated ducts seen on US → MRCP
Pigment Stones: 5%
 Small, black, gritty, fragile Rx
 Calcium bilirubinate  Conservative
 Associated c̄ haemolysis  Rehydrate and NBM
 Opioid analgesia: morphine 5-10mg/2h max
Mixed Stones: 75%  High recurrence rate  surgical Rx favoured
 Often multiple  Surgical
 Cholesterol is the major component  As for conservative + either:
 Urgent lap chole (same admission)
 Elective lap chole @ 6-12wks
Complications
In the Gallbladder
1. Biliary Colic
2. Acute cholecystitis ± empyema
3. Chronic cholecytsitis
4. Mucocele
5. Carcinoma
6. Mirizzi’s syndrome
In the CBD
1. Obstructive jaundice
2. Pancreatitis
3. Cholangitis
In the Gut
1. Gallstone ileus

Acute Cholecystitis Chronic Cholecystitis
Pathogenesis Symptoms: Flatulent Dyspepsia
 Stone or sludge impaction in Hartmann’s pouch  Vague upper abdominal discomfort
 → chemical and / or bacterial inflammation  Distension, bloating
 5% are acalculous: sepsis, burns, DM  Nausea
 Flatulence, burping
Sequelae  Symptoms exacerbated by fatty foods
1. Resolution ± recurrence  CCK release stimulates gallbladder
2. Gangrene and rarely perforation
3. Chronic cholecystitis Differential
4. Empyema  PUD
 IBS
Presentation  Hiatus hernia
 Severe RUQ pain  Chronic pancreatitis
 Continuous
 Radiates to right scapula and epigastrium
Ix
 Fever
 AXR: porcelain gallbladder
 Vomiting
 US: stones, fibrotic, shrunken gallbladder
 MRCP
Examination
 Local peritonism in RUQ
Mx
 Tachycardia c̄ shallow breathing
 Medical
 ± jaundice  Bile salts (not very effective)
 Murphy’s sign  Surgical
 2 fingers over the GB and ask pt. to breath in  Elective cholecystectomy
 → pain and breath catch. Must be –ve on the L  ERCP first if US shows dilated ducts and stones
 Phlegmon may be palpable
 Mass of adherent omentum and bowel
 Boas’ sign
 Hyperaesthesia below the right scapula
Rarer Gallstone Disease
Ix
 Urine: bilirubin, urobilinogen Mucocele
 Bloods  Neck of gallbladder blocked by stone but contents
 FBC: ↑ WCC remains sterile
 U+E: dehydration from vomiting  Can be very large → palpable mass
 Amylase, LFTs, G+S, clotting, CRP  May become infected → empyema
 Imaging
 AXR: gallstone, porcelain gallbladder
 Erect CXR: look for perforation Gallbladder Carcinoma
 US
 Rare
 Stones: acoustic shadow
 Associated c̄ gallstones and gallbladder polyps.
 Dilated ducts (>6mm)
 Calcification of gallbladder → porcelain GB
 Inflamed GB: wall oedema
 Incidental Ca found in 0.5-1% of lap choles.
 If Dx uncertain after US
 HIDA cholescintigraphy: shows failure of GB
filling (requires functioning liver)
 MRCP if dilated ducts seen on US Mirizzi’s Syndrome
 Rare
 Large stone in GB presses on the common hepatic duct
Mx → obstructive jaundice.
 Conservative  Stone may erode through into the ducts
 NBM
 Fluid resuscitation
 Analgesia: paracetamol, diclofenac, codeine Gallstone Ileus
 Abx: cefuroxime and metronidazole  Large stone (>2.5cm) erodes from GB → duodenum
 80-90% settle over 24-48h through a cholecysto-duodenal fistula 2O to chonic inflam.
 Deterioration: perforation, empyema  May impact in distal ileum → obstruction
 Surgical  Rigler’s Triad:
 May be elective surgery @ 6-12wks (↓ inflam)  Pneumobiliia
 If <72h, may perform lap chole in acute phase  Small bowel obstruction
 Empyema  Gallstone in RLQ
 High fever  Rx: stone removal via enterotomy
 RUQ mass  NB. Bouveret’s syn. = duodenal obstruction
 Percutaneous drainage: cholecystostomy

Obstructive Jaundice Pancreatic Carcinoma
Causes Risk Factors: SINED
 30% stones  Smoking
 30% Ca head of the pancreas  Inflammation: chronic pancreatitis
 30% Other  Nutrition: ↑fat diet
 LNs @ porta hepatis: TB, Ca  EtOH
 Inflammatory: PBC, PSC  DM
 Drugs: OCP, sulfonylureas, flucolox
 Neoplastic: Cholangiocarcinoma
 Mirizzi’s syndrome
Pathology
 90% ductal adenocarcinomas
 Present late, metastasise early
Clinical Features  Direct extension to local structures
 Jaundice  Lymphatics
 Noticeable @ ~50mM  Blood → liver and lungs
 Seen @ tongue frenulum first  60% located in head, 25% body, 15% tail
 Dark urine, pale stools
 Itch (bile salts)
Presentation
 Typically male >60yrs
Ix  Painless obstructive jaundice: dark urine, pale stools
 Urine  Epigastric pain: radiates to back, relieved sitting
 Dark forward
 ↑ bilirubin
 Anorexia, wt. loss and malabsorption
 ↓ urobilinogen
 Acute pancreatitis
 Bloods
 Sudden onset DM in the elderly
 FBC: ↑ WCC in cholangitis
 U+E: hepatorenal syndrome
 LFT: ↑cBR, ↑↑ ALP, ↑AST/ALT Signs
 Clotting: ↓ vit K → ↑ INR  Palpable gallbladder
 G+S: may need ERCP  Jaundice
 Immune: AMA, ANCA, ANA  Epigastric mass
 Imaging  Thrombophlebitis migrans (Trousseau Sign)
 AXR  Splenomegaly: PV thrombosis → portal HTN
 May visualise stone  Ascites
 Pneumobilia suggests gas forming infection
 US Courvoisier’s Law
 Dilated ducts >6mm  In the presence of painless obstructive jaundice, a
 Stones (95% accurate) palpable gallbladder is unlikely to be due to stones.
 Tumour
 MRCP or ERCP Ix
 Percutaneous Transhepatic Cholangiography  Bloods: cholestatic LFTs, ↑Ca19-9 (90% sens), ↑Ca
 Imaging
Mx of Stones  US: pancreatic mass, dilated ducts, hepatic
 Conservative mets, guide biopsy
 Monitor LFTs: passage of stone may → resolution  EUS: better than CT/MRI for staging
 Vitamins ADEK  CXR: mets
 Analgesia  Laparoscopy: mets, staging
 Cholestyramine  ERCP
 Interventional  Shows anatomy
 If: no resolution, worsening LFTs or cholangitis  Allows stenting
 ERCP c̄ sphincterotomy and stone extraction  Biopsy of peri-ampullary lesions
 Surgical
 Open / lap stone removal c̄ T tube placement Rx
 T tube cholangiogram 8d later to confirm  Surgery
stone removal.  Fit, no mets, tumour ≤3cm (≤10% of pts)
 Delayed cholecystectomy to prevent recurrence  Whipple’s pancreaticoduodenectomy
 Distal pancreatectomy
Ascending Cholangitis  Post-op chemo delays progression
 May complicate CBD obstruction  5ys = 5-14%
 Charcot’s triad: fever/rigors, RUQ pain, jaundice  Palliation
 Endoscopic / percutaneous stenting of CBD
 Reynolds pentad: Charcot’s triad + shock + confusion
 Palliative bypass surgery:
 Mx
– cholecystojejunostomy + gastrojejunostomy
 Cef and met
 Pain relief – may need coeliac plexus block
 1st: ERCP
 2nd: Open or lap stone removal c̄ T tube drain
Prognosis
 Mean survival <6mo
© Alasdair Scott, 2012  5ys = <2% 38
Acute Pancreatitis
Pathophysiology Ix
 Pancreatic enzymes released and activated in vicious  Bloods
circle → multi-stage process.  FBC: ↑WCC
1. Oedema + fluid shift + vomiting → hypovolaemic  ↑amylase (>1000 / 3x ULN) and ↑lipase
shock while enzymes → autodigestion and fat necrosis  ↑ in 80%
2. Vessel autodigestion → retroperitoneal haemorrhage  Returns to normal by 5-7d
3. Inflammation → pancreatic necrosis  U+E: dehydration and renal failure
4. Super-added infection: 50% of pts. c̄ necrosis  LFTs: cholestatic picture, ↑AST, ↑LDH
 Ca2+: ↓
Epidemiology  Glucose: ↑
 1% of surgical admissions  CRP: monitor progress, >150 after 48hrs = sev
 4th and 5th decades  ABG: ↓O2 suggests ARDS
 10% mortality  Urine: glucose, ↑cBR, ↓urobilinogen
 Imaging
Aetiology  CXR: ARDS, exclude perfed DU
 AXR: sentinel loop, pancreatic calcification
 Gallstones (45%)
 US: Gallstones and dilated ducts, inflammation
 Ethanol (25%)
 Contrast CT: Balthazar Severity Score
 Idiopathic (20%): ?microstones
 Trauma
Conservative Mx
 Steroids
 Manage @ appropriate level: e.g. ITU if severe
 Mumps + other infections: Coxsackie B
 Constant reassessment is key
 Autoimmune: e.g. PAN
 Hrly TPR, UO
 Scorpion (Trinidadian)  Daily FBC, U+E, Ca2+, glucose, amylase ABG
 Hyperlipidaemia (I and V), ↑Ca, Hypothermia
 ERCP: 5% risk Fluid Resuscitation
 Drugs: e.g. thiazides, azathioprine  Aggressive fluid resus: keep UO >30ml/h
 Catheter ± CVP
Symptoms
 Severe epigastric pain → back Pancreatic Rest
 May be relieved by sitting forward  NBM
 Vomiting  NGT if vomiting
 TPN may be required if severe to prevent catabolism
Signs
 ↑HR, ↑RR Analgesia
 Fever  Pethidine via PCA
 Hypovolaemia → shock  Or morphine 5-10mg/2h max
 Epigastric tenderness
 Jaundice Antibiotics
 Ileus → absent bowel sounds  Not routinely given if mild
 Ecchymoses  Used if suspicion of infection or before ERCP
 Grey Turners: flank  Penems often used: e.g. meropenem, imipenem
 Cullens: periumbilical (tracks up Falciform)
Mx Complications
Differential  ARDS: O2 therapy or ventilation
 Perforated DU  ↑ glucose: insulin sliding scale
 Mesenteric infarction  ↑/↓Ca
 MI  EtOH withdrawal: chlordiazepoxide
Modified Glasgow Criteria Interventional Mx: ERCP

 Valid for EtOH and Gallstones  If pancreatitis c̄ dilated ducts 2O to gallstones
 Assess severity and predict mortality  ERCP + sphincterotomy → ↓ complications
 Ranson’s criteria are only applicable to EtOH and can
only be fully applied after 48hrs. Surgical Mx
PANCREAS Indications
 PaO2 <8kPa 1 = mild  Infected pancreatic necrosis
 Age >55yrs 2 = mod  Pseudocyst or abscess
 Neutrophils >15 x109/L 3 = severe  Unsure Dx
 Ca2+ <2mM
 Renal function U>16mM Operations
 Enzymes LDH>600iu/L  Laparotomy + necrosectomy (pancreatic debridement)
AST>200 iu/L  Laparotomy + peritoneal lavage
 Albumin <32g/L  Laparostomy: abdomen left open c̄ sterile packs in ITU
 Sugar >10mM
Complications of Acute Pancreatitis Chronic Pancreatitis
Early: Systemic Causes: AGITS
 Respiratory: ARDS, pleural effusion  Alcohol (70%)
 Shock: hypovolaemic or septic  Genetic
 Renal failure  CF
 DIC  HH
 Metabolic  Immune
 ↓ Ca2+  Lymphoplasmacytic sclerosing pancreatitis (↑IgG4)
 ↑ glucose  Triglycerides ↑
 Metabolic acidosis  Structural
 Obstruction by tumour
 Pancreas divisum
Late (>1wk): Local
 Pancreatic necrosis Presentation
 Pancreatic infection  Epigastric pain
 Pancreatic abscess  Bores through to back
 May form in pseudocyst or in pancreas  Relieved by sitting back or hot water bottle →
 Open or percutaneous drainage erythema ab igne
 Bleeding: e.g. from splenic artery  Exacerbated by fatty food or EtOH
 May require embolisation  Steatorrhoea and wt. loss
 Thrombosis  DM: polyuria, polydipsia
 Splenic A., GDA or colic branches of SMA  Epigastric mass: pseudocyst
 May → bowel necrosis
 Portal vein → portal HTN Ix
 Fistula formation  ↑ glucose
 Pancreato-cutaneous → skin breakdown  ↓ faecal elastase: ↓ exocrine function
 US: pseudocyst
Pancreatic Pseudocyst
 AXR: speckled pancreatic calcifications
 Collection of pancreatic fluid in the lesser sac
 CT: pancreatic calcifications
surrounded by granulation tissue
 Occur in 20% (esp. in EtOH pancreatitis)
 Presentation
Rx
 4-6wks after acute attack  Diet
 Persisting abdominal pain  No EtOH
 Epigastric mass → early satiety  ↓ fat, ↑ carb
 Complications  Drugs
 Infection → abscess  Analgesia: may need coeliac plexus block
 Obstruction of duodenum or CBD  Enzyme supplements: pancreatin (Creon)
 ADEK vitamins
 Ix
 DM Rx
 Persistently ↑ amylase ± LFTs
 US / CT  Surgery
 Indications
 Rx
 <6cm: spontaneous resolution  Unremitting pain
 >6cm  Wt. loss
 Endoscopic cyst-gastrostomy  Duct blockage
 Percutaneous drainage under US/CT  Procedures
 Distal pancreatectomy, Whipple’s
 Pancreaticojejunostomy: drainage
 Endoscopic stenting
Complications
 Pseudocyst
 DM
 Pancreatic Ca
 Pancreatic swelling → biliary obstruction
 Splenic vein thrombosis → splenomegaly

Pancreatic Endocrine Neoplasia Pancreatic Malformations
Epidemiology Ectopic Pancreas
 30-60yrs  Meckel’s diverticulum
 ~15% assoc. c̄ MEN1  Small bowel
Insulinoma Pancreas Divisium

 Fasting / exercise-induced hypoglycaemia  Failure of fusion of dorsal and ventral buds
 Confusion, stupor, LOC  → bulk of pancreas drains through smaller accessory duct.
 ↑ insulin + ↑ c-peptide + ↓glucose  Usually asymptomatic
 May → chronic pancreatitis
Gastrinoma → Zollinger-Ellison
 Hypergastrinaemia → hyperchlorhydria → PUD and Annular Pancreas
chronic diarrhoea (inactivation of pancreatic enzymes)  Fusion of dorsal and ventral buds around duodenum
 May present c̄ infantile duodenal obstruction.
Glucagonoma
 ↑ se glucagon → mild DM
 Characteristic blistering rash
 Necrolytic migratory erythema
VIPoma / Verner-Morrison / WDHA Syn.

 Watery Diarrhoea
 Hypokalaemia
 Achlorhydria
 Acidosis
Somatostatinoma
 Somatostatin
 Inhibits glucagon and insulin release
 Inhibits pancreatic enzyme secretion
 Features
 DM
 Steatorrhoea
 Gall stones
 Usually v. malignant tumour c̄ poor prognosis

Cholangiocarcinoma Hydatid Cyst
Pathology Pathophysiology
 Rare bile duct tumour  Zoonotic infection by Echinococcus granulosus
 Adenocarcinoma  Occurs in sheep-rearing communities
 Typically occur @ confluence of right and left hepatic  Parasite penetrates the portal system and infects the
ducts: called “Klatskin” tumours liver → calcified cyst
Risk Factors Presentation

 PSC  Mostly asymptomatic
 Ulcerative colitis  Pressure effects
 Choledocholithiasis  Non-specific pain
 Hep B/C  Abdominal fullness
 Choledochal cysts  Obstructive jaundice
 Lynch 2  Rupture
 Flukes  Biliary colic
 Jaundice
 Urticaria
Presentation  Anaphylaxis
 Progressive painless obstructive jaundice O
 2 infection
 Gallbladder not palpable
 Steatorrhoea
Ix
 Wt. loss
 Eosinophilia
 CT
Ix
 Cholestatic LFTs
Rx
 CA 19-9
 Medical: albendazole
 Surgical cystectomy
Rx  Indicated for large cysts
 Poor prognosis: no curative Rx
 Palliative stenting by ERCP

Lower GI Surgery
Contents
Paediatric Conditions................................................................................................................................................................... 44
Small Bowel Neoplasms .............................................................................................................................................................. 45
Carcinoid Tumours ...................................................................................................................................................................... 45
Acute Appendicitis ....................................................................................................................................................................... 46
Inflammatory Bowel Disease: Pathology and Presentation ........................................................................................................ 47
Ulcerative Colitis: Management................................................................................................................................................... 48
Crohn’s Disease: Management ................................................................................................................................................... 49
Diverticular Disease..................................................................................................................................................................... 50
Bowel Obstruction: Causes and Investigation ............................................................................................................................. 51
Bowel Obstruction: General Management .................................................................................................................................. 52
Bowel Obstruction: Specific Management .................................................................................................................................. 53
Colorectal Carcinoma: Pathology and Presentation ................................................................................................................... 54
Colorectal Carcinoma: Ix, Mx and Prevention ............................................................................................................................. 55
Familial CRC Syndromes ............................................................................................................................................................ 56
GI Polyps ..................................................................................................................................................................................... 56
Mesenteric Ischaemia ................................................................................................................................................................. 57
Lower GI Bleed ............................................................................................................................................................................ 57

Paediatric Conditions
Meckel’s Diverticulum Intussusception
 Ileal remnant of vitellointestinal duct  Portion of intestine (the intussusception) is invaginated
 Joins yoke sac to midgut lumen into its own lumen (the intussuscipiens)
Features Cause
 A true diverticulum  Hypertrophied Peyer’s patch
 2 inches long  Meckel’s
 2 ft from ileocaecal valve on antimesenteric border  HSP
 2% of population  Peutz-Jeghers
 2% symptomatic  Lymphoma
 Contain ectopic gastric or pancreatic tissue
Presentation
Presentation of Symptomatic Meckel’s  6-12mo
 Rectal bleeding: from gastric mucosa  Colicky abdo pain:
 Diverticulitis mimicking appendicitis  Episodic inconsolable crying, drawing up legs
 Intussusception  ± bilious vomiting
 Volvulus  Redcurrent jelly stools
 Malignant change: adenocarcinoma  Sausage-shaped abdominal mass
 Raspberry tumour: mucosa protruding at umbilicus
 A vitello-intestinal fistula Mx
 Littre’s Hernia: herniation of Meckel’s  Resuscitate, x-match, NGT
 US + reduction by air enema
Dx  Surgery if not reducible by enema
 Tc pertechnecate scan +ve in 70% (detects gastric
mucosa) NB. Intussusception rarely occurs in an adult
 If it does, consider neoplasm as lead-point
Rx
 Surgical resection
Mesenteric Adenitis
 Viral infection / URTI → enlargement of mesenteric LNs
 → pain, tenderness and fever
 Differentiating features
 Post URTI
 Headache + photophobia
 Higher temperature
 Tenderness is more generalised
 Lymphocytosis

Small Bowel Neoplasms Carcinoid Tumours
Benign: 35% Pathology
 Lipoma  Diverse group of neuroendocrine tumours of
 Leiomyoma enterochromaffin cell origin capable of producing 5HT
 Neurofibroma  May be derived from
 Haemangioma  Foregut: respiratory tract
 Adenomatous polyps (FAP, Peutz-Jeghers)  Midgut: stomach, ileum, appendix
 Hindgut: colorectum
Malignant: 65% (only 2% of GI malignancies)  May secrete: 5-HT, VIP, gastrin, glucagon, insulin, ACTH
 Adenocarcinoma (40% of malignant tumours)  Hind gut tumours rarely secrete 5-HT
 Carcinoid (40% of malignant tumours)  Carcinoid syndrome suggest bypass of first-pass
 Lymphoma (esp. c̄ Coeliac disease: EATL) metabolism and is strongly assoc. c̄ metastatic disease.
 GIST  10% part of MEN1
 Sites
Presentation  Appendix: 45%
 Ileum: 30%
 Often non-specific symptoms so present late
 Colorectum: 20%
 N/V, obstruction
 Stomach: 10%
 Wt. loss and abdominal pain
 Elsewhere in GIT
 Bleeding  Bronchus: 10%
 Jaundice from biliary obstruction or liver mets.  Consider all as malignant
Imaging
 AXR: SBO
 Ba follow through Presentation
 CT
Local
Endoscopy  Appendicitis
 Push enteroscopy  Intussusception or obstruction
 Capsule endoscopy  Abdominal pain
Carcinoid Syndrome: FIVE HT

 Flushing: paroxysmal, upper body ± wheals
 Intestinal: diarrhoea
 Valve fibrosis: tricuspid regurg and pulmonary stenosis
 whEEze: bronchoconstriction
st
 Hepatic involvement: bypassed 1 pass metabolism
 Tryptophan deficiency → pellagra (3Ds)
Ix
 ↑ urine 5-hydroxyindoleacetic acid
 ↑ plasma chromogranin A
 CT/MRI: find primary
Rx
 Symptoms: octreotide or loperamide
 Curative
 Resection: tumours are v. yellow
 Give octreotide to avoid carcinoid crisis
Carcinoid Crisis
 Tumour outgrows blood supply or is handled too
much → massive mediator release
 Vasodilatation, hypotension, bronchoconstriction,
hyperglycaemia
 Rx: high-dose octreotide
Prognosis
 Median survival is 5-8yrs (~3yrs if mets present)

Acute Appendicitis
Definition Differential
 Inflammation of the vermiform appendix ranging from  Surgical
oedema to ischaemic necrosis and perforation.  Cholecystitis
 Diverticulitis
Epidemiology  Meckel’s diverticulitis
 Incidence: 6% lifetime incidence, commonest surgical  Gynae
emergency  Cyst accident: torsion, rupture, haemorrhage
 Salpingitis / PID
 Age: rare <2yrs, maximal peak during child, ↓ thereafter
 Ruptured ectopic
 Medical
Pathogenesis  Mesenteric adenitis
 Obstruction of the appendix  UTI
 Faecolith most commonly  Crohn’s
 Lymphoid hyperplasia post-infection
 Tumour (e.g. caecal Ca, carcinoid)
 Worms (e.g. Ascaris lumbicoides, Schisto)
Ix
 Dx is principally clinical
 Gut organisms → infection behind obstruction
 Bloods: FBC, CRP, amylase, G+S, clotting
 → oedema → ischaemia → necrosis → perforation
 Peritonitis  Urine
 Abscess  Sterile pyuria: may indicate bladder irritation
 Appendix mass  Ketones: anorexia
 Exclude UTI
 β-HCG
Pattern of Abdominal Pain  Imaging
 US: exclude gynae path, visualise inflamed
Early inflammation → appendiceal irritation
appendix
 Visceral pain is not well localised cf. somatic pain.  CT: can be used
 Nociceptive info travels in the sympathetic afferent  Diagnostic lap
fibres that supply the viscus
 Pain referred to the dermatome corresponding to the
spinal cord entry level of these sympathetic fibres.
Mx
 Fluids
 Append = midgut = lesser splanch (T10/11) = umb
 Abx: cef 1.5g + met 500g IV TDS
Late inflammation → parietal peritoneum irritation  Analgesia: paracetamol, NSAIDs, codeine phosphate
 Pain localised in RIF  Certain Dx → appendicectomy (open or lap)
 Uncertain Dx → active observation
Symptoms
 Colicky abdo pain Complications
 Central → localised in RIF
 Worse c̄ movement Appendix Mass
 Anorexia  Inflamed appendix c̄ adherent covering of omentum and
 Nausea (vomiting is rarely prominent) small bowel
 Constipation / diarrhoea  Dx: US or CT
 Mx
 Initially: Abx + NBM
Signs  Resolution of mass → interval appendicectomy
 Low-grade pyrexia: 37.5 – 38.5  Exclude a colonic tumour: colonoscopy
 ↑HR, shallow breathing
 Foetor oris Appendix Abscess
 Guarding and tenderness: @ McBurney’s point  Results if appendix mass doesn’t resolve
 +ve cough / percussion tenderness  Mass enlarges, pt. deteriorates
 Appendix mass may be palpable in RIF  Mx
 Pain PR suggests pelvic appendix.  Abx + NBM
 CT-guided percutaneous drainage
Special Signs  If no resolution, surgery may involve right
hemicolectomy.
Rovsing’s Sign
 Pressure in LIF → more pain in RIF Perforation
 Commoner if faecolith present and in young children (as
Psoas Sign Dx is often delayed)
 Pain on extending the hip: retrocaecal appendix  Deteriorating pt. c̄ peritonitis.
Cope Sign
 Flexion + internal rotation of R hip → pain
 Appendix lying close to obturator internus

Inflammatory Bowel Disease: Pathology and Presentation
Epidemiology Pathology
UC Crohn’s UC Crohn’s
Prev 100-200 /100,000 50-100 /100,000 Macroscopic
Age 30s 20s Location Rectum + colon Mouth to anus
Sex F>M (just) ± backwash ileitis esp. terminal ileum
Aet Concordance = 10% Concordance = 70% Distribution Contiguous Skip lesions
Smoking protective Smoking ↑ risk Strictures No Yes
TH2-mediated TH1/TH17-mediated
Microscopic
Inflammation Mucosal Transmural
Ulceration Shallow, broad Deep, thin, serpiginous
→ cobblestone mucosa
Fibrosis None Marked
Granulomas None Present
Pseudoplyps Marked Minimal
Fistulae No Yes
Presentation
UC Crohn’s
Symptoms
Systemic Fever, malaise, anorexia, wt. loss in active disease
Abdominal  Diarrhoea  Diarrhoea (not usually bloody)
 Blood ± mucus PR  Abdominal pain
 Abdominal discomfort  Wt. loss
 Tenesmus, faecal urgency
Signs
Abdominal  Fever  Aphthous ulcers, glossitis
 Tender, distended abdomen  Abdominal tenderness
 RIF mass
 Perianal abscesses, fistulae, tags
 Anal / rectal strictures
Extra-abdominal Skin Joints
 Clubbing  Arthritis (non-deforming, asymmetrical)
 Erythema nodosum  Sacroiliitis
 Pyoderma gang (esp. UC)  Ank spond
HPB
Eyes  PSC + cholangiocarcinoma (esp. UC)
 Iritis  Gallstones (esp. Crohn’s)
 Conjunctivitis  Fatty liver
 Episcleritis Other
 Scleritis  Amyloidosis
 Oxalate renal stones (esp. Crohns)
Complications  Toxic megacolon  Fistulae

 Diameter >6cm  Entero-enteric/colonic → diarrhoea
 Risk of perforation  Enterovesical → frequency, UTI
 Bleeding  Enterovaginal
 Malignancy  Perianal → “pepperpot” anus
 CRC in 15% c̄ pancolitis for 20yrs  Strictures → obstruction
 Cholangiocarcinoma  Abscesses
 Strictures → obstruction  Abdominal
 Venous thrombosis  Anorectal
 Malabsorption
 Fat → Steatorrhoea, gallstones
 B12 → megaloblastic anaemia
 Vit D → osteomalacia
 Protein → oedema
 Toxic megacolon and Ca may occur (< cf.
UC)
Ulcerative Colitis: Management
Ix Inducing Remission in Mild / Mod Disease
 Bloods:  OPD-based
 FBC: ↓Hb, ↑WCC
 LFT: ↓albumin Oral Therapy
 ↑CRP/ESR  1st line: 5-ASAs
 Blood cultures  2nd line: prednisolone
 Stool
 MCS: exclude Campy, Shigella, Salmonella… Topical Therapy: mainly left-sided disease
 CDT: C. diff may complicate or mimic  Proctitis: suppositories
 Imaging  More proximal disease: enemas or foams
 AXR: megacolon (>6cm), wall thickening  5-ASAs ± steroids (prednisolone or budesonide)
 CXR: perforation
 CT Additional Therapy: steroid sparing
 Ba / gastrograffin enema  Azathioprine or mercaptopurine
 Lead-pipe: no haustra  Infliximab: steroid-dependent pts
 Thumbprinting: mucosal thickening
 Pseudopolyps: regenerating mucosal island Maintaining Remission
 Ileocolonoscopy + regional biopsy: Baron Score  1st line: 5-ASAs PO – sulfasalazine or mesalazine
 Topical Rx may be used in proctitis
Severity  2nd line: Azathioprine or mercaptopurine
 Relapsed on ASA or are steroid-dependent
Truelove and Witts Criteria  Give 6-mercaptopurine if azathioprine intolerant
 3rd line: Infliximab / adalimumab
Mild Mod Severe
Motions <4 4-6 >6
Emergency Surgery
PR bleed small moderate large
 20% require surgery at some stage
Temp Apyrexic 37.1-37.8 >37.8
 30% c̄ colitis require surgery w/i 5yrs
HR <70 70-90 >90
Hb >11 10.5-11 <10.5
Indications
ESR <30 >30
 Toxic megacolon
 Perforation
 Massive haemorrhage
Acute Severe UC  Failure to respond to medical Rx
 Resus: Admit, IV hydration, NBM
 Hydrocortisone: IV 100mg QDS + PR Procedures
 Transfuse if required  Total / subtotal colectomy c̄ end ileostomy ± mucus
 Thromboprophylaxis: LMWH fistula
 Monitoring  Followed after ~3mo by either
 Bloods: FBC, ESR, CRP, U+E  Completion proctectomy + Ileal-pouch anal
 Vitals + stool chart anastomosis (IPAA) or end ileostomy
 Twice daily examination  Ileorectal anastomosis (IRA)
 ± AXR  Panproctocolectomy + permanent end ileostomy
 Acute colitis op mortality: 7% (30% if perforated)
NB. RCTs show no benefit of Abx: not routinely recommended
 May use: megacolon, perforation, uncertain Dx
Elective Surgery
Acute Complications
 Perforation Indications
 Bleeding  Chronic symptoms despite medical therapy
 Toxic megacolon (>6cm)  Carcinoma or high-grade dysplasia
 VTE
Procedures
Improvement → oral therapy  Panproctocolectomy c̄ end ileostomy or IPAA
 Switch to oral pred + a 5-ASA  Total colectomy c̄ IRA
 Taper pred after full remission
Surgical Complications
No Improvement → rescue therapy  Abdominal
 On day 3: stool freq >8 or CRP >45  SBO
 Predicts 85% chance of needing a colectomy during  Anastomotic stricture
the admission  Pelvic abscess
 Discussion between pt, physician and surgeon  Stoma: retraction, stenosis, prolapse, dermatitis
 Medical: ciclosporin, infliximab or visilizumab (anti-T cell)  Pouch
 Surgical  Pouchitis (50%): metronidazole + cipro
 ↓ female fertility
 Faecal leakage
Crohn’s Disease: Management
Ix Inducing Remission in Mild / Mod Disease
 Bloods: (top 3 are severity markers)  OPD treatment
 FBC: ↓Hb, ↑WCC
 LFT: ↓albumin Supportive
 ↑CRP/ESR  High fibre diet
 Haematinics: Fe, B12, Folate  Vitamin supplements
 Blood cultures
 Stool Oral Therapy
 MCS: exclude Campy, Shigella, Salmonella…  1st line
 CDT: C. diff may complicate or mimic  Ileocaecal: budesonide
 Imaging  Colitis: sulfasalazine
 AXR: obstruction, sacroileitis  2nd line: prednisolone (tapering)
 CXR: perforation  3rd line: methotrexate
 MRI  4th line: infliximab or adalimumab
 Assess pelvic disease and fistula
 Assess disease severity Perianal Disease
 Small bowel follow-through or enteroclysis  Occurs in ~50%
 Skip lesions  Ix: MRI + EUA
 Rose-thorn ulcers  Rx
 Cobblestoning: ulceration + mural  Oral Abx: metronidazole
oedema  Immunosuppression ± infliximab
 String sign of Kantor: narrow terminal  Local surgery ± seton insertion
ileum
 Endoscopy Maintaining Remission
 Ileocolonoscopy + regional biopsy: Ix of  1st line: azathioprine or mercaptopurine
choice  2nd line: methotrexate
 Wireless capsule endoscopy  3rd line: Infliximab / adalimumab
 Small bowel enteroscopy
Surgery
Severe Attack  50-80% need ≥1 operation in their life
 Never curative
Assessment  Should be as conservative as possible
 ↑temp, ↑HR, ↑ESR, ↑CRP, ↑WCC, ↓albumin
Indications
Management  Emergency
 Resus: Admit, NBM, IV hydration  Failure to respond to medical Rx
 Hydrocortisone: IV + PR if rectal disease  Intestinal obstruction or perforation
 Abx: metronidazole PO or IV  Massive haemorrhage
 Thromboprophylaxis: LMWH  Elective
 Abscess or fistula
 Dietician Review
 Perianal disease
 Elemental diet
 Chronic ill health
 Liquid prep of amino acids, glucose and
 Carcinoma
fatty acids
 Consider parenteral nutrition
Procedures
 Monitoring
 Limited resection: e.g. ileocaecal
 Vitals + stool chart
 Stricturoplasty
 Daily examination
 Defunction distal disease c̄ temporary loop ileostomy
Improvement → oral therapy
 Switch to oral pred (40mg/d) Complications
 Stoma complications
No Improvement → rescue therapy  Enterocutaneous fistulae
 Discussion between pt, physician and surgeon  Anastomotic leak or stricture
 Medical: methotrexate ± infliximab
 Surgical Short gut
 <1-2m small bowel
 Features
 Steatorrhoea
 ADEK and B12 malabsorption
 Bile acid depletion → gallstones
 Hyperoxaluria → renal stones
 Rx
 Dietician
 Supplements or TPN
 Loperamide
Diverticular Disease
Definitions Mx of Acute Diverticulitis
 Diverticulum = out-pouching of tubular structure  Mild Attacks
 True = composed of complete wall (e.g. Meckel’s)  Can be treated at home c̄ bowel rest (fluids only)
 False = composed of mucosa only (pharyngeal, colonic) and augmentin ± metronidazole
 Diverticular disease: symptomatic diverticulosis  Admit if
 Diverticulitis: inflammation of diverticula  Unwell
 Fluids can’t be tolerated
 Pain can’t be controlled
Epidemiology
 Medical
 30% of Westerner’s have diverticulosis by 60yrs
 NBM
 F>M
 IV fluids
 Analgesia
Pathophysiology  Antibiotics: cefuroxime + metronidazole
 Assoc. c̄ ↑ intraluminal pressure  Most cases settle
 Low fibre diet: no osmotic effect to keep stool wet  Surgical
 Mucosa herniates through muscularis propria at points  Indications
of weakness where perforating arteries enter.  Perforation
 Most commonly located in sigmoid colon  Large haemorrhage
 Commoner in obese pts.  Stricture → obstruction
 Uniting factor in Saint’s Triad?  Procedure
 Hiatus Hernia  Hartmann’s to resect diseased bowel
 Cholelithiasis
 Diverticular disease Other Complications
Symptoms of Diverticular Disease Perforation
 Altered bowel habit ± left-sided colic  Sudden onset pain (± preceding diverticulitis)
 Relieved by defecation  Generalised peritonitis and shock
 Nausea  CXR: free air under diaphragm
 Flatulence  Rx: Hartmann’s
 Rx
 High fibre diet, mebeverine may help Haemorrhage
 Elective resection for chronic pain  Sudden, painless bright red PR bleed
 Ix: mesenteric angiography or colonoscopy
Diverticulitis  Rx
 Inspissated faeces → obstruction of diverticulum  Usually stops spontaneously
 Elderly pt. c̄ prev Hx of constipation  May need transfusion
 Colonoscopy ± diathermy / adrenaline
Presentation  Embolisation
 Abdominal pain and tenderness  Resection
 Typically LIF
 Localised peritonitis Abscess
 Pyrexia  Walled-off perforation
 Swinging fever
Ix  Localising signs: e.g. boggy rectal mass
 Bloods  Leukocytosis
 FBC: ↑WCC  Rx: Abx + CT/US-guided drainage
 ↑CRP/ESR
 Amylase Fistulae
 G+S/x-match  Enterocolic
 Imaging  Colovaginal
 Erect CXR: look for perforation  Colovesicular: pneumaturia + intractable UTIs
 AXR: fluid level / air in bowel wall  Rx: resection
 Contrast CT
 Gastrograffin enema Strictures
 Endoscopy  After diverticulitis, colon may heal c̄ fibrous strictures
 Flexi Sig  Rx
 Colonoscopy: not in acute attack O
 Resection (usually c̄ 1 anastomosis)
 Stenting
Hinchey Grading
1 Small confined pericolic abscesses Surgery rarely

needed
2 Large abscess extending into pelvis May resolve w/o
surgery
3 Generalised purulent peritonitis Surgery needed
4 Generalised faecal peritonitis Surgery needed
Bowel Obstruction: Causes and Investigation
Classification Presentation
 Simple  Abdominal Pain
 1 obstructing point + no vascular compromise  Colicky
 May be partial or complete  Central but level depends on gut region
 Closed Loop  Constant / localised pain suggests strangulation
 Bowel obstructed @ two points or impending perforation
 Left CRC c̄ competent ileocaecal valve  Distension
 Volvulus  ↑ c̄ lower obstructions
 Gross distension → perforation  Vomiting
 Strangulated  Early in high obstruction
 Compromised blood supply  Late or absent in low obstructions
 Localised, constant pain + peritonism  Absolute Constipation: flatus and faeces
 Fever + ↑WCC
Examination
Commonest Causes  ↑HR: hypovolaemia, strangulation
 Dehydration, hypovolaemia
SBO  Fever: suggests inflammatory disease or strangulation
 Adhesions: 60%  Surgical scars
 Hernia  Hernias
 Mass: neoplastic or inflammatory
LBO  Bowel sounds
 Colorectal Neoplasia: 60%  ↑: mechanical obstruction
 Diverticular stricture: 20%  ↓: ileus
 Volvulus: 5%  PR
 Empty rectum
 Rectal mass
Other Causes  Hard impacted stool
 Blood from higher pathology
Non-Mechanical = Paralytic Ileus (usually SB)
 Post-op Ix
 Peritonitis  Bloods
 Pancreatitis or any localised inflammation  FBC: ↑WCC
 Poisons / Drugs: anti-AChM (e.g. TCAs)  U+E: dehydration, electrolyte abnormalities
 Pseudo-obstruction  Amylase: ↑↑ if strangulation/perforation
 Metabolic: ↓K, ↓Na, ↓Mg, uraemia  VBG: ↑ lactate in strangulation
 Mesenteric ischaemia  G+S, clotting: may need surgery
 Imaging
Mechanical  Erect CXR
 Intraluminal  AXR: ± erect film for fluid levels
 Impacted matter: faeces, worms, bezoars  CT: can show transition point
 Intussusception  Gastrograffin studies
 Gallstones  Look for mechanical obstruction: no free flow
 Intramural  Follow through or enema
 Benign stricture  Follow through may relieve mild mechanical
 IBD obstruction: usually adhesional
 Surgery  Colonoscopy
 Ischaemic colitis  Can be used in some cases
 Diverticulitis  Risk of perforation
 Radiotherapy  May be used therapeutically to stent
 Neoplasia
 Congenital atresia AXR Findings
 Extramural
 Hernia SBO LBO
 Adhesions Diameter ≥3 ≥6cm (caecum ≥9)
 Volvulus (sigmoid, caecal, gastric) Location Central Peripheral
 Extrinsic Compression Markings Valvulae coniventes Haustra
 Pseudocyst - completely across - partially across
 Abscess LB Gas Absent Present
 Haematoma - not in rectum
 Tumour: e.g. ovarian No. of loops Many Few
 Congenital bands (e.g. Ladd’s) Fluid levels Many, short Few, long
Ileus
 Both small and large bowel may be visible
 No clear transition point
Bowel Obstruction: General Management
Medical Surgical
Resuscitate: “Drip and Suck” Indications
 NBM  Closed loop obstruction
 IV fluids: aggressive as pt. may be v. dehydrated  Obstructing neoplasm
 NGT: decompress upper GIT, stops vomiting, prevents  Strangulation / perforation → sepsis, peritonitis
aspiration  Failure of conservative Mx (up to 72h)
 Catheterise: monitor UO
Principals
Therapy  Aim to treat the cause
 Analgesia: may require strong opioid  Typically involves resection of the obstructing lesion
 Antibiotics: cef+met if strangulation or perforation  Colon has not been cleansed therefore most surgeons
 Gastrograffin study: oral or via NGT utilise a proximal ostomy post-resection.
 Consider need for parenteral nutrition  Pts. c̄ substantial comorbidity or unresectable tumours
may be offered bypass procedures.
Monitoring  Endoscopically placed expanding metal stents offer
 Regular clinical examination is necessary to ensure that palliation or a bridge to surgery allowing optimisation.
the pt. is not deteriorating.
 ↑ distension Procedures
 ↑ pain or tenderness  Must consent pt. for possible resection ± stoma
 ↑ HR/ ↑RR  SBO: adhesiolysis
 Repeat imaging and bloods  LBO
 Non-operative Mx successful in ~80% of pts. c̄ SBO  Hartmann’s
O
w/o peritonitis  Colectomy + 1 anastomosis + on table lavage
 Pts. c̄ LBO are more likely to need surgery.  Palliative bypass procedure
 Transverse loop colostomy or loop ileostomy
 Caecostomy

Bowel Obstruction: Specific Management
Sigmoid Volvulus (80% of volvulus) Paralytic Ileus
Pathophysiology Presentation
 Long mesentery c̄ narrow base predisposes to torsion  Adynamic bowel 2O to the absence of normal peristalsis
 Usually due to sigmoid elongation 2O to chronic  Usually SBO
constipation  Reduced or absent bowel sounds
 ↑ risk in neuropsych pts.: MS, PD, psychiatric  Mild abdominal pain: not colicky
 Disease or Rx interferes c̄ intestinal motility
 → closed loop obstruction Cause
 Post-op
Presentation  Peritonitis
 Commoner in males  Pancreatitis or any localised inflammation
 Often elderly, constipated, co-morbid pts.  Poisons / Drugs: anti-AChM (e.g. TCAs)
 Massive distension c̄ tympanic abdomen  Pseudo-obstruction
 Metabolic: ↓K, ↓Na, ↓Mg, uraemia
AXR  Mesenteric ischaemia
 Characteristic inverted U / coffee bean sign
Prevention
Mx  ↓ bowel handling
 Often relieved by sigmoidoscopy and flatus tube  Laparoscopic approach
insertion  Peritoneal lavage after peritonitis
 Monitor for signs of bowel ischaemia following  Unstarched gloves
decompression.
 Sigmoid colectomy occasionally required Mx
 Failed endoscopic decompression  Conservative “drip and suck” Mx
 Bowel necrosis  Correct any underlying causes
 Often recurs  elective sigmoidectomy may be needed  Drugs
 Metabolic abnormalities
 Consider need for parenteral nutrition
Caecal Volvulus  Exclude mechanical cause if protracted
 Assoc. c̄ congenital malformation where caecum is not
fixed in the RIF.
 Only ~10% of pts. can be detorsed c̄ colonoscopy
Colonic Pseudo-obstruction / Ogilvie’s Syn.
  typically requires surgery
Presentation
 Right hemi c̄ 1O ileocolic anastomosis
 Clinical signs of mechanical obstruction but no
 Caecostomy obstructing lesion found
 Usually distension only: no colic
Gastric Volvulus Cause

 Aetiology unknown
Triad of gastro-oesophageal obstruction  Assoc. c̄
 Vomiting → retching c̄ regurgitation of saliva  Elderly
 Pain  Cardiorespiratory disorders
 Failed attempts to pass an NGT  Pelvic surgery: e.g. hip arthroplasty
 Trauma
Risk Factors
 Congenital Ix
 Bands  Gastrograffin enema: exclude mechanical cause
 Rolling / Paraoesophageal hernia
 Pyloric stenosis Mx
 Acquired  Neostigmine: anti-cholinesterase
 Gastric / oesophageal surgery  Colonoscopic decompression: 80% successful
 Adhesions
Ix
 Gastric dilatation
 Double fluid level on erect films
Mx
 Endoscopic manipulation
 Emergency laparotomy

Colorectal Carcinoma: Pathology and Presentation
Epidemiology Pathology
 3rd commonest cancer  95% adenocarcinoma
 2nd commonest cause of cancer deaths (16,000/yr)  Others: lymphoma, GIST, carcinoid
 Age: peak in 60s  Location
 Sex: rectal Ca commoner in men  Rectum: 35%
 Geo: Western disease  Sigmoid: 25%
 Caecum and ascending colon: 20%
Pathophysiology  Transverse: 10%
 Descending: 5%
Colonic Adenomas  Proximal tumours: sessile or polypoid
 Benign precursors to CRC  Distal tumours: annular stenosing
 Characterised by dysplastic epithelium
 Classification Spread
 Tubular: small, pedunculated, tubular glands  Local
 Villous: large, sessile, covered by villi  Lymphatic
 Tubulovillous: mixture  Blood (liver, lungs)
 Presentation  Transcoelomic
 Typically asymptomatic
 Large polyps can bleed → IDA Presentation
 Villous adenomas can → ↓K + hypoproteinaemia
 Malignant potential Left
 ↑ size  Altered bowel habit
 ↑ dysplasia  PR mass (60%)
 ↑ villous component
 Obstruction (25%)
 Bleeding / mucus PR
APC et al.
 Tenesmus
 -ve regulator of β-catenin (component of WNT pathway)
 APC binds to and promotes degradation of β-catenin.
Right
 APC mutation → ↑ β-catenin → ↑ transcription of genes
 Anaemia
which promote cell proliferation.
 Wt. loss
 Proliferation → mutation of other genes which promote
 Abdominal pain
growth and prevent apoptosis
 KRAS (proto-oncogene)
Either
 p53 (TSG)
 Abdominal mass
Adenoma → Carcinoma Sequence  Perforation
1. First hit: mutation of one APC copy  Haemorrhage
2. Second hit: mutation of second APC copy  Fistula
 → adenoma formation
3. Additional mutations in adenoma → malignant Examination
transformation: e.g KRAS, p53  Palpable mass: per abdomen or PR
 Perianal fistulae
Other Aetiological Factors  Hepatomegaly
 Diet: ↓ fibre + ↑ refined carbohydrate  Anaemia
 IBD: CRC in 15% c̄ pancolitis for 20yrs  Signs of obstruction
 Familial: FAP, HNPCC, Peutz-Jeghers
 Smoking
 Genetics
 No relative: 1/50 CRC risk
st
 One 1 degree: 1/10
 NSAIDs / Aspirin (300mg/d): protective

Colorectal Carcinoma: Ix, Mx and Prevention
Ix Surgery
 Bloods  Use ERAS pathway
 FBC: Hb  Pre-operative bowel prep (except R sided lesions)
 LFTs: mets  E.g. Kleen Prep (Macrogol: osmotic laxative) the
 Tumour Marker: CEA (carcinoembryonic Ag) day before and phosphate enema in the AM.
 Imaging  Consent: discuss stomas
 CXR: lung mets  Stoma nurse consult for siting
 US liver: mets
 CT and MRI Principals
 Staging  Excision depends on lymphatic drainage which follows
 MRI best for rectal Ca and liver mets arterial supply.
 Endoanal US: staging rectal tumours  Mobility of bowel and blood supply at cut ends is also
 Ba / gastrograffin enema: apple-core lesion important.
 Endoscopy + Biopsy  Hartmann’s often used if obstruction.
 Flexi sig: 65% of tumours accessible  Laparoscopic approach is the standard of care
 Colonoscopy
Rectal Ca
 Neo-adjuvant radiotherapy may be used to ↓ local
Staging recurrence and ↑5ys
 Anterior resection: tumour 4-5cm from anal verge
Dukes (Sir Cuthbert Dukes: St. Mary’s Pathologist)  Defunction c̄ loop ileostomy
 AP resection: <4cm from anal verge
Spread % 5ys  + Total mesorectal excision for tumours of the middle
A Confined to bowel wall 90 and lower third.
B Through bowel wall but no LNs 60  Aims to ↓ recurrence
C Regional LNs 30  ↑ anastomotic leak and faecal incontinence
D Distant mets <10
Other Tumours
TNM  Sigmoid: high anterior resection or sigmoid colectomy
 TIS: carcinoma in situ  Left: left hemicolectomy
 T1: submucosa  Transverse: extended right hemicolectomy
 T2: muscularis propria  Caecal / right: right hemicolectomy
 T3: subserosa
 T4: through the serosa to adjacent organs
 N1: 1-3 nodes Other Rx
 N2: >4 nodes  Local excision: e.g. Transanal Endoscopic Microsurg
 Bypass surgery: palliation
 Hepatic resection: if single lobe mets only
Grading  Stenting: palliation or bridge to surgery in obstruction
 Grading from low to high  Chemo
 Based on cell morphology  Adjuvant 5-FU for Dukes’ C ↓ mortality by 25%
 Dysplasia, mitotic index, hyperchromatism  i.e. LN +ve pts.
 High grade tumour
 Palliation of metastatic disease
Mx
 Manage in an MDT
 Confirmation of Dx NHS Screening for CRC
 Stage c̄ CT or MRI
 60% amenable to radical surgery FOB Testing
 Introduced in 2006
 60-75yrs
 Home FOB testing every 2yrs: ~1/50 have +ve FOB
 Colonoscopy if +ve: ~1/10 have Ca
 Lindholm et al. BJS 2008
 Screening ↓ risk of dying from CRC by 25%
Flexi Sig
 Introduced in 2011/12
 55-60yrs
 Once only flexi Sig
 Atkin et al. Lancet 2010
 ↓ CRC incidence by 33%
 ↓ CRC mortality by 43%

Familial CRC Syndromes GI Polyps
Familial Adenomatous Polyposis Inflammatory Pseudopolyps
 Autosomal dominant  Regenerating islands of mucosa in UC
 APC gene on 5q21
Hyperplastic Polyps
Presentation  Piling up of goblet cells and absorptive cells
 100-1000s of adenomas by ~16yrs  Serrated surface architecture
 Mainly in large bowel  No malignant potential
 Also stomach and duodenum (near ampulla)
 100% develop CRC, often by ~40yrs Hamartomatous
 May be assoc. c̄ congenital hypertrophy of the retinal  Tumour-like growths composed of tissues present at
pigment epithelium (CHPRE) site where they develop.
 Sporadic or part of familial syndromes
Variants  Juvenile polyp: solitary hamartoma in children
 Attenuated FAP: <100 adenomas, later CRC (>50yrs)  “Cherry on a stalk”
 Gardener’s (TODE)
 Thyroid tumours Neoplastic
 Osteomas of the mandible, skull and long bones  Tubular or Villous adenomas
 Dental abnormalities: supernumerary teeth  Usually asympto
 Epidermal cysts  May have blood / mucus PR, tenesmus
 Turcot’s: CNS tumours: medullo- and glio-blastomas
Mx Other Hamartomatous Polyposis Syndromes

 Prophylactic colectomy before 20yrs
 Total colectomy + IRA Juvenile Polyposis
 Requires life-long stump surveillance  Autosomal dominant
 Proctocolectomy + IPAA  >10 hamartomatous polyps
 Remain @ risk of Ca in stomach and duodenum  ↑ CRC risk: need surveillance and polypectomy
 Regular endoscopic screening
Cowden Syndrome
 Auto dominant
Hereditary Non-Polyposis Colorectal Cancer  Macrocephaly + skin stigmata
 Autosomal dominant  Intestinal hamartomas
 Mutation of mismatch repair enzymes  ↑ risk of extra-intestinal Ca
 E.g. MSH2 on Chr 2p
 Commonest cause of hereditary CRC: 3% of all CRC
Presentation
 Lynch 1: right sided CRC
 Lynch 2: CRC + gastric, endometrial, prostate, breast
Dx: “3, 2, 1, rule”

 ≥3 family members over 2 generations c̄ one <50yrs
Peutz-Jeghers Syndrome
 Autosomal dominant
 STK11 mutation
Presentation
 ~ 10-15yrs
 Mucocutaneous hyperpigmentation
 Macules on palms, buccal mucosa
 Multiple GI hamartomatous polyps
 Intussusception
 Haemorrhage
 ↑ Ca risk
 CRC, pancreas, breast, lung, ovaries, uterus

Mesenteric Ischaemia Lower GI Bleed
Acute Causes
Causes Common / Important

 Arterial: thrombotic (35%), embolic (35%)  Rectal: haemorrhoids, fissure
 Non-occlusive (20%)  Diverticulitis
 Splanchnic vasoconstriction: e.g. 2O to shock  Neoplasm
 Venous thrombosis (5%)
 Other: trauma, vasculitis, strangulation Other
 Inflammation: IBD
Presentation  Infection: shigella, campylobacter, C. diff
 Nearly always small bowel  Polyps
 Triad  Large upper GI bleed (15% of lower GI bleeds)
 Acute severe abdominal pain ± PR bleed  Angio: dysplasia, ischaemic colitis, HHT
 Rapid hypovolaemia → shock
 No abdominal signs Ix
 Degree of illness >> clinical signs  Bloods: FBC, U+E, LFT, x-match, clotting, amylase
 May be in AF  Stool: MCS
 Imaging
Ix  AXR, erect CXR
 Bloods  Angiography: necessary if no source on endoscopy
 ↑Hb: plasma loss  Red cell scan
 ↑WCC  Endoscopy
 ↑ amylase  1st: Rigid proctoscopy / sigmoidoscopy
 Persistent metabolic acidosis: ↑lactate  2nd: OGD
 Imaging  3rd: Colonoscopy: difficult in major bleeding
 AXR: gasless abdomen
 Arteriography / CT/MRI angio Mx
 Resuscitate
Complications  Urinary catheter
 Septic peritonitis  Abx: if evidence of sepsis or perf
 SIRS → MODS  PPI: if upper GI bleed possible
 Keep bed bound: need to pass stool may be large bleed
Mx
→ collapse
 Fluids
 Stool chart
 Abx: gent + met
 Diet: keep on clear fluids (allows colonoscopy)
 LMWH
 Surgery: only if unremitting, massive bleed
 Laparotomy: resect necrotic bowel
Chronic Small Bowel Ischaemia Angiodysplasia

 Cause: atheroma + low flow state (e.g. LVF)  Submucosal AV malformations
 Presentation:  70-90% occur in right colon
 Severe, colicky post-prandial abdo pain
 Can affect anywhere in GIT
 “gut claudication”
 PR bleeding
Presentation
 Malabsorption
 Elderly
 Wt. loss
 Fresh PR bleeding
 Mx: angioplasty
Ix
Chronic Large Bowel Ischaemia  Exclude other Dx
 Cause: follows low flow in IMA territory  PR exam
 Presentation  Ba enema
 Lower, left-sided abdominal pain  Colonoscopy
 Bloody diarrhoea  Mesenteric angiography or CT angiography
 Pyrexia  Tc-labelled RBC scan: identify active bleeding
 Tachycardia
 Ix Rx
 ↑WCC  Embolisation
 Ba enema: thumb-printing  Endoscopic laser electrocoagulation
 MR angiography
 Resection
 Complications
 May → peritonitis and septic shock
 Strictures in the long-term
 Mx
 Usually conservative: fluids and Abx
 Angioplasty and endovascular stenting
Perianal Surgery
Contents
Key Anatomy ............................................................................................................................................................................... 59
Minor Anal Conditions ................................................................................................................................................................. 59
Haemorrhoids .............................................................................................................................................................................. 60
Anal Fissure ................................................................................................................................................................................. 61
Fistula in Ano ............................................................................................................................................................................... 61
Peri-anal Sepsis / Abscess .......................................................................................................................................................... 62
Pilonidal Sinus ............................................................................................................................................................................. 62
Anal Carcinoma ........................................................................................................................................................................... 63
Rectal Prolapse ........................................................................................................................................................................... 63

Key Anatomy Minor Anal Conditions
Rectum Perianal Haematoma
 12cm
 Sacral promontory to levator ani muscle Definition
 The 3 tenia coli fuse around the rectum to form a  Subcutaneous bleeding from a burst venule caused by
continuous muscle layer. straining or the passage of hard stool.
 Also called an external pile: a misnomer
Anal Canal
 4cm Presentation
 Levator ani muscle to anal verge  Tender blue lump at the anal margin
 Upper 2/3 of canal  Pain worsened by defecation or movement
 Lined by columnar epithelium
 Insensate Rx
 Sup. rectal artery and vein  Analgesia + spontaneous resolution
 Internal iliac nodes  Evacuation under LA
 Lower 1/3 of canal
 Lined by squamous epithelium
 Sensate Proctalgia Fugax
 Middle and inf. rectal arteries and veins  Young, anxious men
 Superficial inguinal nodes  Crampy anorectal pain, worse @ night
 Dentate line = squamomucosal junction  Unrelated to defecation
 White line = where anal canal becomes true skin  Assoc. c̄ trigeminal neuralgia
 Rx
 Reassurance
Anal Sphincters  GTN cream
Internal
 Thickening of rectal smooth muscle Perineal Warts
 Involuntary control
 Commonly seen in MSM
 Condylomata accuminata
External
 HPV
 Three rings of skeletal muscle
 Rx: podophyllin paint, cryo, surgical excision
 Deep
 Condylomata lata
 Superficial
 Syphilis
 Subcutaneous
 Rx: penicillin
 Voluntary control
Anorectal Ring
 Deep segment of external sphincter which is continuous
Pruritis Ani
c̄ puboretalis muscle (part of levator ani)  50% idiopathic
 Poor hygiene
 Palpable on PR ~5cm from the anus
 Haemorrhoids
 Demarcates junction between anal canal and rectum.
 Anal fissure
 Must be preserved to maintain continence
 Anal fistula
 Fungi, worms
 Crohn’s
 Neoplasia

Haemorrhoids
Definition Symptoms
 Disrupted and dilated anal cushions  Fresh painless PR bleeding
 Bright red
Pathophysiology  On paper, on stool, may drip into pan
 Anal cushion: mass of spongy vascular tissue  Pruritis ani
 Positioned @ 3, 7 and 11 O’clock  Lump in perianal area
 Where the three major arteries that feed the  Severe pain = thrombosis
vascular plexuses enter the anal canal
 Gravity, straining → engorgement and enlargement of Examination
anal cushions  Full abdo exam, palpating for masses
 Hard stool disrupts connective tissue around cushions.  Inspect perianal area: masses, recent bleeding
 Cushions protrude and can be damaged by hard stool  DRE: can’t palpate piles unless thrombosed
 → bright red (capillary) bleeding.  Rigid sig to identify higher rectal pathology
 Haemorrhoids arise above dentate line  not painful  Proctoscopy (also allows Rx)
 May be gripped by anal sphincter → thrombosis
 Strangulated piles are acutely painful Differential
 May ulcerate or infarct  Perianal haematoma
 Fissure
Causes  Abscess
 Constipation c̄ prolonged straining  Tumour (must exclude in all cases)
 Venous congestion may contribute
 Pregnancy Mx
 Abdominal tumour
 Portal HTN Conservative
 ↑ fibre and fluid intake
Classification  Stop straining @ stool
 1st degree: never prolapse
 2nd: prolapse on defecation but spontaneously reduce Medical
 3rd: prolapse on defecation but require digital reduction  Topical preparations
 4th: remain permanently prolapsed  Anusol: hydrocortisone
 Topical analgesics
 Laxatives: lactulose, Fybogel
Interventional
 Injection c̄ sclerosant (5% phenol in Almond oil)
 Injection above dentate line
 SE: impotence, prostatitis
 Barron’s banding → thrombosis and separation
 SE: bleeding, infection
 Cryotherapy
 SE: watery discharge post-procedure
 Infra-red coagulation
Surgical: Haemorrhoidectomy
 Excision of piles + ligation of vascular pedicles
 Lactulose + metronidazole 1wk pre-op
 Discharge c̄ laxatives post-op
 SE: bleeding, stenosis
Mx of Thrombosed Piles
 Analgesia
 Ice-packs
 Stool softeners
 Bed rest c̄ elevated foot of bed
 Pain usually resolves in 2-3wks
 Haemorrhoidectomy is not usually necessary

Anal Fissure Fistula in Ano
Definition Definition
 Tear of squamous epithelial lining in lower anal canal  Abnormal connection between ano-rectal canal and the
skin.
Causes
 Mostly trauma 2O to the passage of hard stool Pathogenesis
 Assoc. c̄ constipation  Usually occur 2O to perinanal sepsis
 Spasm of internal anal sphincter contributes to  Blockage of intramuscular glands → abscess
pain and → ischaemia + poor healing  Abscess discharges to form a fistula
 Commoner in women  Associations
 Rarer causes, often → multiple ± lateral fissures  Crohn’s
 Crohn’s  Diverticular disease
 Herpes  Rectal Ca
 Anal Ca  Immunosuppression
Presentation Classification
 Intense anal pain  High: cross sphincter muscles above dentate line
 Especially on defecation  Low: don’t cross sphincter muscles above dentate line
 May prevent pt. from passing stools
 Fresh rectal bleeding Goodsall’s Rule
 On paper mostly  Determines path of fistula tract
 Fistula anterior to anus track in a straight line (radial)
Examination  Fistula posterior to anus always have internal opening
 PR often impossible at the 6 o’clock position → curved track
 Midline ulcer is seen
Anterior
 Usually posterior @ 6 O’clock
 May be anterior
 May be a mucosal tag – sentinel pile
 Usually posterior @ 6 O’clock
 Groin LNs suggest complicating factor: e.g. HIV
Mx
 If fissure recurrent, chronic or difficult to Rx the patient
requires EUA.
Conservative
 Soaks in warm bath Posterior
 Toileting advice
 Dietary advice: ↑ fibre and fluids
Presentation
Medical  Persistent anal discharge
 Laxatives: lactulose + fybogel  Perianal pain or discomfort
 Topical → resolution in 75%
 Lignocaine Examination
 GTN  May visualise external opening: may be pus
 Diltiazem  Induration around the fistula on DRE
 Botulinum injection  Proctosopy may reveal internal opening
Surgical: Lateral partial sphincterotomy Ix

 Division of internal anal sphincter @ 3 O’clock  MRI
 Pre-op anorectal US and mannometry  Endoanal US
 Complications
 Minor faecal/flatus incontinence (= GTN)
 Perianal abscess
Rx
 Extent of fistula must first be delineated by probing the
NB. Lord’s operation (anal dilatation under anaesthesia) is no fistula @ EUA
longer used due to high rates of incontinence.
Low Fistula
 Fistulotomy and excision
 Laid open to heal by 2O intention
High Fistula
 Fistulotomy could damage the anorectal ring
 Suture – a seton – passed through fistula and gradually
tightened over months
 Stimulates fibrosis of tract
© Alasdair Scott, 2012
 Scar tissue holds sphincter together 61
Peri-anal Sepsis / Abscess Pilonidal Sinus
Pathogenesis Definition
 Anal gland blockage → infection → abscess  Pilonidal: lat “nest of hair”
 E.g. coli, bacteroides  Sinus: blind ending tract, lined by epithelial or
 May develop from skin infections granulation tissue, which opens onto an epithelial
 E.g. sebaceous gland or hair follicle surface.
 Staphs
Pathophysiology
Associations  Hair works its way beneath skin → foreign body
 Crohn’s reaction → formation of abscess
 DM  Usually occur in the natal cleft.
 Malignancy
Risk Factors
Classification  M>F=4:1
 Perianal: 45%  Geo: Mediterranean, Middle east, Asians
 Discrete local red swelling close to the anal verge  Often overweight c̄ poor personal hygiene
 Ischiorectal: ≤30%  Occupations c̄ lots of sitting: e.g. truck drivers
 Systemic upset
 Extremely painful on DRE Presentation
 Interphincteric / intermuscular: >20%  Persistent discharge of purulent or clear fluid
 Pelvirectal / supralevator: ~5%  Recurrent pain
 Systemic upset
 Abscesses
 Bladder irritation
Presentation Rx
 Throbbing perianal pain
Conservative
 Worse on sitting
 Hygiene advice
 Occasionally a purulent anal discharge
 Shave / remove hair from affected area
Examination Surgical
 Perianal mass or cellulitic area  Incision and drainage of abscesses
 Fluctuant mass on PR  Elective sinus excision
 Septic signs: fever, tachycardia  Methylene blue to outline tract
 Recurrence in 4-15%
Rx
 Abx may suffice if Rx instigated v. early in course
 Most cases require EUA c̄ I&D
 Wound packed
 Heals by 2O intention
 Daily dressing for 7-10d
 Look for an anal fistula which complicates ~30% of
abscesses.

Anal Carcinoma Rectal Prolapse
Epidemiology Definition
 Relatively uncommon: 250-300 cases/yr in the UK  Protrusion of rectal tissue through the anal canal.
Pathology Classification
 80% SCCs
 Others: melanomas, adenocarcinomas Type 1: Mucosal Prolapse
 Anal Margin tumours  Partial prolapse of redundant mucosa
 Well differentiated keratinising lesions  Common in children: esp. c̄ CF
 Commoner in men  Essentially large piles  same Rx
 Good prognosis
 Anal Canal tumours Type 2: Full Thickness Prolapse
 Arise above dentate line  Commoner cf. type 1
 Poorly differentiated, non-keratinising  Usually elderly females c̄ poor O&G Hx
 Commoner in women
 Worse prognosis
Presentation
 Spread
 Mass extrudes from rectum on defecation
 Above dentate line → internal iliac nodes
 May reduce spontaneously or require manual
 Below dentate line → inguinal nodes
reduction
 May become oedematous and ulcerated
Aetiology  → pain and bleeding
 HPV (16, 18, 31, 33) is important factor  Faecal soiling
 ↑ incidence in MSM  Assoc. c̄ vaginal prolapse and urinary incontinence
 ↑ incidence if perianal warts
Presentation Examination
 Visible prolapse: brought out on straining
 Perianal pain and bleeding
 ± excoriation and ulceration
 Pruritis ani
 ↓ sphincter tone on PR
 Faecal incontinence
 Assoc. uterovaginal prolapse
 70% have sphincter involvement @ presentation
 May → rectovaginal fistula
Ix
Examination  Sigmoidoscopy to exclude proximal lesions
 Anal manometry
 Palpable lesion in only 25%
 Endoanal US
 ± palpable inguinal nodes
 MRI
Ix
 ↓ Hb (ACD)
Rx
 Endoanal US
Partial Prolapse
 Rectal EUA + biopsy
 Phenol injection
 CT / MRI: assess pelvic spread
 Rubber band ligation
 Surgery: Delorme’s Procedure
Rx
 Chemoradiotherapy: most pts Complete Prolapse
 50% 5ys  Conservative
 Surgery: reserved for  Pelvic floor exercises
 Tumours that fail to respond to radiotherapy  Stool softeners
 GI obstruction  Surgery
 Small anal margin tumours w/o sphincter  Abdominal Approach: Rectopexy
involvement  Lap or open
 Mobilised rectum fixed to sacrum c̄ mesh
 Perineal Approach: Delorme’s Procedure
 Resect mucosa and suture the two
mucosal boundaries.

Hernias
Contents
Hernia Definitions ........................................................................................................................................................................ 65
Inguinal Hernia ............................................................................................................................................................................ 66
Femoral Hernia ............................................................................................................................................................................ 67
Incisional Hernia .......................................................................................................................................................................... 67
Other Hernia Types ..................................................................................................................................................................... 68

Hernia Definitions
Term Definition
Hernia Protrusion of a viscus or part of a viscus through the walls of its containing cavity into an abnormal position.
Reducible Sac can return to the abdominal cavity either spontaneously or c̄ manipulation.
Irreducible Sac cannot be reduced despite pressure or manipulation.
Strangulated Blood supply of contents is compromised due to pressure at the neck of the hernia.
Sliding hernia Part of the sac is formed by bowel (e.g. caecum or sigmoid): take care when excising the sac.
Maydl’s hernia Herniating double loop of bowel. Strangulated portion may reside as a single loop inside the abdomen.
Littre’s hernia Hernial sac containing strangulated Meckel’s diverticulum.
Amyand’s Inguinal hernia containing strangulated Appendix
Richter’s Only part of circumference of bowel is within sac

Most commonly seen with femoral hernias.
Can strangulate w/o obstructing.
Pantaloon Simultaneous direct and indirect hernia.
Herniotomy Excision of hernial sac

Herniorrhaphy Suture repair of hernial defect
Hernioplasty Mesh repair of hernial defect

Inguinal Hernia
Epidemiology Clinical Features
 3% of adults will require hernioplasty
 ~4% of male neonates have hernia (↑ c̄ prems) Children
 M>>F = 9:1 (descent of testes)  Lump in groin which may descend into scrotum
 Majority present in 50s.  Exacerbated by crying
 Commonly obstruct
Adults
Pathology
 Lump in groin, exacerbated by straining/cough
 Commoner on R (?damage to ilioinguinal N. @
 May be clear ppting event: e.g. heavy lifting
appendicectomy → muscle weakness)
 Dragging pain radiating to groin
 5% bilateral
 May present c̄ obstruction/strangulation
 8-15% present as emergency c̄ strangulation/obstruction
Questions
 Reducible?
Aetiology  Ever episodes of obstruction / strangulation?
 Predisposing factors: cough, straining, lifting?
Congenital: patent processus vaginalis  Occupation and social circumstances?
 Processus vaginalis should obliterate following descent of
the testes.
 If it stays patent it may fill with
 Fluid → hydrocele Mx
 Bowel/omentum → indirect hernia
Non-surgical
Acquired: mainly things which ↑IAP  Rx RFs: cough, constipation
 Chronic cough: COPD, asthma  Lose weight
 Prostatism  Truss
 Constipation
 Severe muscular effort: e.g. heavy lifting Surgical
 Previous incision/repair  Tension-free mesh (e.g. Lichtenstein repair) better
cf. suture repair (e.g. Shouldice repair)
 Ascites / obesity
 Recurrence < 2% vs. 10%
 Appendicectomy
 Open approach can be done under LA or GA
 Lap approach allows bilateral repair and improved
cosmesis. Also preferred for recurrent hernias.
Classification  1O unilateral repairs should be open (NICE)
 Children only require sac excision (herniotomy)
Indirect
 80%: commoner in young Complications
 Congenital patent processus vaginalis  Early
 Emerge through deep ring  Haematoma / seroma formation: 10%
 Same 3 coverings as cord and descend into the scrotum  Intra-abdominal injury (lap)
 Can strangulate  Infection: 1%
 Urinary retention
Direct  Late
 20%: commoner in elderly  Recurrence (<2%)
 Acquired  Ischaemic orchitis: 0.5%
 Emerge through Hesselbach’s triangle  Chronic groin pain / paraesthesia: 5%
 Can acquire internal and external spermatic fascia
 Rarely descend into scrotum
 Rarely strangulate
Ix
 US if Dx in doubt

Femoral Hernia Incisional Hernia
 Protrusion of viscus through the femoral canal  Hernia arises through a previously acquired defect
Epidemiology Epidemiology
 F>M  6% of surgical incisions
 Inguinal hernias still more common in F
 Middle aged and elderly
Risk Factors
Aetiology Pre-operative
 Acquired: ↑ intra-abdominal pressure  ↑ age
 Femoral canal larger in females due to shape of pelvis  Obesity or malnutrition
and changes in its configuration due to childbirth  Comorbidities: DM, renal failure, malignancy
 Drugs: steroids, chemo, radio
Clinical features Intra-operative

 Surgical technique/skill (major factor)
Painless groin lump  Too small suture bites
 Neck inferior (and lateral) to the pubic tubercle.  Inappropriate suture material
 Cough impulse.  Incision type (e.g. midline)
 Often irreducible (tight boarders)  Placing drains through wounds
Commonly present c̄ obstruction or strangulation Post-operative

 Tender, red and hot  ↑ IAP: chronic cough, straining, post-op ileus
 Abdo pain, distension, vomiting, constipation  Infection
 Haematoma
Mx
 50% risk of strangulation w/i 1mo
Mx
 Urgent surgery  Surgery is not appropriate for all patients.
 Must balance risk of operation and recurrence c̄ risk of
Elective: Lockwood Approach obstruction / strangulation and pt. choice.
 Low incision over hernia c̄ herniotomy and  Usually broad-necked  low risk of strangulation
herniorrhaphy (suture ing. ligt. to pectineal ligt.)
Conservative
Emergency: McEvedy Approach  Manage RFs: e.g. constipation, cough
 High approach in inguinal region to allow inspection and  Weight loss
resection of non-viable bowel.  Elasticated corset or truss
 Then herniotomy and herniorrhaphy
Surgical
 Pre-Op
 Optimise cardiorespiratory function
 Encourage wt. loss
 Nylon mesh repair: open or lap

Other Hernia Types
Umbilical Features Management
 Congenital  Usually resolves by 2-3yrs
 3% of LBs  Mesh repair if no closure.
 Defect in the umbilical scar  Can recur in adults: pregnancy or gross ascites
Risk Factors
 Afro-Caribbean
 Trisomy 21
 Congenital hypothyroidism
Paraumbilical Features Management

 Acquired: middle aged obese men  Mayo (double-breast linea alba c̄ sutures) /
 Defect through linea alba just above or below mesh repair
umbilicus
 Small defect  strangulation (often omentum)
Risk Factors
 Chronic cough
 Straining
Epigastric Features Management

 Young M >F  Mesh repair
 Pea-sized swelling caused by defect in linea
alba above the umbilicus.
 Usually contains omentum: can strangulate
Spigelian Features
 Hernia through linea semilunaris
 Hernia lies between layers of abdo wall
 Palpable mass more likely to be colon Ca
Obturator Features
 Old aged F>M
 Sac protrudes through obturator foramen
 Pain on inner aspect of thigh or knee
 Frequently present obstructed / strangulated
Lumbar Features
 Middle-aged M>F
 Typically follow loin incisions
 Hernias through sup./inf. lumbar triangles
Sciatic Features
 Hernia through lesser sciatic foramen
 Usually presents as SBO + gluteal mass
Gluteal Features
 Hernia through greater sciatic foramen
 Usually presents as SBO + gluteal mass

Superficial Lesions
Contents
Skin Lumps .................................................................................................................................................................................. 70
Malignant and Pre-malignant Skin Lesions ................................................................................................................................. 72
Neck Lumps: General Approach ................................................................................................................................................. 73
Anterior Triangle Lumps .............................................................................................................................................................. 73
Midline Neck Lumps .................................................................................................................................................................... 74
Posterior Triangle Lumps ............................................................................................................................................................ 74
Cervical Lymphadenopathy ......................................................................................................................................................... 75
Hypertrophic and Keloid Scars .................................................................................................................................................... 75
Thyroid Lumps ............................................................................................................................................................................. 76
Benign Thyroid Disease .............................................................................................................................................................. 77
Malignant Thyroid Disease .......................................................................................................................................................... 78
Salivary Glands ........................................................................................................................................................................... 79

Skin Lumps
Lump Pathology Features Viva Mx
Lipoma Benign tumour of mature adipocytes Inspection Occur anywhere fat can expand Dercum’s Disease / Adiposis Non-surgical
- i.e. NOT scalp or palms dolorosa
Sarcomatous change probably doesn’t - inc. spermatic cord, submucosa - Multiple, painful lipomas Surgical Excision
occur. - Assoc. peripheral neuropathy
May be a scar from recurrence - Obese postmen women
Liposarcomas arise de novo
- Older pts. Familial Multiple Lipomatosis
- Deeper tissues of the lower limbs Palpation Soft
Subcutaneous Madelung’s Disease
Imprecise margin
Fluctuant Bannayan-Zonana Syndrome
- Multiple lipomas
- Macrocephaly
- Haemangiomas
Sebaceous Epithelial-lined cyst containing keratin Inspection Occur @ sites of hair growth Complications Non-surgical
cyst - Scalp, face, neck, chest and back - Infection: pus discharge
Two histological subtypes - NOT soles or palms - Ulceration Surgical Excision
Central Punctum - Calcification
1) Epidermal Cyst
- Arise from hair follicle Cock’s Peculiar Tumour
infundibulum - Large ulcerating trichilemmal cyst
Palpation Firm on the scalp
2) Trichilemmal Cyst / Wen Smooth - Resemble an SCC
- Arise from hair follicle epithelium Intradermal
- Often multiple Gardener’s Syndrome: FAP +
- May be autosomal dominant - Thyroid tumours
- Osteomas
- Dental abnormalities
- Epidermal cysts
Ganglion Cystic swelling related to a synovial Inspection Can be found anywhere Differential Non-Surgical
lined structures: joint, tendon 90% on dorsum of hand or wrist - Bursae - Aspiration followed by
Dorsum of ankle - Cystic protrusion from synovial 3wks of immobilisation
Myxoid degeneration of fibrous tissue May be scar from recurrence cavity of arthritic joint.
Weakly transilluminable Surgical Excision
Contain thick, gelatinous material - Recurrence can be 50%
Palpation Soft - Neurovascular damage
Subcutaneous
May be tethered to tendon
Seborrheic Benign hyperplasia of basal epithelial Stuck on appearance Non-surgical
keratosis layer Dark brown
- Hyperkeratosis: keratin layer Greasy
thickening
- Acanthosis: prickle layer thickening
Lump Pathology Features Viva Mx
Neurofibroma Benign nerve sheath tumour arising Inspection Solitary or multiple NF 1: von Recklinghausen’s Surgical excision only
from schwann cells. Pedunculated nodules - AD, Chr 17 indicated if malignant
- Cafe-au-lait spots (>6) growth suspected.
Palpation Fleshy consistency - Freckling
Pressure can → paraesthesia - Neurofibromas Local regrowth is common
Extras Examine the eyes - Lisch nodules (iris)
Examine the axilla
Examine the cranial nerves (esp. 8)
BP
Papilloma Overgrowth of all layers of the skin c̄ a Skin tag / fibroepithelial polyp Excision + diathermy to
central vascular core. control bleeding.
Pedunculated
Flesh coloured
Pyogenic Rapidly growing capillary Inspection Most commonly on hands, face, gums Possible assoc. c̄ prev trauma Non-surgical
granuloma haemangioma. and lips. More common in pregnancy - regression is uncommon
Bright red hemispherical nodule
Neither pyogenic, nor a granuloma May have serous / purulent discharge Surgical
Palpation Soft - curettage c̄ diathermy of
Bleed very easily the bases
Dermoid Cyst Epidermal-lined cyst deep to the skin Inspection Smooth spherical swelling Child / young adult: congenital Congenital
Sites of embryological fusion - CT to establish extent
Congenital / Inclusion Cysts Scar from recurrence Adult: congenital - Surgical excision
- Developmental inclusion of - Ask re. trauma
epidermis along lines of skin fusion Acquired
- Midline of neck and nose - Surgical excision
- Medial and lateral ends of eyebrows Palpation Soft
Non-tender
Acquired / Implantation Cyst Subcutaneous
- Implantation of epidermis in dermis
- Often 2O to trauma (e.g. piercing)
Dermato- Benign neoplasm of dermal fibroblasts Inspection Can occur anywhere Differential Excision + histology
fibroma Mostly on the lower limbs of young to - Malignancy: melanoma, BCC
middle-aged women
Small, brown pigmented nodule

Palpation Firm, woody feel: characteristic
Intradermal: mobile over deep tissue
Kerato- Benign overgrowth of hair follicle cells Fast-growing Regress w/i 6wks
acanthoma Cytologically similar to well- Dome-shaped c̄ a keratin plug Excise to reduce scarring
differentiated SCCs Intradermal and obtain histology

Malignant and Pre-malignant Skin Lesions
Malignant Melanoma Poor prognostic indicators
 Male sex (more tumours on trunk cf. females)
Epidemiology  ↑ mitoses
 F>M = 1.5:1 Satellite lesions (lymphatic spread)
 UK incidence = 10 000/yr and 2000 deaths/yr Squamous Cell Carcinoma
 ↑80% in 20yrs  Ulcerated lesion c̄ hard, raised everted edges
 Sun exposed areas
Features
 Asymetry Causes
 Boarder: irregular  Sun exposure: scalp, face, ears, lower leg
 Colour: non-uniform  May arise in chronic ulcers: Marjolin’s Ulcer
 Diameter >6mm  Xeroderma pigmentosa
 Evolving / Elevation
Evolution
Risk Factors  Solar/actinic keratosis → Bowen’s → SCC
 Sunlight: esp. intense exposure in early years.  Lymph node spread is rare
 Fair skinned (low Fitzpatrick skin type)
 ↑ no. of common moles Rx
 +ve FH  Excision + radiotherapy to affected nodes
 ↑ age
 Immunosuppression
Actinic Keratoses
Classification  Irregular, crusty warty lesions.
 Superficial Spreading: 80%  Pre-malignant (~1%/yr)
 Irregular boarders, colour variation
 Commonest in Caucasians Rx
 Grow slowly, metastasise late = better prognosis  Cautery
 Lentigo Maligna Melanoma  Cryo
 Often elderly pts.
 5-FU
 Face or scalp
 Imiquimod
 Acral Lentiginous
 Photodynamic phototherapy
 Asians/blacks
 Palms, soles, subungual (c̄ Hutchinson’s sign)
 Nodular Melanoma
 All sites
Bowen’s Disease
 Younger age, new lesion  Red/brown scaly plaques
 Invade deeply and metastasis early = poor prog  Typically on the legs of older women
 Amelanotic  SCC in situ
 Atypical appearance → delayed Dx
Rx
Staging and Prognosis  As for AKs
 Breslow Depth
 Thickness of tumour to deepest point of dermal
invasion Basal Cell Carcinoma
 <1mm = >75% 5ys  Commonest cancer
 >4mm = 50% 5ys  Pearly nodule c̄ rolled telangiectactic edge
 Clark’s Staging  May ulcerate
 Stratifies depth by 5 anatomical levels  Typically on face in sun-exposed area
 Stage 1: Epidermis  Above line from tragus → angle of mouth
 Stage 5: sc fat
Behaviour
Metastasis  Low-grade malignancy → very rarely metastasise
 Liver  Locally invasive
 Eye
Rx
Mx  Excision
O
 Excision + 2 margin excision depending on Bres depth  Mohs: complete circumferential margin
 ± lymphadenectomy assessment using frozen section histology
 ± adjuvant chemo (may use isolated limb perfusion)  Cryo/radio may be used.

Neck Lumps: General Approach Anterior Triangle Lumps
Diagnosis Branchial Cysts
 85% of neck lumps are LNs: esp. if present < 3wks  Embryological remnant 2nd branchial cleft
 Infection: EBV, tonsillitis, HIV
 Ca: lymphoma or mets Presentation
 8% are goitres  Age <20yrs
 7% other: e.g. sebaceous cyst or lipoma  Ant. margin of SCM at junction of upper and middle 3rd
 May become infected → abscess
Ix: Triple Assessment  May be assoc. c̄ branchial fistula
 Clinical assessment
 Imaging: US Pathology
 Cyto/Histo: aspiration or biopsy  Lined by squamous epithelium
 Contain “glary” fluid c̄ cholesterol crystals
Anterior triangle Rx
 Ant. margin of SCM
 Med
 Midline  Abx for infection
 Ramus of the mandible  Sclerotherapy c̄ OK-432 can be used
 Roof: investing fascia  Surgical excision
 Floor: pre-vertebral fascia  Definitive Rx
 May be difficult due to proximity of carotids
Causes
 Pulsatile
 Carotid artery aneurysm
Branchial sinus or fistula
 Tortuous carotid artery
 Small opening in lower 3rd of neck on ant. margin of SCM
 Carotid body tumour (chemodectoma)
 Between tonsillar fossa and ant. border of SCM
 Non-pulsatile
 Branchial cysts  May discharge mucus
 Laryngocele
 Goitre
 Parotid tumour (lump in postero-superior area) Carotid Body Tumour: Chemodectoma
 Very rare
 Carotid bodies
 Located @ carotid bifurcation
Submandibular Triangle  Detect pO2, pCO2 and H+
 Mental process
 Ramus of the mandible Presentation
 Line between two angles of the mandible  Just anterior to upper 3rd of SCM.
 Pulsatile
Causes  Move laterally but not vertically
 Salivary stone  May be bilateral
 Sialadenitis  Pressure may → dizziness and syncope
 Salivary tumour  Mostly benign (5% malignant)
Ix: Doppler or angio: splaying of bifurcation

Posterior Triangle
 Post. margin of SCM Rx: extirpation by a vascular surgeon
 Ant. margin of trapezius
 Mid 1/3 of clavicle.
Laryngocele
Causes  Cystic dilatation of the laryngeal saccule
 LNs  Congenital or acquired
 Cervical ribs  Exacerbated by blowing
 Pharyngeal pouch
 Cystic hygromas
 Pancoast’s tumour
Midline Lumps
 <20yrs
 Thyroglossal cyst
 Dermoid cyst
 >20yrs
 Thyroid isthmus mass
 Ectopic thyroid tissue

Midline Neck Lumps Posterior Triangle Lumps
Dermoid Cyst Cervical ribs
 Developmental inclusion of epidermis along lines of  Overdevelopment of transverse process of C7
skin fusion.  Occur in 1:150
Presentation Presentation
 Common <20yrs  Mostly asymptomatic
 Found at junctions of embryological fusion  Hard swelling
 Neck midline  ↓ radial pulse on abduction and external rotation of arm
 Lateral angles of eyebrow  Can → vascular symptoms
 Under tongue  Compresses subclavian A
 Contains ectodermal elements  Raynaud’s
 Hair follicles, sebaceous glands  Subclavian steal
 ↓ venous outflow → oedema
Rx: excision  Can → neurological symptoms
 Compresses lower trunk of brachial plexus, T1 nerve
root or stellate ganglion.
Thyroglossal Cyst  Wasting of intrinsic hand muscles
 Cyst formed from persistent thyroglossal duct  Paraesthesia along medial border of arm
 Path of thyroid descent from base of tongue
Presentation Pharyngeal Pouch: Zenker’s Diverticulum

 Can be located anywhere between foramen caecum  Herniation of pharyngeal mucosa through its muscular coat
and the thyroid at its weakest point.
 Usually just inferior to the hyoid: subhyoid  Pulsion diverticulum
 Or, just above the hyoid: suprahyoid  Killian’s dehiscence
 Fluctuant lump that moves up c̄ tongue protrusion  Between thyro- and crico-pharyngeal muscles that
 Can become infected → thyroglossal fistula form the inferior constrictor
Rx Presentation
 Sistrunk’s Op: excision of cyst and thyroglossal duct  Swelling on left side of neck
 Regurgitation and aspiration
 Halitosis
 Gurgling sounds
 Food debris → pouch expansion → oesophageal
compression → dysphagia.
Ix: barium swallow
Rx
 Excision and cricopharyngeal myotomy
 Endoscopic stapling
Cystic Hygroma
 Congenital multiloculated lymphangioma arising from the
jugular lymph sac
Presentation
 Infants
 Lower part of post. triangle but may extend to axilla.
 ↑ in size when child coughs/cries
 Transilluminates brilliantly
Rx: excision or hypertonic saline sclerosant

 May recur

Cervical Lymphadenopathy Hypertrophic and Keloid Scars
Key Features Features
 Consistency  Scar more prominent than surrounding skin
 Number
 Fixation Hypertrophic
 Symmetry  Scar confined to wound margins
 Tenderness  Across flexor surfaces and skin creases
 Appear soon after injury and regress spontaneously
Additional Examination  Any age: commonly 8-20yrs
 Face and scalp for infection or neoplasm  M=F
 Chest exam: infection or neoplasm  All races
 Breast examination
 Formal full ENT examination Keloid
 Rest of reticuloendothelial system  Scar extends beyond wound margins
 Earlobes, chin, neck, shoulder, chest
History  Appear months after injury and continue to grow
 Symptoms from the lumps  Puberty to 30yrs
 E.g. EtOH-induced pain  F>M
 General symptoms  Black and Hispanic
 Fever, malaise, wt. loss
 Systemic disease
 PMH Wound Associations
 Previous operations  Infection
 Social history  Trauma
 Ethnic origin  Burns
 HIV risk factors  Tension
 Certain body areas
Causes: LIST
 Lymphoma and Leukaemia Mx
 Infection
 Sarcoidosis Non-surgical
 Tumours  Mechanical-pressure therapy
 Topical silicone gel sheets
Infection  Intralesional steroid and LA injections
 Bacterial
 Tonsillitis, dental abscess Surgical
 TB  Revision of scar c̄ closure by direct suturing
 Bartonella henselae (Cat scratch disease)
 Viral
 EBV
 HIV
 Protozoal
 Toxoplasmosis
Ix
Blood
 FBC, ESR, film (atypical lymphocytes)
 TFTs, serum ACE
 Monospot test, HIV test
Radiological
 US
 CT scan
Pathology
 FNAC
 Excision biopsy

Thyroid Lumps
Congenital Thyroid Disease Ix
 Lingual thyroid
 Ectopic thyroid tissue Bloods
 Thyroglossal cyst  TFTs: TSH, fT3, fT4
 Other: FBC, Ca2+, LFTs, ESR
Embryology  Antibodies: anti-TPO, TSH
 Thyroid migrates from its origin at the foramen caecum
at the base of the tongue. Imaging
 Passes behind the hyoid bone  CXR: goitres and mets
rd th
 Lies anterior to 3 -4 tracheal rings in the  High resolution US
pretracheal fascia.  CT
 Leaves behind the thyroglossal cyst which atrophies  Radionucleotide (Tc or I) scan (hot vs. cold)
 Persistence → thyroglossal cyst
 Ectopic thyroid tissue can be found anywhere along this Histology or cytology
descent  FNAC (can’t distinguish adenoma vs. follicular Ca)
 Biopsy
Goitre Differential
Laryngoscopy
Diffuse  Important pre-op to assess vocal cords
 Simple colloid goitre
 Endemic: iodine deficiency
 Sporadic: autoimmune, hereditary, goitrogens
(e.g. sulphonylureas)
 Graves’
 Thyroiditis
 Hashimoto’s
 De Quervain’s
 Subacute lymphocytic (e.g. post-partum)
 (multinodular goitre c̄ nodules too small to palpate)
Multinodular
 Multinodular colloid goitre (commonest)
 Multiple cysts
 Multiple adenomas
Solitary nodule
 Dominant nodule in multinodular goitre
 Adenoma (hot or cold)
 Cyst
 Malignancy

Benign Thyroid Disease
Disease Clinical Features Cause Management
Simple goitre Diffuse painless goitre Endemic Thyroxine
Mass effects: - iodine deficiency
- dysphagia Total or subtotal
- stridor Sporadic thyroidectomy if pressure
- SVC obstruction - autoimmune symptoms.
- goitrogens (e.g. sulphonylureas)
Usually euthyroid, may →hypothyroid - hereditary (dyshormogenic)
Multinodular Evolves from long-standing simple As for simple goitre Thyroxine
goitre goitre.
Mass effects.
Euthyroid (or subclinical hyperthyroid) Total or subtotal
thyroidectomy if pressure
symptoms.
Plummer’s Multinodular goitre Autonomous nodule develops on Carbimazole
Toxic multinodular Thyrotoxicosis background multinodular goitre Radioiodine
goitre Uneven iodine uptake with hot nodule Total or subtotal
thyroidectomy.
Graves’ Diffuse goitre c̄ bruit Autoimmune (T2 hypersensitivity) Propanolol
Ophthalmopathy - anti-TSH Carbimazole
Dermopathy Radioiodine
Thyrotoxicosis Thyroidectomy
Assoc. c̄ other AI disease (T1DM, PA)
↑ uptake on radionucleotide scan
Hashimoto’s Diffuse painless goitre Autoimmune (T2 and T4) Levothyroxine
thyroiditis May have transient thyrotoxicosis, then - anti-TPO, -Tg
hypothyroidism
Assoc. c̄ other AI disease (T1DM, PA)
de Quervain’s Diffuse painful goitre Viral: Coxsackie common Self-limiting
Preceding viral URTI common
Thyrotoxicosis → hypo→eu Autoimmune
↓ iodine uptake
Subacute Diffuse painless goitre Autoimmune Self-limiting
lymphocytic May occur post-partum
Thyrotoxicosis → hypo→eu
Riedel’s thyoiditis Firm, fixed, irregular thyroid mass Autoimmune fibrosis Conservative
Mass effects
Assoc. c̄ retroperitoneal fibrosis
Follicular Single thyroid nodule Hemithyroidectomy
adenoma ± thyrotoxicosis (majority are cold)
May get pressure symptoms
Thyroid cysts Solitary thyroid nodule Aspiration or excision
Asympto or pressure symptoms
Can → localised pain due to cyst bleed

Malignant Thyroid Disease
Disease Frequency Age Cell Origin Spread Mx
Papillary 80% 20-40 Follicular cells Nodes and lung Total thyroidectomy
- JDG node = ± node excision
Assoc. c̄ Tg tumour marker lateral aberrant ± radioiodine
irradiation thyroid T4 to suppress TSH
Often multifocal >95% 10ys

Follicular 10% 40-60 Follicular cells Blood → bone Total thyroidectomy +
F>M = 3:1 and lungs T4 suppression +
Tg tumour marker Radioiodine
>95% 10ys
Medullary 5% MEN2: young Parafollicular C-cells Do phaeo screen pre-op
30% are familial Sporadic: 40-50 Thyroidectomy +
- e.g. MEN2 CEA and calcitonin Node clearance
markers Consider radiotherapy
Anaplastic Rare >60 Undifferentiated Rapid growth Usually palliative
F>M = 3:1 follicular cells
Aggressive: local, May try thyroidectomy +
LN and blood. radiotherapy
<1% 10ys
Lymphoma 5% Lymphocytes Chemoradiotherapy
- MALToma in Hashi’s
Presentation Complications of Thyroid Surgery

 Non-functional (cold)
 Painless neck mass Early
 Cervical mets  Reactionary haemorrhage → haematoma (<1%)
 Compression symptoms  Can → airway obstruction.
 Dysphagia  Call anaesthetist and remove wound clips
 Stridor  Evacuate haematoma and re-explore wound
 SVC obstruction  Laryngeal oedema
 Damage during intubation or surgical
Risk factors for malignancy in thyroid nodules manipulation
 Solitary  Can → airway obstruction
 Solid  Recurrent laryngeal nerve palsy (0.5%)
 Younger  Right RLN more common (oblique ascent)
 Damage to one → hoarse voice
 Male
 Damage to both → obstruction needing
 Cold
tracheostomy
 Radiation exposure
 Hypocalcaemia (3-5%)
 Usually parathyroid dysfunction but may be
permanent if parathyroids removed.
Thyroid Surgery  Presents @ 24-48hrs
 Tingling in fingers and lips
Indications: 5 Ms  Wheeze / stridor → airway obstruction
Mechanical obstruction  Chvostek’s and Trousseau’s
Malignancy  Rx: 10ml 10% Ca gluconate IV
Marred beauty: cosmetic reasons  Thyroid storm
Medical Rx failure: thyrotoxicosis  Severe hyperthyroidism
Mediastinal extension: can’t monitor changes  Rx: propranolol, antithyroid drugs, Lugol’s iodine
and hydrocortisone sodium succinate
Practicalities
 Render euthyroid pre-op c̄ antithyroid drugs Late
 Stop 10 days prior to surgery (they ↑ vascularity)  Hypothyroidism
 Alternatively just give propronalol  Recurrent hyperthyroidism
 Check for phaeo pre-op in medullary carcinoma  Keloid scar
 Laryngoscopy: check vocal cords pre- and post-op
Procedure
 Collar incision

Salivary Glands
History Salivary Gland Neoplasms
 Swelling/pain related to food: calculi  80% are in the parotid (80% are superficial)
 Malaise, fever, mumps  80% are pleiomorphic adenomas
 Dry eyes/mouth: Sjogrens (Sicca, Mickulicz)  Deflection of ear outwards is classic sign
 CN VII palsy = malignancy
Causes of Salivary Gland Enlargement
 Whole gland Classification
 Parotitis  Benign
 Sjogren’s / Sicca Syndrome  1st: Pleiomorphic adenoma
 Sarcoid  2nd: Adenolymphoma (Warthin’s)
 Amyloid  Malignant (CN7 palsy + fast growing)
 ALL  1st: Mucoepidermoid
 Chronic liver disease  2nd: Adenoid cystic
 Anorexia or bulimia
 Localised Ix
 Tumours  ENT examination
 Stones  US ± CT
 FNAC
Acute Parotitis
 Viral: mumps, coxsackie A, HIV Pleiomorphic Adenoma
 Bacterial: S. aureus  Commonest salivary gland neoplasm (80%)
 Assoc. c̄ calculi and poor oral hygiene  Presentation
 90% occur in parotid
 Occur in middle age
Calculi  F>M
 Recurrent unilateral swelling and pain  Benign and slow growing
 Worse on eating  Histo: different tissue types (hence name)
 Red, tender, swollen gland (80% submandibular)  Rx: superficial parotidectomy
 Ix: plain x-ray or sialography
 Rx: gland excision Adenolymphoma (Warthin’s tumour)
 Benign soft cystic tumour
 Older men
 Rx: enucleation
Adenoid-cystic carcinoma
 One of the commonest malignant salivary tumours
 Highly malignant and often incurable
 Rapid growth
 Hard fixed mass
 Pain
 Facial palsy
Surgery
 Superficial or radical parotidectomy
 Facia lata face lift for facial palsy
Complications
 Facial palsy
 Salivary fistula
 Frey’s Syndrome (gustatory sweating)
 Redness and sweating skin over parotid area
 Occurs in relation to food (inc. thinking)
 Auriculotemporal branch of CN V3 carries
sympathetic fibres to sweat glands over parotid
area and parasympathetic fibres to the parotid
 Reinervation of divided sympathetic nerves by
fibres from the secretomotor branch of
auriculotemporal branch of CN V3

Breast Surgery
Contents
Breast Cancer: Pathology, Presentation and Assessment ......................................................................................................... 81
Breast Cancer: Management ...................................................................................................................................................... 82
Other Breast Disease .................................................................................................................................................................. 83

Breast Cancer: Pathology, Presentation and Assessment
Epidemiology Presentation
 Affects 1/10 women  Lump: commonest presentation of Ca breast
 20 000 cases/yr in UK  Usually painless
 Commonest cause of cancer death in females 15-54  50% in upper outer quadrant
 Second commonest cause of cancer deaths overall  ± axillary nodes
 Skin changes
Aetiology / Risk Factors  Paget’s: persistent eczema
 Peau d’orange
Family Hx  Nipple
 10% Ca breast is familial  Discharge
 One 1st degree relative = 2x risk  Inversion
 5% assoc. c̄ BRCA mutations  Mets
 BRCA1 (17q) → 80% breast Ca, 40% + ov Ca  Pathological #
 BRCA2 (13q) → 80% breast Ca  SOB
 Abdominal pain
Oestrogen Exposure  Seizures
 Early menarche, late menopause  May present through screening
 HRT, OCP (Million Women Study)
 First child >35yrs Differential
 Obesity  Cysts
 Fibroadenomas
Other Factors  DCIS
 Proliferative breast disease c̄ atypia  Duct ectasia
 Previous Ca breast
 ↑ age (v. rare <30) Triple Assessment: any breast lump
 Breast feeding is protective  Hx and Clinical Examination
 Radiology
Pathology  <35yrs: US
 >35ys: US + mammography
DCIS/LCIS  Pathology
 Non-invasive pre-malignant condition  Solid lump: tru-cut core biopsy
 Microcalcification on mammography  Cystic lump: FNAC (green / 18G needle)
 10x ↑ risk of invasive Ca  Reassure if clear fluid
 Send cytology if bloody fluid
Invasive Ductal Carcinoma, NST/NOS  Core biopsy residual mass
 Commonest: ~70% of cancers  Core biopsy if +ve cytology
 Feels hard (scirrhous)
Other Ix
Other subtypes  Bloods
 Invasive lobular: ~20% of cancers  FBC, LFTs, ESR, bone profile
 Medullary: affects younger pts, feels soft  Imaging: help staging
 Colloid/mucinous: occur in elderly  CXR
 Inflammatory: pain, erythema, swelling, peau d’orange  Liver US
 Papillary  CT scan
 Breast MRI: multifocal disease or c̄ implants
Phyllodes Tumour  Bone scan and PET-CT
 Stromal tumour  May need wire-guided excision biopsy
 Large, non-tender mobile lump
Clinical Staging
Spread  Stage 1: confined to breast, mobile, no LNs
 Direct extension → muscle and/or skin  Stage 2: Stage 1 + nodes in ipsilateral axilla
 Lymph → p’eau d’orange + arm oedema  Stage 3: Stage 2 + fixation to muscle (not chest wall)
 Blood → LNs matted and fixed, large skin involvement
 Bones: bone pain, #, ↑Ca  Stage 4: Complete fixation to chest wall + mets
 Lungs: dyspnoea, pleural effusion
 Liver: abdo pain, hepatic impairment TNM Staging
 Brain: headache, seizures  Tis (no palpable tumour): CIS
 T1: <2cm, no skin fixation
Screening  T2: 2-5cm, skin fixation
 Every 3yrs from 47-73  T3: 5-10cm, ulceration + pectoral fixation
 Craniocaudal and oblique views  T4: >10cm, chest wall extension, skin involved
 ↓ breast Ca deaths by 25%  N1: mobile nodes
 10% false negative rate.  N2: fixed nodes

Breast Cancer: Management
Principals Nottingham Prognostic Index
 Manage in an MDT c̄ an individual approach  Predicts survival and risk of relapse
 Oncologist  Guides appropriate adjuvant systemic therapy
 Breast surgeon  (0.2 x tumour size) + histo grade + nodal status
 Breastcare nurse  Histo grade: Bloom-Richardson system (1-3)
 Radiologist
 Histopathologist Systemic Rx
 Try to enrol pts. in a trial
 Factors: age, fitness, wishes, clinical stage Radiotherapy
 1-2: surgical  Post-WLE: ↓ local recurrence
 3-4: chemo and palliation  Post-mastectomy: only if high risk of local recurrence
 Large, poorly differentiated, node +ve
Surgery  Axillary: node +ve disease
 Aim = gain local control  Palliation: bone pain
 Two options
 WLE + radiotherapy (80% treated like this) Chemotherapy
 Mastectomy  Pre-menopausal, node +ve, high grade or recurrent
 Typically large tumours >4cm tumours.
 Multifocal or central tumours  Neo-adjuvant chemo improves survival in large tumours
 Nipple involvement  6 x FEC: 5-FU, Epirubicin, Cyclophosphamide
 Pt. choice  Trastuzumab (anti-Her2) is used if Her2+ve
 Not radical: no longer used  SE: cardiac toxicity
 Same survival, but WLE has ↑ recurrence rates
Endocrine Therapy
Sentinel Node Biopsy: gold standard  Used in ER or PR +ve disease: ↓ recurrence, ↑ survival
 5yrs of adjuvant therapy
Rational  Tamoxifen
 SN = first node that a section of breast drains to.  SERM: antagonist @ breast, agonist @ uterus
 If clinically –ve axillary LNs, no need for further dissection  SE: menopausal symptoms, endometrial Ca
if SN is clear.  Anastrazole
 Aromatase inhibitor → ↓ oestrogen
Procedure  Better cf. tamoxifen if post-men (ATAC trial)
 Blue dye / radiocolloid injected into tumour  SE: menopausal symptoms
 Visual inspection / gamma probe @ surgery to ID SN  If pre-menopausal and ER+ve may consider ovarian
 SN removed and sent for frozen section ablation or GnRH analogues (e.g. goserelin)
 If node +ve → axillary clearance or radiotherapy
Treating Advanced Disease (Stage 3-4)
Evidence  Tamoxifen if ER+ve
 2 RCTs compared SNB vs. SNB + axillary clearance  Chemo for relapse
 No differences in overall or disease-free survival  Her2+ve tumours may respond to trastuzumab
 ↓ morbidity c̄ SNB alone
 Lymphoedema Supportive
 Pain  Bone pain: DXT, bisphosphonates, analgesia
 Numbness  Brain: occasional surgery, DXT, steroids, AEDs
 Lymphoedema: decongestion, compression
Other Axillary Options
 For clinically -ve axilla options included Reconstruction
 Axillary sampling  Offered either at 1O surgery or as delayed procedure.
 Removal of lower nodes
 Clearance or DXT if +ve Implants: silastic or saline inflatable
 Axillary clearance
 Can be done to various levels Lat dorsi myocutaneous flap
 Pedicled flap: skin, fat, muscle and blood supply
Surgical Complications  Supplied by thoracodorsal A. via subscapular A.
 Haematoma, seroma  Usually used c̄ an implant
 Frozen shoulder
 Long-thoracic nerve palsy Transverse rectus abdominis myocutaneous flap
 Lymphoedema  Gold-standard
 Pedicled (inf. epigastric A.)
 Or free: attached to internal thoracic A
 No implant necessary and combined tummy tuck
 CI if poor circulation: smokers, obese, PVD, DM
 Risk of abdominal hernia
Nipple Tattoo
Other Breast Disease
Congenital Mastalgia
 Amastia: complete absence of breast and nipple
 Hypoplasia more common: some asymmetry normal Cyclical
 Accessory nipples  ~35yrs
 Can occur anywhere along the milk line  Pre-menstrual pain
 Present in 1%  Relieved by menstruation
 Commonly in upper outer quadrants bilaterally
Gynaecomastia
 Occurs in 30% of boys at puberty Non-cyclical
 Hormone secreting tumours: e.g. sex-cord testicular  ~45yrs
 Chronic liver disease: hypogonadism + ↓E2  Severe lancing breast pain (often left)
metabolism  May be assoc. c̄ back pain
 Drugs: spironolactone, digoxin, cimetidine
Rx
 Reassurance + good bra for most
st
 1 line: EPO (contains gamma-linoleic acid)
 OCP
 Topical NSAIDs (e.g. ibuprofen)
 Bromocriptine
 Danazol
 Tamoxifen
Inflammatory
Disease Patient Presentation Treatment

Acute Mastitis Usually lactating Painful, red breast Fluclox alone in early stages
May → Abscess (lump near nipple) Fluclox + I&D if fluctuant abscess
Fat Necrosis Associated with previous trauma Analgesia
Painless, palpable, non-mobile mass No f/up necessary
May calcify simulating Ca
Duct Ectasia Post-menopausal Slit-like nipple Need to distinguish from Ca
Duct dilatation - 50-60yrs Often bilateral
± peri-areolar mass Surgical duct excision if mass
Thick white/green discharge present or discharge troublesome
May be calcified on mammography
Close f/up
Periductal Smokers Painful, erythematous sub-areolar mass Broad-spectrum Abx
Mastitis 30yrs Assoc. with inverted nipple ± purulent discharge
May → abscess or discharging fistula
Benign Epithelial Lesions

Benign 30-50yrs Pre-menstrual breast nodularity and pain Triple assessment.
Mammary Often in upper outer quadrant
Dysplasia - Tender “lumpy-bumpy” breasts Reassurance
Analgesia
Aberration of Normal Development and Good Bra
Involution (ANDI) ± evening primrose oil
- Fibroadenosis
- Cyst formation Danazol may occasionally be
- Epitheliosis (hyperplasia) used
- Papillomatosis
Cystic Disease Peri-menopausal >40 Distinct, fluctuant round mass Aspiration: green-brown fluid
Often painful
Persistence or blood → triple
assessment.
Duct Papilloma 40-50yrs Common cause of bloody discharge Triple assessment.
Not usually palpable Excise due to ↑ risk of Ca

Stromal Tumours

Fibroadenoma <35yrs Commonest benign tumour Reassurance + f/up if <2.5cm
Rare post-menopause Painless, mobile, rubbery mass Shell-out surgically
↑ in Blacks Often multiple and bilateral - >2.5cm
- FH of breast Ca
Popcorn calcification - Pt. choice
Phyllodes tumour 50s+ Large, fast growing mass WLE
Mobile, non-tender
Epithelial and connective tissue elements
Malignant Conditions
Disease Clinical Treatment

DCIS Presents as Microcalcification on mammogram WLE + radiotherapy
Rarely assoc. with symptoms:
- lump Extensive or multifocal → mastectomy + reconstruction + SNB
- discharge
- eczematous change = Paget’s disease
→ Ca @ 1%/yr (10x ↑ risk) in ipsilateral breast
Paget’s Unilat, scaly, erythematous, itchy Usually underlying invasive or DCIS breast cancer.
+/- palpable mass (invasive carcinoma) Mastectomy + radio ± chemo/endo
LCIS Incidental biopsy finding (no calcification) Bilateral prophylactic mastectomy or close watching c̄
Often bilat (20-40%) mammographic screening
Young women
↑ risk Ca risk (x10) in both breasts

Vascular Surgery
Contents
Chronic Limb Ischaemia: Presentation and Classification .......................................................................................................... 86
Chronic Limb Ischaemia: Investigation and Management .......................................................................................................... 87
Acute Limb Ischaemia ................................................................................................................................................................. 88
Carotid Artery Disease ................................................................................................................................................................ 89
Aneurysms ................................................................................................................................................................................... 89
Popliteal Aneurysm...................................................................................................................................................................... 89
Abdominal Aortic Aneurysms ...................................................................................................................................................... 90
Thoracic Aortic Dissection ........................................................................................................................................................... 91
Gangrene ..................................................................................................................................................................................... 91
Varicose Veins............................................................................................................................................................................. 92
Leg Ulcers ................................................................................................................................................................................... 93
Leg Swelling ................................................................................................................................................................................ 93

Chronic Limb Ischaemia: Presentation and Classification
Incidence Presentation
 5% of males >50yrs have intermittent claudication
Intermittent Claudication
 Cramping pain after walking a fixed distance
Definition  Pain rapidly relieved by rest
 European Working Group Definition (1991)  Calf pain = superficial femoral disease (commonest)
 Ankle artery pressure <50mmHg (toe <30mmHg)  Buttock pain = iliac disease (internal or common)
 And either:
 Persistent rest pain requiring analgesia for ≥2wks Critical Limb Ischaemia: Fontaine 3 or 4
 Ulceration or gangrene  Rest pain
 Especially @ night
 Usually felt in the foot
Cause  Pt. hangs foot out of bed
 Atherosclerosis  Due to ↓ CO and loss of gravity help
 Typically asymptomatic until 50% stenosis  Ulceration
 (vasculitis and fibromuscular dysplasia are v. rare  Gangrene
causes)
Leriche’s Syndrome: Aortoiliac Occlusive Disease
 Atherosclerotic occlusion of abdominal aorta and iliacs
Atherosclerosis Summary  Triad
1. Endothelial injury: haemodynamic, HTN, ↑ lipids  Buttock claudication and wasting
2. Chronic inflammation  Erectile dysfunction
 Lipid-laden foam cells produce GFs, cytokines,  Absent femoral pulses
ROS and MMPs
 → lymphocyte and SMC recruitment Buerger’s Disease: Thromboangiitis Obliterans
3. SM proliferation: conversion of fatty streak to  Young, male, heavy smoker
atherosclerotic plaque  Acute inflammation and thrombosis of arteries and
veins in the hands and feet → ulceration and gangrene
NB. Arteriosclerosis = general arterial hardening
Atherosclerosis = arterial hardening specifically due to Signs
atheroma  Pulses: pulses and ↑ CRT (norm ≤2sec)
 Ulcers: painful, punched-out, on pressure points
 Nail dystrophy / Onycholysis
Atheroma Pathology  Skin: cold, white, atrophy, absent hair
 Fibrous cap: SM cells, lymphocytes, collagen  Venous guttering
 Necrotic centre: cell debris, cholesterol, Ca, foam cells  Muscle atrophy
 ↓ Buerger’s Angle
 ≥90: normal
Risk Factors  20-30: ischaemia
 <20: severe ischaemia
Modifiable Non-modifiable  +ve Buerger’s Sign
 Smoking  FH and PMH  Reactive hyperaemia due to accumulation of
 BP  Male deoxygenated blood in dilated capillaries
 DM control  ↑ age
 Hyperlipidaemia  Genetic
 ↓ exercise Clinical Classification
Fontaine Rutherford
Associated Vascular Disease 1. Asympto (subclinical) 1. Mild claudication
2. Intermittent claudication 2. Moderate claudication
 IHD: 90%
a. >200m 3. Severe claudication
 Carotid stenosis:15% b. <200m 4. Ischaemic rest pain
 AAA 3. Ischaemic rest pain 5. Minor tissue loss
 Renovascular disease 4. Ulceration / gangrene 6. Major tissue loss
 DM microvascular disease

Chronic Limb Ischaemia: Investigation and Management
Ix Conservative Mx
 Most pts. c̄ claudication can be managed conservatively
Doppler Waveforms  ↑ exercise and employ exercise programs
 Normal: triphasic  Stop smoking
 Mild stenosis: biphasic  Wt. loss
 Severe stenosis: monophasic  Foot care
 Prog: 1/3 improve, 1/3 stay the same, 1/3 deteriorate
ABPI
Clinical Fontaine ABPI Medical Mx

Calcification: CRF, DM >1.4  Risk factors: BP, lipids, DM
Normal ≥1  β-B don’t worsen intermittent claudication but use
c̄ caution in CLI
Asymptomatic Fontaine 1 0.8-0.9
Claudication Fontaine 2 0.6-0.8  Antiplatelets: aspirin / clopidogrel
Rest pain Fontaine 3 0.3-0.6  Analgesia: may need opiates
Ulceration and gangrene Fontaine 4 <0.3  (Parenteral prostanoids ↓ pain in pts. unfit for surgery)
NB. Falsely high results may be obtained in DM / CRF due Endovascular Mx

to calcification of vessels: mediasclerosis  Percutaneous Transluminal Angioplasty ± stenting
 Use toe pressure with small cuff: <30mmHg  Good for short stenosis in big vessels: e.g. iliacs, SFA
 Lower risk for pt.: performed under LA as day case
Walk test  Improved inflow → ↓ pain but restoration of foot pulses is
 Walk on treadmill @ certain speed and incline to required for Rx of ulceration / gangrene.
establish maximum claudication distance.
 ABPI measured before and after: 20% ↓ is sig
Surgical Reconstruction
Bloods
Indications
 FBC + U+E: anaemia, renovascular disease
 V. short claudication distance (e.g. <100m)
 Lipids + glucose
 Symptoms greatly affecting pts. QoL
 ESR: arteritis
 Development of rest pain
 G+S: possible procedure
Pre-op assessment
Imaging: assess site, extent and distal run-off
 Need good optimisation as likely to have
 Colour duplex US cardiorespiratory co-morbidities.
 CT / MR angiogram: gadolinium contrast
 Digital subtraction angiography Practicalities
 Invasive  not commonly used for Dx only.  Need good proximal supply and distal run-off
 Used when performing therapeutic angioplasty  Saphenous vein grafts preferred below the IL
or stenting  More distal grafts have ↑ rates of thrombosis
Other Classification
 ECG: ischaemia  Anatomical: fem-pop, fem-distal, aortobifemoral
 Extra-anatomical: axillo-fem / -bifem, fem-fem crossover
Other
 Endarterectomy: core-out atheromatous plaque
 Sympathectomy: chemical (EtOH injection) or surgical
 Caution in DM c̄ neuropathy
 Amputation
Prognosis
1yr after onset of CLI
 50% alive w/o amputation
 25% will have had major amputation
 25% dead (usually MI or stroke)
Following amputation
 Perioperative mortality
 BK: 5-10%
 AK: 15-20%
 1/3 → complete autonomy
 1/3 → partial autonomy
© Alasdair Scott, 2012
 1/3 → dead 87
Acute Limb Ischaemia
Definitions General Mx
 Acute: ischaemia <14d  In an acutely ischaemic limb discuss immediately c̄ a
 Acute on chronic: worsening symptoms and signs <14d senior as time is crucial.
 Chronic: ischaemia stable for >14d  NBM
 Rehydration: IV fluids
Severity  Analgesia: morphine + metoclopramide
 Incomplete: limb not threatened  Abx: e.g augmentin if signs of infection
 Complete: limb threatened  Unfractionated heparin IVI: prevent extension
 Loss of limb unless intervention w/i/ 6hrs  Complete occlusion?
 Irreversible: requires amputation  Yes: urgent surgery: embolectomy or bypass
 No: angiogram + observe for deterioration
Causes
 Thrombosis in situ (60%) Angiography
 A previously stenosed vessel c̄ plaque rupture  Not performed if there is complete occlusion as it
 Usually incomplete ischaemia introduces delay: take straight to theatre.
 Embolism (30%)  If incomplete occlusion, pre-op angio will guide any
 80% from LA in AF distal bypass.
 Valve disease
 Iatrogenic from angioplasty / surgery Embolus Mx
 Cholesterol in long bone #
 Paradoxical (venous via PFO) 1. Embolectomy
 Typically lodge at femoral bifurcation  Under LA or GA
 Often complete ischaemia  Wire fed through embolus
 Graft / stent occlusion  Fogarty catheter fed over the top
 Trauma  Balloon inflated and catheter withdrawn, removing the
 Aortic dissection embolism.
 Send embolism for histo (exclude atrial myxoma)
Presentation: 6Ps  Adequacy confirmed by on-table angiography
 Pale
 Pulseless 2. Thrombolysis
 Perishingly cold  Consider if embolectomy unsuccessful
 Painful  E.g. local injection of TPA
 Paraesthesia
 Paralysis 3. Other options
 Emergency reconstruction
 Amputation
Thrombosis vs. Embolus
Post-embolectomy
 Anticoagulate: heparin IVI → warfarin
Thrombosis Embolus
 ID embolic source: ECG, echo, US aorta, fem and pop
Onset Hrs-days Sudden
Severity Less severe Profound ischaemia  Complications
- collaterals  Reperfusion injury
Embolic source Present  Local swelling → compartment syndrome
O
- often AF  Acidosis and arrhythmia 2 to ↑K
Claudication Hx Present Absent  ARDS
Contralat pulses Absent Present  GI oedema → endotoxic shock
Dx Angiography Clinical  Chronic pain syndromes
Rx Thrombolysis Embolectomy +
Bypass surgery Warfarin
Thrombosis Mx
Ix  Emergency reconstruction if complete occlusion
 Blood  Angiography + angioplasty
 FBC, U+E, INR, G+S  Thrombolysis
 CK  Amputation
 ECG
 Imaging
 CXR Manage Cardiovascular Risk Factors
 Duplex doppler

Carotid Artery Disease Aneurysms
Definitions Definition
 Stroke: sudden neurological deficit of vascular origin  Abnormal dilatation of a blood vessel > 50% of its
lasting >24h normal diameter.
 TIA: sudden neurological deficit of vascular origin
lasting <24h (usually lasts <1h) c̄ complete recovery Classification
 True Aneurysm
Pathogenesis  Dilatation of a blood vessel involving all layers of
 Turbulent flow → ↓ shear stress @ carotid bifurcation the wall and is >50% of its normal diameter
promoting atherosclerosis and plaque formation.  Two different morphologies
 Plaque rupture → complete occlusion or distal emboli  Fusiform: e.g AAA
 Cause 15-25% of CVA/TIA  Saccular: e.g Berry aneurysm
 False Aneurysm
Presentation  Collection of blood around a vessel wall that
 Bruit communicates c̄ the vessel lumen.
 CVA/TIA  Usually iatrogenic: puncture, cannulation
 Dissection
Ix  Vessel dilatation caused by blood splaying apart
 Duplex carotid Doppler the media to form a channel w/i the vessel wall.
 MRA
Causes
Mx  Congenital
 ADPKD → Berry aneurysms
Conservative  Marfan’s, Ehlers-Danlos
 Aspirin or clopidogrel  Acquired
 Control risk factors  Atherosclerosis
 Trauma: e.g. penetrating trauma
Surgical: Endarterectomy  Inflammatory: Takayasu’s aortitis, HSP
 Symptomatic (ECST, NASCET)  Infection
 ≥70% (5% stroke risk per yr)  Mycotic: SBE
 ≥50% if low risk (<3%, typically <75yrs)  Tertiary syphilis (esp. thoracic)
 Perform w/i 2wks of presentation
 Asymptomatic (ACAS, ACST) Complications
 ≥60% benefit if low risk  Rupture
 Thrombosis
Complications of Endarterectomy  Distal embolization
Stroke or death: 3%  Pressure: DVT, oesophagus, nutcracker syndrome
HTN: 60%  Fistula (IVC, intestine)
Haematoma
MI
Nerve injury
Hypoglossal: ipsilateral tongue deviation Popliteal Aneurysm
Great auricular: numb ear lobe  Less common cf. AAA
Recurrent laryngeal: hoarse voice, bovine cough  50% of pts. c̄ popliteal aneurysm also have AAA
Stenting Presentation
 Less invasive: ↓ hospital stay, ↓ infection, ↓ CN injury  Very easily palpable popliteal pulse
 There is concern over ↑ stroke risk, esp. pts. >70yrs  50% bilateral
 Meta-analysis shows no sig difference in mortality vs.  Rupture is relatively rare
CEA @ 120d  Thrombosis and distal embolism is main complication
 Younger pts. have best risk / benefit ratio  → acute limb ischaemia
Mx
 Acute: embolectomy or fem-distal bypass
 Stable: elective grafting + tie off vessel

Abdominal Aortic Aneurysms
Epidemiology AAA Rupture
 Prevalence: ~5% >50yrs
 Mortality: 10,000 deaths/yr Rupture Rates
 Sex: M>F=3:1  <5.5cm = 1% / yr
 >6cm = 25% / yr
Pathology  ↑ risk if:
 Dilatation of the abdominal aorta ≥3cm  ↑BP
 90% infrarenal  Smoker
 30% involve the iliac arteries  Female
 Strong FH
Presentation Rupture Presentation
 Usually asympto: discovered incidentally  Sudden onset severe abdominal pain
 May → back pain or umbilical pain radiating to groin  Intermittent or continuous
 Acute limb ischaemia  Radiates to back or flanks (don’t dismiss as colic)
 Blue toe syndrome: distal embolisation  Collapse → shock
 Acute rupture  Expansile abdominal mass
Examination Mx: a surgical emergency

 Expansile mass just above the umbilicus  High flow O2
 Bruits may be heard  2 x large bore cannulae in each ACF
 Tenderness + shock suggests rupture  Give fluid if shocked but keep SBP <100mmHg
 Give O- blood if desperate
Ix  Blood: FBC, U+E, clotting, amylase, xmatch 10u
 AXR: calcification may be seen  Instigate the major haemorrhage protocol
 Abdo US: screening and monitoring  Call vascular surgeon, anaesthetist and warn theatre
 CT / MRI: gold-standard  Analgesia
 Angiography  Abx prophylaxis: cef + met
 Won’t show true extent of aneurysm due to  Urinary catheter + CVP line
endoluminal thrombus.  If stable + Dx uncertain: US or CT may be feasible
 Useful to delineate relationship of renal arteries  Take to theatre: clamp neck, insert dacron graft
Mx Mortality
 100% w/o surgery
Conservative  50% c̄ surgery
 Manage cardiovascular risk factors: esp. BP
 UK Small Aneurysm Trial suggested that AAA <5.5cm
in maximum diameter can be monitored by US (/CT)
 <4cm: yearly monitoring
 4-5.5cm: 6 monthly monitoring
Surgical
 Aim to treat aneurysm before it ruptures.
 Elective mortality: 5%
 Emergency mortality: 50%
 Operate when risk of rupture > risk of surgery
 Indications
 Symptomatic (back pain = imminent rupture)
 Diameter >5.5cm
 Rapidly expanding: >1cm/yr
 Causing complications: e.g. emboli
 Open or EVAR
 EVAR has ↓ perioperative mortality
 No ↓ mortality by 5yrs due to fatal endograft
failures.
 EVAR not better than medical Rx in unfit pts.
Screening
MASS trial revealed 50% ↓ aneurysm-related mortality in
males aged 65-74 screened c̄ US.
UK men offered one-time US screen @ 65yrs

Thoracic Aortic Dissection Gangrene
 Blood splays apart the laminar planes of the media to form  Death of tissue from poor vascular supply.
a channel w/i the aortic wall.
Classification
Aetiology  Wet: tissue death + infection
 Atherosclerosis and HTN cause 90%  Dry: tissue death only
 Minority caused by connective tissue disorder  Pregangrene: tissue on the brink of gangrene
 Marfan’s, Ehlers Danlos
 Vitamin C deficiency Presentation
 Black tissues ± slough
Presentation  May be suppuration ± sepsis
 Sudden onset, tearing chest pain
 Radiates through to the back Gas Gangrene
 Tachycardia and hypertension (1O + sympathetic)  Clostridium perfringes myositis
 Distal propagation → sequential occlusion of branches  RFs: DM, trauma, malignancy
 Left hemiplegia  Presentation
 Unequal arm pulses and BP  Toxaemia
 Paraplegia (anterior spinal A.)  Haemolytic jaundice
 Anuria  Oedema
 Proximal propagation  Crepitus from surgical emphysema
 Aortic regurgitation  Bubbly brown pus
 Tamponade  Rx
 Rupture into pericardial, pleural or peritoneal cavities  Debridement (may need amputation)
 Commonest cause of death  Benzylpenicillin + metronidazole
 Hyperbaric O2
Stanford Classification
Type A: Proximal Synergistic Gangrene
 70%  Involves aerobes + anaerobes
 Involves ascending aorta ± descending  Fournier’s: perineum
 Higher mortality due to probable cardiac involvement  Meleney’s: post-op ulceration
 Usually require surgery  Both progress rapidly to necrotising fasciitis + myositis
Type B: Distal Mx
 30%  Take cultures
 Involves descending aorta only: distal to L SC artery  Debridement (including amputation)
 Usually best managed conservatively  Benzylpenicillin ± clindamycin
Ix
 ECG: exclude MI
 TTE / TOE: can be used in haemodynamically unstable pts
 CT/MRI: not suitable for unstable pts.
Mx
Resuscitate
Investigate
 Bloods: x-match 10u, FBC, U+E, clotting, amylase
 ECG: 20% show ischaemia due to involvement of the
coronary ostia
 Imaging
 CXR
 CT/MRI: not if haemodynamically unstable
 TOE: can be used if haemodynamically unstable
Treat
 Analgesia
 ↓SBP
 Labetalol or esmolol (short t½)
 Keep SBP 100-110mmHg
 Type A: open repair
 Acute operative mortality: <25%
 Type B: conservative initially
 Surgery if persistent pain or complications
 Consider TEVAR if uncomplicated
Varicose Veins
Definition CEAP Classification
 Tortuous, dilated veins of the superficial venous system  Chronic venous disease can be classified according to
 Clinical signs (1-6 + sympto or asympto)
Pathophysiology  Etiology
 One-way flow from sup → deep maintained by valves  Anatomy
 Valve failure → ↑ pressure in sup veins → varicosity  Pathophysiology
 3 main sites where valve incompetence occurs:
 SFJ: 3cm below and 3cm lateral to pubic tubercle Conservative Mx
 SPJ: popliteal fossa  Treat any contributing factors
 Perforators: draining GSV  Lose weight
 3 medial calf perforators (Cockett’s)  Relieve constipation
 1 medial thigh perforator (Hunter’s)  Education
 Avoid prolonged standing
Causes  Regular walks
 Class II Graduated Compression Stockings
Primary  18-24mmHg
 Idiopathic (congenitally weak valves)  Symptomatic relief and slows progression
 Prolonged standing  Skin Care
 Pregnancy  Maintain hydration c̄ emollients
 Obesity  Treat ulcers rapidly
 OCP
 FH Minimally Invasive Therapies
 Congenital valve absence (v. rare)
Indications
Secondary Small below knee varicosities not involving GSV or SSV
 Valve destruction → reflux: DVT, thrombophlebitis
 Obstruction: DVT, foetus, pelvic mass Techniques
 Constipation Local or GA
 AVM Injection sclerotherapy: 1% Na tetradecyl sulphate
 Overactive pumps (e.g. cyclists) Endovenous laser or radiofrequency ablation
 Klippel-Trenaunay
 PWS, varicose veins, limb hypertrophy Post-Operatively
Compression bandage for 24hrs
Symptoms Compression stockings for 1mo
 Cosmetic defect
 Pain, cramping, heaviness
 Tingling
Surgical Mx
 Bleeding: may be severe
Indications
 Swelling
 SFJ incompetence
 Major perforator incompetence
Signs  Symptomatic: ulceration, skin changes, pain
 Skin changes
 Venous stars Procedures
 Haemosiderin deposition
 Trendelenberg: saphenofemoral ligation
 Venous eczema
 SSV ligation: in the popliteal fossa
 Lipodermatosclerosis (paniculitis)
 LSV stripping: no longer performed due to potential for
 Atrophie blanche
saphenous nerve damage.
 Ulcers: medial malleolus / gaiter area
 Multiple avulsions
 Oedema
 Perforator ligation: Cockett’s operation
 Thrombophlebitis
 Subfascial endoscopic perforator surgery (SEPS)
Ix Post-op
 Duplex ultrasonography  Bandage tightly
 Anatomy  Elevate for 24h
 Presence of incompetence
 Discharged c̄ compression stockings and instructed to
 Caused by obstruction or reflux
walk daily.
 Surgery: FBC, U+E, clotting, G+S, CXR, ECG
Complications
Referral Criteria  Haematoma (esp. groin)
 Bleeding  Wound sepsis
 Pain  Damage to cutaneous nerve (e.g. long saphenous)
 Ulceration  Superficial thrombophlebitis
 Superficial thrombophlebitis  DVT
 Severe impact on QoL  Recurrence: may approach 50%
Leg Ulcers Leg Swelling
Definition Differential
 Interruption in the continuity of an epithelial surface
Bilateral
Causes ↑ Venous Pressure
 Venous: commonest RHF
 Arterial: large or small vessel Venous insufficiency
 Neuropathic: EtOH, DM Drugs: e.g. nifedipine
↓ Oncotic Pressure
 Traumatic: e.g. pressure
Nephrotic syndrome
 Systemic disease: e.g. pyoderma gangrenosum
Hepatic failure
 Neoplastic: SCC Protein losing enteropathy
Lymphoedema
Venous: 75% Myxoedema
 Painless, sloping, shallow ulcers Hyper- / hypo-thyroidism
 Usually on medial malleolus: “gaiter area”
 Assoc. c̄ haemosiderin deposition and Unilateral
lipodermatosclerosis Venous insufficiency
 RFs: venous insufficiency, varicosities, DVT, obesity DVT
Infection or inflammation
Arterial: 2% Lymphoedema
 Hx of vasculopathy and risk factors
 Painful, deep, punched out lesions Lymphoedema
 Occur @ pressure points  Collection of interstitial fluid due to blockage or absence
 Heal of lymphatics
 Tips of. and between, toes
 Metatarsal heads (esp. 5th) Primary
 Other signs of chronic leg ischaemia  Congenital absence of lymphatics
 May or may not be familial
Neuropathic  Presentation
 Painless c̄ insensate surrounding skin  Congenital: evident from birth
 Warm foot c̄ good pulses  Praecox: after birth but <35yrs
 Tarda: >35yrs
Complications Milroy’s Syndrome
 Osteomyelitis  Familial AD subtype of congenital lymphoedema
 Development of SCC in the ulcer (Marjolin’s ulcer)  F>M
Ix Secondary: FIIT
 ABPI if possible  Fibrosis: e.g. post-radiotherapy
 Duplex ultrasonography  Infiltration
 Biopsy may be necessary  Ca: prostate, lymphoma
 Look for malignant change: Marjolin’s ulcer  Filariasis: Wuchereria bancrofti
 Infection: TB
Mx of Venous Ulcers  Trauma: block dissection of lymphatics
 Refer to leg ulcer community clinic
 Focus on prevention Ix
 Graduated compression stockings  Doppler US
 Venous surgery  Lymphoscintigraphy
 Optimise risk factors: nutrition, smoking  CT / MRI
Specific Rx Mx
 Analgesia  Conservative
 Bed Rest + Elevate leg  Skin care
 4 layer graded compression bandage (if ABPI >0.8)  Compression stocking
 Pentoxyfylline PO  Physio
 ↑ microcirculatory blood flow  Treat or prevent comorbid infections
 Improves healing rates  Surgical: debulking operation
Other Options (no proven benefit)

 Desloughing: e.g. larval therapy, hydrogel
 Topical antiseptics: iodine, Manuka honey
 Split-thickness skin grafting may be considered

Urology
Contents
Urinary Tract Obstruction ............................................................................................................................................................ 95
Urethral Stricture ......................................................................................................................................................................... 95
Obstructive Uropathy ................................................................................................................................................................... 95
Urinary Retention......................................................................................................................................................................... 96
Haematuria .................................................................................................................................................................................. 97
Peri-Aortitis .................................................................................................................................................................................. 97
Urolithiasis: Pathophysiology and Presentation .......................................................................................................................... 98
Urolithiasis: Ix and Mx ................................................................................................................................................................. 99
Renal Tumours .......................................................................................................................................................................... 100
Bladder Tumours ....................................................................................................................................................................... 101
Benign Prostatic Hypertrophy .................................................................................................................................................... 102
Prostate Cancer......................................................................................................................................................................... 103
Prostatitis ................................................................................................................................................................................... 104
Urinary Incontinence.................................................................................................................................................................. 104
Undescended Testes................................................................................................................................................................. 105
Testicular Torsion ...................................................................................................................................................................... 105
Lumps in the Groin and Scrotum............................................................................................................................................... 106
Testicular Tumours .................................................................................................................................................................... 107
The Penis .................................................................................................................................................................................. 108

Urinary Tract Obstruction Urethral Stricture
Causes Aetiology
 Trauma
Luminal  Instrumentation
 Stones  Pelvic #s
 Blood clots  Infection: e.g. gonorrhoea
 Sloughed papilla  Chemotherapy
 Balantitis xerotica obliterans
Mural
 Congenital / acquired stricture Presentation: voiding difficulty
 Tumour: renal, ureteric, bladder  Hesitancy
 Neuromuscular dysfunction  Strangury
 Poor stream
Extramural  Terminal dribbling
 Prostatic enlargement  Pis en deux
 Abdo / pelvic mass / tumour
 Retroperitoneal fibrosis Examination
 PR: exclude prostatic cause
Presentation  Palpate urethra through penis
Acute  Examine meatus
 Upper Urinary Tract
 Loin pain → groin
Ix
 Lower Urinary Tract
 Urodynamics
 Bladder outflow obstruction precedes severe
 ↓ peak flow rate
suprapubic pain c̄ distended palpable bladder
 ↑ micturition time
 Urethroscopy and cystoscopy
Chronic
 Retrograde urethrogram
 Upper Urinary Tract
 Flank pain
 Renal failure (may be polyuric) Mx
 Lower Urinary Tract  Internal urethrotomy
 Frequency, hesitancy, poor stream, terminal  Dilatation
dribbling, overflow incontinence  Stent
 Distended, palpable bladder ± large prostate
PR
Ix Obstructive Uropathy
 Bloods: FBC, U+E
 Urine: dip, MC+S Pathogenesis
 Imaging  Acute retention on a chronic background may go
 US: hydronephrosis or hydroureter unnoticed for days due to lack of pain.
 Anterograde / retrograde ureterograms  Se Cr may be up to 1500uM
 Allow therapeutic drainage  Renal function should return to normal over days
 Radionucleotide imaging: renal function  Some background impairment may remain.
 CT / MRI
Complications
Mx
Upper Urinary Tract Hyperkalaemia
 Nephrostomy Metabolic acidosis
 Ureteric stent
Post-obstructive diuresis
Lower Urinary Tract  Kidneys produce a lot of urine in the acute phase
 Urethral or suprapubic catheter after relief of obstruction.
 May be a large post-obstructive diuresis  Must keep up c̄ losses to avoid dehydration.
Complications of Ureteric Stents Na and HCO3 losing nephropathy

Common  Diuresis may → loss of Na and HCO3
 Infection  May require replacement c̄ 1.26% NaHCO3
 Haematuria
 Trigonal irritation Infection
 Encrustation
Rare
 Obstruction
 Ureteric rupture
 Stent migration
Urinary Retention
Causes Chronic Urinary Retention (CUR)
Obstructive Classification
 Mechanical  High Pressure
 BPH  High detrusor pressure @ end of micturition
 Urethral stricture  Typically bladder outflow obstruction
 Clots, stones  → bilateral hydronephrosis and ↓ renal function
 Constipation  Low Pressure
 Dynamic: ↑ smooth muscle tone (α-adrenergic)  Low detrusor pressure @ end of micturition
 Post-operative pain  Large volume retention c̄ very compliant bladder
 Drugs  Kidney able to excrete urine
 No hydronephrosis  normal renal function
Neurological
 Interruption of sensory or motor innervation Presentation
 Pelvic surgery  Insidious as bladder capacity ↑↑ (>1.5L)
 MS  Typically painless
 DM  Overflow incontinence / nocturnal enuresis
 Spinal injury / compression  Acute on chronic retention
 Lower abdo mass
Myogenic
 UTI
 Over-distension of the bladder
 Renal failure
 Post-anaesthesia
 High EtOH intake
Mx
High-Pressure
Acute Urinary Retention (AUR)  Catheterise if
 Renal impairment
Clinical Features  Pain
 Suprapubic tenderness  Infection
 Palpable bladder  Hrly UO + replace: post-obstruction diuresis
 Dull to percussion  Consider TURP before TWOC
 Can’t get beneath it
 Large prostate on PR Low-Pressure
 Check anal tone and sacral sensation  Avoid catheterisation if possible
 <1L drained on catheterisation  Risk of introducing infection
 Early TURP
Ix  Often do poorly due to poor detrusor function
 Blood: FBC, U+E, PSA (prior to PR)  Need CISC or permanent catheter
 Urine: dip, MC+S
 Imaging
 US: bladder volume, hydronephrosis Suprapubic Catheterisation
 Pelvic XR
Advantages
Mx  ↓ UTIs
 ↓ stricture formation
Conservative  TWOC w/o catheter removal
 Analgesia  Pt. preference: ↑ comfort
 Privacy  Maintain sexual function
 Walking
 Running water or hot bath Disadvantages
 More complex: need skills
Catheterise  Serious complications can occur
 Use correct catheter: e.g. 3-way if clots
 ± STAT gent cover CI
 Hrly UO + replace: post-obstruction diuresis  Known or suspected bladder carcinoma
 Tamsulosin: ↓ risk of recatheterisation after retention  Undiagnosed haematuria
 TWOC after 24-72h  Previous lower abdominal surgery
 May d/c and f/up in OPD  → adhesion of small bowel to abdo wall
 More likely to be successful if predisposing factor
and lower residual volume (<1L)
Clean Intermittent Self-Catheterisation
TURP  Alternative to indwelling catheter in AUR and CUR
 Failed TWOC  Also useful in pts. who fail to void after TURP
 Impaired renal function
 Elective
Haematuria Peri-Aortitis
False Aetiology
 Beetroot  Idiopathic retroperitoneal fibrosis
 Rifampicin  Inflammatory AAAs
 Porphyria  Perianeurysmal RPF
 PV bleed  RPF 2O to malignancy: e.g. lymphoma
Idiopathic Retroperitoneal Fibrosis

True  Autoimmune vasculitis
 Fibrinoid necrosis of vasa vasorum
General  Affects aorta and small/medium sized retroperitoneal
 HSP vessels.
 Bleeding diathesis  Ureters are embedded in dense, fibrous tissue →
bilateral obstruction
Renal
 Infarct Associations
 Trauma: inc. stones  Drugs: β-B, bromocriptine, methysergide, methyldopa
 Infection  AI disease: thyroiditis, SLE, ANCA+ vasculitis
 Neoplasm  Smoking
 GN  Asbestos
 Polycystic kidneys
Presentation
Ureter
 Middle–aged male
 Stone
 Vague loin, back or abdo pain
 Tumour
 ↑ BP
 Chronic urinary tract obstruction
Bladder
 Infection
 Stones Ix
 Tumour  Blood: ↑U and Cr, ↑ESR/CRP, ↓Hb
 Exercise  US: bilateral hydronephrosis + medial ureteric deviation
 CT/MRI: peri-aortic mass
Prostate  Biopsy: exclude Ca
 BPH
 Prostatitis Rx
 Tumour  Relieve obstruction: retrograde stent placement
 Ureterolysis: dissection of ureters from retroperitoneal
Urethra tissue.
 Infection  ± immunosuppression
 Stones
 Trauma
 Tumour
Clinical Features
 Timing?
 Beginning of stream: urethral
 Throughout stream: renal / systemic, bladder
 End of stream: bladder stone, schisto
 Painful or painless?
 Obstructive symptoms?
 Systemic symptoms: wt. loss, appetite
Ix
 Bloods: FBC, U+E, clotting
 Urine: dip, MC+S, cytology
 Imaging
 Renal US
 IVU
 Flexible cystoscopy + biopsy
 CT/MRI
 Renal angio

Urolithiasis: Pathophysiology and Presentation
Epidemiology Presentation
 Lifetime incidence: 15%
 Young men Ureteric Colic
 Peak age: 20-40yrs  Severe loin pain radiating to the groin
 Sex: M>F=3:1  Assoc. c̄ n/v
 Pt. cannot lie still
Pathophysiology Bladder or Urethral Obstruction

 ↑ concentration of urinary solute  Bladder irritability: frequency, dysuria, haematuria
 ↓ urine volume  Strangury: painful urinary tenesmus
 Urinary stasis  Suprapubic pain radiating → tip of penis or in labia
 Pain and haematuria worse at the end of micturition
Other Possible Features

Common Anatomical Sites  UTI
 Pelviureteric junction
 Haematuria
 Crossing the iliac vessels at the pelvic brim
 Sterile pyuria
 Under the vas or uterine artery
 Anuria
 Vesicoureteric junction
Examination
Stone Types  Usually no loin tenderness
 Calcium oxalate: 75%
 Haematuria
 ↑ risk in Crohn’s
 Triple phosphate (struvite): 15%
 Ca Mg NH4 – phosphate
 May form staghorn calculi
 Assoc. c̄ proteus infection
 Urate: 5% (radiolucent)
 Double if confirmed gout
 Cystine: 1% (faint)
 Assoc. c̄ Fanconi Syn.
Associated Factors
 Dehydration
 Hypercalcaemia: 1O HPT, immobilisation
 ↑ oxalate excretion: tea, strawberries
 UTIs
 Hyperuricaemia: e.g. gout
 Urinary tract abnormalities: e.g. bladder diverticulae
 Drugs: frusemide, thiazides

Urolithiasis: Ix and Mx
Urine Initial Rx
 Dip: haematuria  Analgesia
 MC+S  Diclofenac 75mg PO/IM or 100mg PR
 Opioids if NSAIDs CI: e.g. pethidine
Blood  Fluids: IV if unable to tolerate PO
 FBC, U+E, Ca, PO4, urate  Abx if infection: e.g cefuroxime 1.5mg IV TDS
Conservative: <5mm in lower 1/3 of ureter

 90-95% pass spontaneously
Imaging
 Can discharge pt. c̄ analgesia
KUB XR  Sieve urine to collect stone for OPD analysis
 90% of stones radio-opaque
 Urate stones are radiolucent, cysteine stones are faint Medical Expulsive Therapy (MET)
USS: hydronephrosis Indications

 Stone 5-10mm
Spiral non-contrast CT-KUB  Stone expected to pass
 99% of stones visible
 Gold standard Drugs
 Nifedipine or tamsulosin
IVU  ± prednisolone
 600x radiation dose of KUB  Most pass w/i 48h, 80% w/i 30d
 IV contrast injected and control, immediate and serial
films taken until contrast @ level of obstruction Active Stone Removal
 Abnormal findings
 Failure of flow to the bladder Indications
 Standing column of contrast  Low likelihood of spontaneous passage: e.g. >10mm
 Clubbing of the calyces: back pressure  Persistent obstruction
 Delayed, dense nephrogram: no flow from kidney  Renal insufficiency
 CI  Infection
 Contrast allergy
 Severe asthma Extracorporeal Shockwave Lithotripsy (SWL)
 Metformin  Stones <20mm in kidney or proximal ureter
 Pregnancy  SE: renal injury may → ↑BP
 CI: pregnancy, AAA, bleeding diathesis
Functional Scans
 DMSA: dimercaptosuccinic acid
Ureterorenoscopy (URS) + Dormier Basket Removal
 DTPA: diethylenetriamene penta-acetic acid  Stone >10mm in distal ureter or if SWL failed
 MAG-3  Stone >20mm in renal pelvis
Percutaneous Nephrolithotomy (PNL)

Prevention  Stone >20mm in renal pelvis
 Drink plenty  E.g. staghorn calculi: do DMSA first
 Treat UTIs rapidly
 ↓ oxalate intake: chocolate, tea, strawberries Lap or Open Surgery: rare
Febrile c̄ Renal Obstruction

 Surgical emergency
 Percutaneous nephrostomy or ureteric stent
 IV Abx: e.g. cefuroxime 1.5g IV TDS
Rx Summary
Conservative: stone <5mm in distal ureter
MET: stone 5-10mm and expected to pass
Active: stones >10mm, persistent pain, renal insufficiency
Location Size 1st line 2nd line

Pelvis >20mm PNL or URS SWL
<20mm SWL URS, PNL
Proximal >10mm URS or SWL
ureter <10mm SWL URS
Distal ureter >10mm URS SWL
© Alasdair Scott, 2012 <10mm URS or SWL 99
Renal Tumours
Renal Cell Carcinoma / Hypernephroma Transitional Cell Carcinoma
Epidemiology Epidemiology
 90% of renal cancers  2nd commonest renal cancer
 Age: 55yrs  Age: 50-80yrs
 Sex: M>F=2:1  Sex: M>F=4:1
Risk Factors Risk Factors

 Obesity  Smoking
 Smoking  Amine exposure (rubber industry)
 HTN  Cyclophosphamide
 Dialysis (15% of pts. develop RCC)
 4% heritable: e.g. VHL syndrome Pathology
 Highly malignant
Pathology  Locations
 Adenocarcinoma from proximal renal tubular epithelium  Bladder: 50%
 Subtypes  Ureter
 Clear Cell (glycogen): 70-80%  Renal pelvis
 Papillary: 15%
 Chromophobe: 5% Presentation
 Collecting duct: 1%  Painless haematuria
 Frequency, urgency, dysuria
Presentation  Urinary tract obstruction
 50% incidental finding
 Triad: Haematuria, loin pain, loin mass Ix
 Systemic: anorexia, malaise, wt. loss, PUO  Urine cytology
 Clot retention  CT/MRI
 Invasion of L renal vein → varicocele (1%)  IVU: pelviceal filling defect
 Cannonball mets → SOB
Mx
Paraneoplastic Features  Nephrouretectomy
 EPO → polycythaemia  Regular f/up: 50% develop bladder tumours
 PTHrP → ↑ Ca
 Renin → HTN
 ACTH → Cushing’s syn. Nephroblastoma: Wilm’s Tumour
 Amyloidosis  Childhood tumour of primitive renal tubules and
mesenchymal cells
Spread  May be assoc. c̄ Chr 11 mutation
 Direct: renal vein  May be assoc. c̄ WAGR syndrome
 Lymph  Wilms, Aniridia, GU abnormalities, Retardation
 Haematogenous: bone, liver and lung
Presentation
Ix  2-5yrs
 Blood: polycythaemia, ESR, U+E, ALP, Ca  5-10% bilat
 Urine: dip, cytology  Abdo mass (doesn’t cross the midline)
 Imaging  Haematuria
 CXR: cannonball mets  Abdo pain
 US: mass  HTN
 IVU: filling defect
 CT/MRI
Other Neoplasms
Robson Staging
1. Confined to kidney
Benign
2. Involves perinephric fat, but not Garota’s fascia
 Cysts: very common
3. Spread into renal vein
4. Spread to adjacent / distant organs  Renal papillary adenomas
 Oncocytoma: eosinophilic cells c̄ numerous
Mx mitochondria
 Medical  Angiomyolipoma: seen in tuberous sclerosis
 Reserved for pts. c̄ poor prognosis
 Temsirolimus (mTOR inhibitor) Malignant
 Surgical  SCC: assoc. c̄ chronic infected staghorn calculi
 Radical nephrectomy
 Consider partial if small tumour or 1 kidney NB. Benign tumours commonly require nephrectomy to
exclude malignancy.
Prognosis: 45% 5ys
Bladder Tumours
Epidemiology Ix
 Incidence: 1:5000/yr  Urine: dip (sterile pyuria), cytology
 Sex: M>F=4:1  IVU: filling defects
 Cystoscopy c̄ biopsy: diagnostic
Pathology  Bimanual EUA: helps to assess spread
 Transitional cell carcinomas account for 90%  CT/MRI: helps stage
 SCCs: assoc. c̄ schistosomiasis
 Adenocarcinoma Mx
 Depends on histological grade and the presence of
Natural Hx dissemination.
 Low-Grade Tumours
 80% TIS, Ta and T1 (Superficial)
 Non-invasive, generally not life-threatening  80% of all pts.
 High rate of recurrence  Diathermy via transurethral cystoscopy / Transurethral
 High-Grade Tumours Resection of Bladder Tumour (TURBT)
 20%  Intravesicular chemo: mitomycin C
 Invasive and life-threatening  Intravesicular immunotherapy: Bacille Calmette-Guérin
 High recurrence rates
T2, T3 (Invasive)
Risk Factors  Radical cystectomy c̄ ileal conduit is gold standard
 Smoking  Radiotherapy: worse 5ys but preserves bladder
 Amine exposure (rubber industry)  Salvage cystectomy can be performed
 Previous renal TCC  Adjuvant chemo: e.g. M-VAC
 Chronic cystitis  Neoadjuvant chemo may have a role
 Schistosomiasis (SCC)
 Urechal remnants (adenocarcinomas) T4
 Embryological remnant of communication  Palliative chemo / radiotherapy
between umbilicus and bladder  Long-term catheterisation
 Pelvic irradiation  Urinary diversions
Presentation Complications
 Painless haematuria  Massive bladder haemorrhage
 Voiding irritability: dysuria, frequency, urgency  Cystectomy → Sexual and urinary malfunction
 Recurrent UTIs
 Retention and obstructive renal failure Follow-Up
 Up to 70% of bladder tumours recur therefore intensive
Examination f/up is required.
 Anaemia  History, examination and regular cystoscopy
 Palpable bladder mass  High-risk tumours: every 3mo for 2yrs, then every 6mo
 Palpable liver  Low-risk tumours: @ 9mo, then yrly
TNM Staging Prognosis

 80% confined to mucosa  Depends on age and stage
 20% penetrate muscle (↑ mortality)  TIS, Ta and T1: 95% 5ys
 T2: 40-50% 5ys
TIS Carcinoma in situ Not felt at EUA  T3: 25% 5ys
Ta Confined to epithelium Not felt at EUA  T4: <1yr median survival
T1 Tumour in lamina propria Not felt at EUA
T2 Superficial muscle involved Rubbery thickness
T3 Deep muscle involved Mobile mass
T4 Invasion of prostate, uterus or vag Fixed mass
Spread
 Local → pelvic structures
 Lymph → iliac and para-aortic nodes
 Haem → bones, liver and lungs
Histological Classification
 Grade 1: well differentiated
 Grade 2: intermediate
 Grade 3: poorly differentiated

Benign Prostatic Hypertrophy
Epidemiology Mx
 70% @ 60yrs
 90% @ 80yrs Conservative
 ↓ caffeine, EtOH
 Double voiding
Pathophysiology  Bladder training: hold on → ↑ time between voiding
 Benign nodular or diffuse hyperplasia of stromal and
epithelial cells Medical
 Affects inner (transitional) layer of prostate (cf. Ca)  Useful in mild disease and while awaiting TURP
st
 → urethral compression  1 : α-blockers
 DHT produced from testosterone in stromal cells by 5α-  Tamsulosin, doxazosin
reducatase enzyme.  Relax prostate smooth muscle
 DHT-induced GFs → ↑ stromal cells and ↓ epithelial cell  SE: drowsiness, ↓BP, depression, EF, wt. ↑,
death. extra-pyramidal signs
 2nd: 5α-reductase inhibitors
 Finasteride
Presentation  Inhibit conversion of testosterone → DHT
 Preferred if significantly enlarged prostate.
 Storage Symptoms
 SE: excreted in semen (use condoms), ED
 Nocturia
 Frequency
Surgical Mx
 Urgency
 Overflow incontinence  Indications
 Symptoms affect QoL
 Voiding Symptoms
 Complications of BPH
 Hesitancy
 Straining  TURP
 Poor stream/flow + terminal dribbling  Cystoscopic resection of lateral and middle lobes
 Strangury (urinary tenesmus)  ≤14% become impotent
 Incomplete emptying: pis en deux  Transurethral incision of prostate (TUIP)
O
 Bladder stones (2 to stasis)  < destruction → ↓ risk to sexual function
O  Similar benefits to TURP if small prostate (<30g)
 UTI (2 to stasis)
 Tranurethral ElectroVaporisation of Prostate
 Electric current → tissue vaporisation
 Laser prostatectomy
Examination  ↓ ED and retrograde ejaculation
 PR  Similar efficacy as TURP
 Smoothly enlarged prostate
 Open retropubic prostatectomy
 Definable median sulcus
 Used for very large prostates (>100g)
 Bladder not usually palpable unless acute-on-chronic
obstruction
TURP Complications
Ix
Immediate
 Blood: U+E, PSA (after PR)
 TUR syndrome
 Urine: dip, MC+S
 Absorption of large quantity of fluids → ↓Na
 Imaging
 Haemorrhage
 Transrectal US ± biopsy
 Urodynamics: pressure / flow cystometry
Early
 Voiding diary
 Haemorrhage
 Infection
 Clot retention: requires bladder irrigation
Late
 Retrograde ejaculation: common
 ED: ~10%
 Incontinence: ≤10%
 Urethral stricture
 Recurrence

Prostate Cancer
Epidemiology Gleason Grade

 Score two worst affected areas
 Commonest male Ca
 Sum is inversely proportional to prognosis
 3rd commonest cause of male Ca death
 Prevalence: 80% of men >80yrs
 Race: ↑ in Blacks
TNM Stage
TIS Carcinoma in situ
Pathology T1 Incidental finding on TURP or ↑PSA
 Adenocarcinoma
T2 Intracapsular tumour c̄ deformation of prostate
 Peripheral zone of prostate
T3 Extra-prostatic extension
T4 Fixed to pelvis + invading neighbouring structures
Presentation N1-4 1 or more lymph nodes involved
 Usually asymptomatic M1 Distant mets, e.g. spine
 Urinary: nocturia, frequency, hesitancy, poor stream,
terminal dribbling, obstruction
 Systemic: wt. loss, fatigue
Prognostic Factors
 Help determine whether to pursue radical Rx
 Mets: bone pain
 Age
 Pre-Rx PSA
Examination
 Tumour stage
 Hard irregular prostate on PR
 Tumour grade
 Loss of midline sulcus
Spread Mx
 Local: seminal vesicles, bladder, rectum  Difficult to know which tumours are indolent and will not
 Lymph: para-aortic nodes → mortality before something else.
 Haem: sclerotic bony lesions  Radical therapy assoc. c̄ significant morbidity.
Ix Conservative: Active Monitoring

 Bloods: PSA, U+E, acid and alk phos, Ca  Close monitoring c̄ DRE and PSA
 Imaging
 XR chest and spine Radical Therapy
 Transrectal US + biopsy  Radical prostatectomy (+ goserelin if node +ve)
 Bone scan  Performed laparoscopicaly c̄ robot
 Staging MRI  Only improves survival vs. active monitoring if
 Contrast enhancing magnetic nanoparticles <75yrs
↑s detection of affected nodes.  Brachytherapy: implantation of palladium seeds
 SEs: ED, urinary incontinence, death (0.2-0.5%)
PSA
 Proteolytic enzyme used in liquefaction of ejaculate Medical
 Not specific for prostate Ca  Used for metastatic or node +ve disease
 ↑ c̄ age, PR, TURP, and prostatitis  LHRH analogues
 >4ng/ml: 40-90% sensitivity, 60-90% specificity  E.g. goserelin
 Only 1-in-3 will have Ca  Inhibit pituitary gonadotrophins → ↓ testosterone
 Normal in 30% of small cancers  Anti-androgens
 E.g. cyproterone acetate, flutamide
Symptomatic
 TURP for obstruction
 Analgesia
 Radiotherapy for bone mets / cord compression
Screening c̄ PSA
 Population based screening not recommended in UK
 PSA not an accurate tumour marker
 ERSPC trial showed small mortality benefit, PLCO trial
showed no benefit.
 Must balance mortality benefit c̄ harm caused by over
diagnosis and over treatment of indolent cancers.

Prostatitis Urinary Incontinence
Aetiology Male
 S. faecalis  Usually caused by prostatic enlargement
 E. coli  Urge incontinence or dribbling may result from
 Chlamydia partial retention.
 Retention may → overflow (palpable bladder after
Presentation voiding)
 Usually >35yrs  TURP and pelvic surgery may weaken external urethral
 UTI / dysuria sphincter.
 Pain
 Low backache Women
 Pain on ejaculation  Stress Incontinence
 Haematospermia  Leakage from incompetent sphincter when IAP ↑
 Fever and rigors  Loss of small amounts of urine when coughing
 Retention  Pelvic floor weakness
 Malaise  Urge Incontinence / Overactive Bladder
 Can’t hold urine for any length of time
 May have precipitant: arriving home, running water,
Examination coffee
 Pyrexia  Dx: urodynamic studies
 Swollen / boggy / tender prostate on PR
 Examine testes to exclude epididymo-orchitis
Mx
 Check
Ix  PR: faecal impaction
 Blood: FBC, U+E, CRP  Palpable bladder after voiding: retention c̄ overflow
 Urine: dip, MC+S  UTI
 DM
Rx  CNS: MS, Parkinson’s stroke, spinal trauma
 Analgesia  Diuretics
 Levofloxacin 500mg/d for 28d  Stress Incontinence
 Pelvic floor exercises
 Ring pessary
 Duloxetine
 Surgery: tension-free vaginal tape
 Urge Incontinence
 Bladder training
 Wt. loss
 Anti-AChM: tolterodine, imipramine

Undescended Testes Testicular Torsion
Epidemiology Aetiology
 3% @ birth  Usually 2O to some exertion or minor trauma
 1% @ 1yr  Occurs because testicle doesn’t have a large “bare
 Unilateral 4x commoner cf. bilateral area” to attach to scrotal wall.
 Should have genetic testing if bilateral  Tunica vaginalis invests whole of testicle
 Noonan’s Prader-Willi  Free-hanging “clapper bell” testicle can twist on
 Commoner in prems: incidence up to 30% its mesentery.
Normal Descent Presentation

 Testes remain in abdomen (retroperitoneal) until 7mo  Usually 10-25yrs
 Gubernaculum connects inferior pole of testis to scrotum.  Sudden onset severe pain in one testis
 Testis descends through inguinal canal to scrotum c̄ an  May have lower abdominal pain (testis supplied by T10)
out-pouching of peritoneum: processus vaginalis.  Assoc. c̄ n/v
 May be Hx of previous testicular pain or torsion
Classification
Examination
Cryptorchidism  Inflam of one testis: hot, swollen, extremely tender
 Complete absence of testis from scrotum  Testis rides high and lies transversely
 Anorchism = absence of both testes
Differential
Retractile Testis  Epididymo-orchitis
 Normal development but excessive cremasteric reflex  Older pt.
 Testicle often found at external inguinal ring  UTI symptoms
 Will descend: no Rx required  More gradual onset
 Torted Hydatid of Morgagni
Maldescended Testis  Remnant of Mullerian duct
 Found anywhere along normal path of descent  Younger pt.
 Testis and scrotum are usually under-developed  Less pain
 Often assoc. c̄ patent processus vaginalis  Tiny blue dot visible on scrotum
 Tumour
Ectopic Testis  Trauma
 Found outside line of descent  Strangulated hernia
 Usually in sup. inguinal pouch (ant. to external oblique  Appendicitis
aponeurosis)
 Abdominal, perineal, penile, femoral triangle Ix
 Doppler US may demonstrate absence of flow
Complications  Must not delay surgical exploration
 Infertility
 10x ↑ risk of malignancy (remains after surgery) Mx
 ↑ risk of trauma  Surgical emergency
 ↑ risk of torsion  4-6h window from onset of pain to salvage testis
 Assoc. c̄ hernias (90%) or urinary tract abnormalities  Inform senior
 NBM
Mx  IV access
 Restores potential for spermatogenesis  Analgesia
 Makes Ca easier to Dx  Bloods: FBC, U+E, G+S, clotting
 Surgery
Surgical: Orchidopexy by Dartos Pouch Procedure  Consent for possible orchidectomy
 Perform before 2yrs  Bilateral orchidopexy: suture testes to scrotum
 Mobilisation of testis and cord  If no torsion found and epididymo-orchitis Dx, take fluid
 Removal of patent processus sample from scrotum for bacteriology and Rx c̄ Abx.
 Testicle brought through a hole made in the dartos
muscle to lie in a subcutaneous pouch.
 Dartos prevents retraction.
Hormonal
 β-HCG may be tried if testis is in inguinal canal.

Lumps in the Groin and Scrotum
Differential Epididymo-Orchitis
 Can’t get above: inguinoscrotal hernia
 Separate, cystic: epididymal cyst Aetiology
 Separate, solid: varicocele, sperm granuloma, epididymitis  STI: Chlamydia, gonorrhoea
 Testicular, cystic: hydrocele  Ascending UTI: e. coli
 Testicular, solid: tumour, orchitis, haematocele  Mumps
Epididymal Cyst Features

 Develop in adulthood  Sudden onset tender swelling
 Contain clear or milky (spermatocele) fluid  Dysuria
 Lie above and behind testis  Sweats, fever
 Remove if symptomatic
Examination
 Tender, red, warm, swollen testis and epididymis
Varicocele  Elevating testicle may relieve pain
 Dilated veins of pampiniform plexus
 Secondary hydrocele
 Presentation
 Urethral discharge
 Feel like bag of worms in the scrotum
 May be visible dilated veins
Ix
 ↓ size on lying down
 Blood: FBC, CRP
 Pt. may c/o dull ache
 May → oligospermia (↓ fertility)  Urine: dip, MC+S (fist catch may be best)
 Pathology  Urethral swab and STI screen
 1O: Left side commoner: drain into left renal vein  US: may be needed to exclude abscess
 2O: left renal tumour has tracked down renal vein →
testicular vein obstruction. Complications
 Mx  May → infertility
 Conservative: scrotal support
 Surgical: clipping the testicular vein (open or lap) Mx
 Bed rest
Sperm Granuloma  Analgesia
 Painful lump of extravasated sperm after vasectomy  Scrotal support
 Abx: doxycycline or cipro
 Drain abscess if present
Hydrocele
 Collection of serous fluid w/i tunica vaginalis
 Primary
 assoc. c̄ patent processus vaginalis
 Commoner, larger, tense, younger men
 Secondary
 Tumour, trauma, infection
 Smaller, less tense
 Ix
 US testicle to exclude tumour
 Mx
 May resolve spontaneously
 Surgery
 Lord’s Repair: plication of the sac
 Jaboulay’s Repair: eversion of the sac
 Aspiration
st
 Usually recur so not 1 line.
 Send fluid for cytology and MC+S
Haematocele
 Blood in the tunica vaginalis
 Hx of trauma
 May need drainage or excision

Testicular Tumours
Epidemiology Staging: Royal Marsden Classification
 Commonest male malignancies from 15-44yrs 1. Disease only in testis
 Whites > Blacks = 5:1 2. Para-aortic nodes involved (below diaphragm)
3. Supra- and infra-diaphragmatic LNs involved
Presentation 4. Extra-lymphatic spread: lungs, liver
 Painless testicular lump
 Often noticed after trauma Ix
 Haematospermia  Tumour markers
 2O hydrocele  Useful for monitoring
 Mets: SOB from lung mets  ↑AFP and ↑hCG in 90% of teratomas
 Abdo mass: para-aortic lymphadenopathy  ↑hCG in 15% of seminomas
 Hormones: gynaecomastia, virilisation  Normal AFP in pure seminomas
 Contralateral tumour in 5%  Scrotum US
 Staging
 CXR
Risk Factors  CT
 Undescended testis NB. Percutaneous biopsy should not be performed as it may
 10% occur in undescended testes → seeding along needle tract
 Infant hernia
 Infertility
Mx
 If both testes are abnormal, semen can be
Pathology cryopreserved
Germ Cell: 95% of tumours Seminomas
 Pure Seminomas: 40%  Stage 1-2: inguinal orchidectomy + radiotherapy
 Commonest single subtype  Groin incision allows cord clamping to prevent
 30-40yrs seeding
 ↑ βhCG in 15%  Stage 3-4: as above + chemo (BEP)
 ↑ placental ALP in some  Bleomycin, Etoposide, cisPlatin
 Very radiosensitive
 Non-seminomas (inc.mixed): 60% Non-seminomas / Teratomas
 Mixed: commonest NSGCT  Stage 1: inguinal orchidectomy + surveillance
 Teratoma
 Stage 2: orchidectomy + chemo + para-aortic LN
 Arise from all 3 germ layers dissection
 Common and benign in children  Stage 3: orchidectomy + chemo
 Rare and malignant in adults: 15-30yrs
 Secrete βhCG and/or AFP Close f/up to detect relapse
 Chemosensitive  Typically w/i 18-24mo
 Yolk Sac  Repeat CT scanning and tumour markers
 Commonest testicular tumour in children
 Choriocarcinoma Prognosis
 ↑↑ βhCG
 Stage 1: 98% 5ys
 Stage 2: 85% 5ys
Sex-cord Stromal
 Stage 4: 60% 5ys
 Leydig Cell
 Mostly benign
 May secrete androgens or oestrogens
 Sertoli Cell
 Mostly benign
 May secrete oestrogens
Lymphoma / Leukaemia
 NHL: commonest malignant testicular mass >60yrs
 ALL: commonest malignant testicular mass <5yrs

The Penis
Balanitis Penile Cancer
 Acute inflammation of the foreskin and glans
 Cause: Strep, staph infection, Candida (DM) Epidemiology
 RFs: DM, young children c̄ tight foreskin  Incidence: 1:100,000/yr in UK
 Rx: hygiene advice, Abx, circumcision  Geo: commoner in Far East and Africa
Aetiology
 V. rare if circumcised
Phimosis
 Risk factors
 Foreskin occludes the meatus
 HPV (16, 18, 31) infection
 Children O
 Chronic irritation 2 to smegma
 Pres: recurrent balanitis and ballooning
 Mx: Gentle retraction, steroid creams, circumcision Pathology
 Adults  Erythroplasia of Querat: penile CIS
 Pres: dyspareunia, infection
 SCC
 Mx: circumcision
 Assoc. c̄ balanitis xerotica obliterans: thickening of
Presentation
foreskin and glans → phimosis + meatal narrowing  Chronic fungating ulcer
 Bloody / purulent discharge
 50% have inguinal nodes at presentation
Paraphimosis
 Tight foreskin is retracted and becomes irreplaceable. Mx
 ↓ venous return → oedema and swelling of the glans  Medical
 Can rarely → glans ischaemia  Early growths c̄ no urethral involvement
 Causes: catheterisation, masturbation, intercourse  DXT and iridium wires
 Mx:  Surgical
 Manual reduction: use ice and lignocaine jelly  Amputation required if urethral involvement
 May require glans aspiration or dorsal slit  Lymph node dissection
Hypo- / epi-spadias
 Developmental abnormality of the position of the urethral
opening
 Hypospadia: opens on ventral surface of penis
 Epispadia: opens on dorsal surface

Orthopaedics
Contents
Bone and Fracture Physiology .................................................................................................................................................. 110
Fracture Classification ............................................................................................................................................................... 110
Fracture Management: 4Rs ....................................................................................................................................................... 111
Fracture Complications ............................................................................................................................................................. 112
Hip Fracture ............................................................................................................................................................................... 114
Distal Forearm Fractures ........................................................................................................................................................... 115
Scaphoid Fractures ................................................................................................................................................................... 115
Radial and Ulna Shaft Fractures ............................................................................................................................................... 115
The Shoulder ............................................................................................................................................................................. 116
Supracondylar Fractures of the Humerus ................................................................................................................................. 117
Femoral and Tibial Fractures .................................................................................................................................................... 118
Ankle Injuries ............................................................................................................................................................................. 118
Knee Injuries.............................................................................................................................................................................. 119
Osteoarthritis ............................................................................................................................................................................. 120
Back Pain .................................................................................................................................................................................. 121
Osteochondritis.......................................................................................................................................................................... 122
Traction Apophysitis .................................................................................................................................................................. 122
Osteochondritis Dissecans ........................................................................................................................................................ 122
Avascular Necrosis .................................................................................................................................................................... 122
The Limping Child...................................................................................................................................................................... 123
Acute Osteomyelitis ................................................................................................................................................................... 124
Septic Arthritis ........................................................................................................................................................................... 124
Bone Tumours ........................................................................................................................................................................... 125
Brachial Plexus Injuries ............................................................................................................................................................. 127
Other Nerve Injuries .................................................................................................................................................................. 127
Carpal Tunnel Syndrome .......................................................................................................................................................... 128
Minor Hand Conditions .............................................................................................................................................................. 129
Minor Leg and Foot Conditions ................................................................................................................................................. 130

Bone and Fracture Physiology Fracture Classification
Composition Classification
 Traumatic #
Cells: osteoblasts, osteoclasts, osteocytes, OPCs  Direct: e.g. assault c̄ metal bar
 Indirect: e.g. FOOSH → clavicle #
Matrix  Avulsion
 Organic = osteoid (40%)  Stress #
 Collagen Type I  Bone fatigue due to repetitive strain
 Resists tension, twisting and bending  E.g. foot #s in marathon runners
 Inorganic (60%)  Pathological #
 Calcium hydroxyapatite  Normal forces but diseased bone
 Resists compressive forces  Local: tumours
 General: osteoporosis, Cushing’s, Paget’s
Classification Describing a fracture: PAID

 Radiographs must be orthogonal: request AP and lat. films.
Woven Bone  Need images of joint above and joint below #.
 Disorganised bone that forms the embryonic skeleton
and fracture callus. 1. Demographics
 Pt. details
Lamellar Bone  Date radiograph taken
 Mature bone that can be of two types:  Orientation and content of image
 Cortical/compact: dense outer layer
 Cancellous/trabecular: porous central layer 2. Pattern
 Transverse  Crush
 Oblique  Greenstick
Formation  Spiral  Avulsion
 Multifragmentary
Intramembranous Ossification
 Direct ossification of mesenchymal bone models 3. Anatomical Location
formed during embryonic development.
 Skull bones, mandible and clavicle. 4. Intra- / extra-articular
 Dislocation or subluxation
Endochondral Ossification
 Mesenchyme → cartilage → bone 5. Deformity (distal relative to proximal)
 Most bones ossify this way  Translation
 Angulation or tilt
 Rotation
 Impaction (→shortening)
Fracture Healing
6. Soft Tissues
Reactive Phase (injury – 48hrs)  Open or closed
1. Bleeding into # site → haematoma  Neurovascular status
2. Inflammation → cytokine, GF and vasoactive  Compartment syndrome
mediator release → recruitment of leukos and
fibroblasts → granulation tissue 7. ? Specific # classification/type
 Salter-Harris
Reparative Phase (2 days – 2 wks)  Garden
3. Proliferation of osteoblasts and fibroblasts →  Colles’, Smith’s, Galeazzi, Monteggia
cartilage and woven bone production → callus
formation.
4. Consolidation (endochondral ossification) of woven
bone → lamellar bone
Remodelling Phase (1wk – 7yrs)

5. Remodelling of lamellar bone to cope c̄ mechanical
forces applied to it (Wolff’s Law: “form follows
function”)
Healing Time
 Closed, paediatric, metaphyseal, upper limb: 3wks
 “Complicating factor” doubles healing time
 Adult
 Lower limb
 Diaphyseal
 Open

Fracture Management: 4Rs
1: Resuscitation 3: Restriction
Principles Principles
 Follow ATLS guidelines  Interfragmentary strain hypothesis dictates that tissue
 Trauma series in 1O survey: C-spine, chest and pelvis formed @ # site depends on strain it experiences.
 # usually assessed in 2O survey  Fixation → ↓ strain → bone formation
 Assess neurovascular status and look for dislocations  Fixation also → ↓ pain, ↑ stability, ↑ ability to function.
 Consider reduction and splinting before imaging
 ↓ pain Methods
 ↓ bleeding  Non-rigid
 ↓ risk of neurovascular injury  Slings
 X-ray once stable  Elastic supports
 Plaster
Open fractures require urgent attention: 6As  POP
 Analgesia: M+M  In first 24-48h use back-slab or split cast due to
 Assess: NV status, soft tissues, photograph risk of compartment syndrome
 Antisepsis: wound swab, copious irrigation, cover with  Functional bracing
betadine-soaked dressing.  Joints free to move but bone shafts supported in
 Alignment: align # and splint cast segments.
 Anti-tetanus: check status (booster lasts 10yrs)  Continuous traction
 e.g. collar-and-cuff
 Abx
 Fluclox 500mg IV/IM + benpen 600mg IV/IM  Ex-Fix
 Fragments held in position by pins/wires which
 Or, augmentin 1.2g IV
are then connected to an external frame.
Mx: debridement and fixation in theatre  Intervention is away from field of injury.
 Useful in open #s, burns, tissue loss to allow
wound access and ↓ infection risk.
Gustillo Classification of Open #s
1. Wound <1cm in length  Risk of pin-site infections
2. Wound ≥1cm c̄ minimal soft tissue damage  Internal fixation
 Pins, plates, screws, IM nails
3. Extensive soft tissue damage
 Usually perfect anatomical alignment
 ↑ stability
Clostridium perfringes
 Aid early mobilisation
 Most dangerous complication of open #
 Wound infections and gas gangrene
 ± shock and renal failure
4: Rehabilitation
 Rx: debride, benpen + clindamycin
Principles
2: Reduction  Immobility → ↓ muscle and bone mass, joint stiffness
 Need to maximise mobility of uninjured limbs
Principles
 Quick return to function ↓s later morbidity
 Displaced #s should be reduced
 Unless no effect on outcome, e.g. ribs Methods
 Aim for anatomical reduction (esp. if articular surfaces  Physiotherapy: exercises to improve mobility
involved)
 OT: splints, mobility aids, home modification
 Alignment is more important than opposition
 Social services: meals on wheels, home help
Methods
 Manipulation / Closed reduction
 Under local, regional or general anaesthetic
 Traction to disimpact
 Manipulation to align
 Traction
 Not typically used now.
 Employed to overcome contraction of large
muscles: e.g. femoral #s
 Skeletal traction vs. skin traction
 Open reduction (and internal fixation)

 Accurate reduction vs. risks of surgery
 Intra-articular #s
 Open #s
 2 #s in 1 limb
 Failed conservative Rx
 Bilat identical #s
Fracture Complications
General Complications Specific Complications
Tissue Damage Immediate
 Haemorrhage and shock  Neurovascular damage
 Infection  Visceral damage
 Muscle damage → rhabdomyolysis Early
Anaesthesia  Compartment syn.
 Anaphylaxis  Infection (worse if assoc. c̄ metalwork)
 Damage to teeth  Fat embolism → ARDS
 Aspiration Late
Prolonged Bed Rest  Problems c̄ union
 Chest infection, UTI  AVN
 Pressure sores and muscle wasting  Growth disturbance
 DVT, PE  Post-traumatic osteoarthritis
 ↓ BMD  Complex regional pain syndromes
 Myositis ossificans
Neurological Complications Problems with union

 Severance is rare, stretching over bone edge commoner
 Seddon classification describes three types of injury Delayed Union: union takes longer than expected
Non-union: # fails to unite
Neuropraxia
 Temporary interruption of conduction w/o loss of axonal Causative Factors: 5 Is
continuity.  Ischaemia: poor blood supply or AVN
 Infection
Axonotmesis  ↑ interfragmentary strain
 Disruption of nerve axon → distal Wallerian degeneration.  Interposition of tissue between fragments
 Connective tissue framework of nerve preserved.  Intercurrent disease: e.g. malignancy or malnutrition
 Regeneration occurs and recovery is possible.
Non-union Classification
Neurotmesis  Hypertrophic
 Disruption of entire nerve fibre  Bone end is rounded, dense and sclerotic
 Surgery required and recovery not usually complete.  Atrophic
 Bone looks osteopenic
Common Palsies
Injury Palsy Test/Result Management
Ant. shoulder dislocation Axillary N. Numb chevron  Optimise biology: infection, blood supply, bone
Humeral surgical neck Weak abduction graft, BMPs
# humeral shaft Radial N. Waiter’s tip  Optimise mechanics: ORIF
Elbow dislocation Ulnar N. Claw hand
Hip dislocation Sciatic N. Foot drop Malunion: # healed in an imperfect position
# neck of fibula Fibular N. Foot drop  Poor appearance and/or function
Knee dislocation  E.g. Gunstock deformity
Compartment Syndrome
 Osteofacial membranes divide limbs into separate Avascular Necrosis
compartments of muscles.  Death of bone due to deficient blood supply.
 Oedema following # → ↑ compartment pressure → ↓  Sites: femoral head, scaphoid, talus
venous drainage → ↑ compartment pressure  Consequence: bone becomes soft and deformed
 If compartment pressure > capillary pressure → ischaemia → pain, stiffness and OA.
 Muscle infarction →  X-ray: sclerosis and deformity.
 Rhabdomyolysis and ATN
 Fibrosis → Volkman’s ischaemic contracture
Myositis Ossificans
Presentation
 Heterotopic ossification of muscle @ sites of
 Pain > clinical findings
haematoma formation
 Pain on passive muscle stretching
 → restricted, painful movement
 Warm, erythematous, swollen limb
 Commonly affects the elbow and quadriceps
 ↑ CRT and weak/absent peripheral pulses
 Can be excised surgically
Rx Pellegrini-Stieda disease
 Elevate limb  form of MO
 Remove all bandages and split/remove cast  Calcification of the superior attachment of MCL @
 Fasciotomy the knee following traumatic injury.
Complex Regional Pain Syndrome Type 1
= Reflex Sympathetic Dystrophy, Sudek’s Atrophy
Definition Rx
 Complex disorder of pain, sensory abnormalities,  Usually self-limiting
abnormal blood flow, sweating and trophic changes in  Refer to pain team
superficial or deep tissues.  Amitryptilline, gabapentin
 No evidence of nerve injury.  Sympathetic nerve blocks can be tried.
Causes CRPS Type II (= Causalgia)

 Injury: #s, carpal tunnel release, ops for Dupuytren’s  Persistent pain following injury caused by nerve
 Zoster, MI, Idiopathic lesions.
Presentation
 Wks – months after injury
 NOT traumatised area that is affected: affects a
NEIGHBOURING area.
 Lancing pain, hyperalgesia or allodynia
 Vasomotor: hot and sweaty or cold and cyanosed
 Skin: swollen or atrophic and shiny.
 NM: weakness, hyper-reflexia, dystonia, contractures
Growth Disturbance
 In children, damage to the physis (growth plate) can result in abnormal bone growth.
 The Salter-Harris classification (1963) categorises growth plate injuries:
Salter Harris Classification
1. Straight across
2. Above
3. Lower
4. Through
5. CRUSH
 ↑ing risk of growth plate injury

 SH 1: e.g. SUFE. Normal growth c̄ good reduction.
 SH 4: union across physis may interfere c̄ bone growth
 SH 5: crush → physis injury → growth arrest

Hip Fracture
Epidemiology Classification
 80/100,000  Intracapsular: subcapital, transcervical, basicervical
 50% in >80yrs  Extracapsular: Intertrochanteric, subtrochanteric
 F>M = 3:1
Garden Classification of Intracapsular Fractures
Pathophysiology 1. Incomplete #, undisplaced
 Old = osteoporosis c̄ minor trauma (e.g. fall) 2. Complete #, undisplaced
3. Complete #, partially displaced
 Young = major trauma
4. Complete #, completely displaced
Osteoporosis Risk Factors: Age + SHATTERED
 Steroids
 Hyper- para/thyroidism
 Alcohol and Cigarettes D
 Thin (BMI<22)
 Testosterone low
 Early Menopause
 Renal / liver failure
 Erosive / inflame bone disease (e.g. RA, myeloma)
 Dietary Ca low / malabsorption, DM
Presentation
 O/E: shortened and externally rotated
 Key Qs:
 Mechanism
 RFs for osteoporosis / pathological # F
 Premorbid mobility
 Premorbid independence
 Comorbidities Surgical Management
 MMSE
Intracapsular
Initial Management  1,2: ORIF c̄ cancellous screws
 Resuscitate: dehydration, hypothermia  3,4:
 Analgesia: M+M  <55: ORIF c̄ screws.
 Assess neurovascular status of limb  f/up in OPD and do arthroplasty if AVN
 Imaging: AP and lateral films develops (in 30%)
 Prep for theatre  55-75: total hip replacement
 Inform Anaesthetist and book theatre  >75: hemiarthroplasty
 Bloods: FBC, U+E, clotting, X-match (2u)  Mobilises: cemented Thompson’s
 CXR  Non-mobiliser: uncemented Austin Moore
 DVT prophylaxis: TEDS, LMWH
 ECG Extracapsular
 Films: orthogonal X-rays  ORIF c̄ DHS
 Get consent
Discharge
Imaging  Involve OT and physios
 Ask for AP and lateral film  Discharge when mobilisation and social circumstances
 Look @ Shenton’s lines permit.
 Intra- or extra-capsular?
 Displaced or non-displaced Specific Complications
 Osteopaenic?  AVN of fem head in displaced #s (30%)
 Non / mal-union (10-30%)
Key Anatomy  Infection
 Capsule attaches proximally to acetabular margin and  Osteoarthritis
distally to intertrochanteric line.
Prognosis
 Blood supply to fem head:
1. Retinacular vessels, in capsule, distal → prox  30% mortality @ 1yr
2. Intramedullary vessels  50% never regain pre-morbid functioning
3. Artery of ligamentum teres.  >10% unable to return to premorbid residence
 If retinacular vessels damaged there is risk of AVN of  Majority will have some residual pain or disability.
the femoral head → pain, stiffness and OA

Distal Forearm Fractures Scaphoid Fractures
Colles’ Fracture Clinical Features
 FOOSH
Clinical Features  Pain in anatomical snuffbox
 Fall onto an outstretched hand  Pain on telescoping the thumb
 Most common in elderly females c̄ osteoporosis
 Dinner fork deformity Specific Management
 Request scaphoid x-ray view
Radiographic Features  If clinical hx and exam suggest a scaphoid #, it should
 Extra-articular # of dist. radius (w/i 1.5” of joint) initially be treated even if the x-ray is normal.
 Dorsal displacement of distal fragment  # may become apparent after 10 days due to
localised decalcification.
 Dorsal angulation of distal fragment
 Normally 11 degrees volar tilt  Place wrist in scaphoid plaster (beer glass position)
 ↓ radial height (norm =11mm)  If initial x-ray is negative, pt. returns to # clinic after 10
days for re-xray.
 ↓ radial inclination (norm=22O)
 # visible → plaster for 6 wks
 ± avulsion of ulna styloid
 No visible # but clinically tender → plaster for 2
 ± impaction
wks
 # not visible and not clinically tender → no plaster
Specific Management
 Examine for neurovascular injuries as median nerve Specific Complications
and radial artery lie close.  Main risk is AVN of the scaphoid as blood supply runs
 If much displacement → reduction distal to proximal.
 Under haematoma block, IV regional anaesthesia  → stiffness and pain at the wrist
(Bier’s block) or GA.
 Disimpact and correct angulation.
 Position: ulnar deviation + some wrist flexion
 Apply dorsal backslab: provide 3-point pressure Radial and Ulna Shaft Fractures
 Re X-Ray – satisfactory position?
 No: ortho review and consider MUA ± K wires Classification
 Yes: home c̄ # clinic f/up w/i 48hrs for completion  Monteggia
of POP  # of proximal 3rd of ulna shaft
 6 wks in POP + physio  Anterior dislocation of radial head at capitellum
 If comminuted, intra-articular or re-displaces:  May → palsy of deep branch of radial nerve →
 Surgical fixation c̄ ex-fix, Kirschner-wires or weak finger extension but no sensory loss
ORIF and plates.
 Galleazzi
Specific Complications  # of radial shaft between mid and distal 3rds
 Median N. injury  Dislocation of distal radio-ulna joint
 Frozen shoulder / adhesive capsulitis
 Tendon rupture: esp. EPL Specific Management
 Carpal tunnel syn.  Unstable fractures
 Mal- /non-union  Adults: ORIF
 Children: MUA + above elbow plaster
 Sudek’s atrophy / CRPS
 Fractures of forearm should be plastered in most stable
position:
 Proximal #: supination
 Distal #: pronation
Other Distal Forearm Fractures  Mid-shaft #: neutral
Smith’s / Reverse Colles’

 Fall onto back of flexed wrist
 Fracture of distal radius c̄ volar displacement and
angulation of distal fragment.
 Reduce to restore anatomy and POP for 6wks
Barton’s Fracture
 Oblique intra-articular # involving the dorsal aspect of
distal radius and dislocation of radio-carpal joint
 Reverse Barton’s involves the volar aspect of the radius

The Shoulder
Shoulder Dislocation Impingement Syndrome / Painful Arc
Classification Pathology
 Anterior  Entrapment of supraspinatus tendon and subacromial
 95% of shoulder dislocations. bursa between acromion and grater tuberosity of
 Direct trauma or falling on hand humerus.
 Humeral head dislocates antero-inferiorly  → subacromial bursitis and/or supraspinatous
 Posterior tendonitis
 Caused by direct trauma or muscle contraction
(seen in epileptics). Presentation
O
 Painful arc: 60-120
Associated Lesions  Weakness and ↓ ROM
 +ve Hawkin’s test
Bankart Lesion
 Damage to anteroinferior glenoid labrum. Ix
 Plain radiographs: may see bony spurs
Hill-Sachs Lesion  US
 Cortical depression in the posterolateral part of the  MRI arthrogram
humeral head following impaction against the glenoid
rim during anterior dislocation. Rx
 Occurs in 35-40% of anterior dislocations.  Conservative
 Rest
Presentation  Physiotherapy
 Shoulder contour lost: appears square  Medical
 Bulge in infraclavicular fossa: humeral head  NSAIDs
 Subacromial bursa steroid ± LA injection
 Arm supported in opposite hand
 Surgical
 Severe pain
 Arthroscopic acromioplasty
Specific Management Differential of Painful Arc
 Assess for neurovascular deficit: esp. axillary N.  Impingement
 Sensation over “chevron” area before and after  Supraspinatous tear or partial tear
reduction.
 AC joint OA
 Occurs in 5%
 X-ray: AP and transcapular view
 Reduction under sedation (e.g. propafol) Frozen Shoulder: Adhesive Capsulitis
 Hippocratic: Longitudinal traction c̄ arm in 30O
abduction and counter traction @ the axilla Presentation
 Kocher’s: external rotation of adducted arm,  Progressive ↓ active and passive ROM
anterior movement, internal rotation  ↓ ext. rotation <30O
 Rest arm in a sling for 3-4wks  ↓ abduction <90O
 Physio  Shoulder pain, esp. @ night (can’t lie on affected side)
Complications Cause
 Recurrent dislocation  Unknown, may follow trauma in elderly
 90% of pts. <20yrs with traumatic dislocation  Commonly assoc. c̄ DM
 Axillary N. injury
Rx
 Conservative: rest, physio
 Medical
Recurrent Shoulder Instability  NSAIDs
 Subacromial bursa steroid ± LA injection
TUBS: Traumatic Unilateral dislocations with a Bankart lesion
often require Surgery Rotator Cuff Tear
 Mostly young patients: 15-30yrs  2O to degeneration or a sudden jolt or fall
 Surgery involves a Bankart repair  Partial tears → painful arc
 Complete tear
AMBRI: Atraumatic Multidirectional Bilateral shoulder
 Shoulder tip pain
dislocation is treated with Rehabilitation, but may require
 Full range of passive movement
Inferior capsular shift
 Inability to abduct the arm
 Active abduction possible following passive
abduction to 90O
 Lowering the arm beneath this → sudden drop
 “drop arm” sign
Rx: open or arthroscopic repair

Supracondylar Fractures of the Humerus
Presentation Specific Complications
 Common in children after FOOSH
 Elbow very swollen and held semi-flexed. Neurovascular Injury
 Sharp edge of proximal humerus may injure brachial  Brachial artery
artery which lies anterior to it.  Radial nerve
 Median nerve: esp. anterior interosseous branch
Classification  Supplies deep forearm flexors (FPL, lateral half
of FDP and pronator quadratus)
Extension
 Commonest type Compartment syndrome
 Distal fragment displaces posteriorly  Monitor closely during the first 24h
 Gartland further classified extension type:  Pain on passive extension of the fingers (stretches
 Type 1: non-displaced flexor compartment) is early sign.
 Type 2: angulated c̄ intact posterior cortex  Mx: try extension of the elbow, surgical Rx may be
 Type 3: displaced c̄ no cortical contact needed.
 Volkmann’s ischaemic contracture can result → fibrosis
Flexion of flexors → claw hand.
 Less common
 Distal fragment displaces anteriorly Gunstock Deformity
 Valgus, varus and rotational deformities in the coronal
plane do not remodel and → cubitus varus.
Specific Management
 Cubitus varus deformity is referred to as a “gunstock”
 Ensure there is no neurovascular damage deformity.
 If radial pulse absent or damage to brachial
artery suspected, take urgently to theatre for
reduction ± on-table angiogram.
 Median nerve is also vulnerable
 Restore the anatomy

 No displacement → flex the arm as fully as
possible and apply a collar and cuff for 3wks –
triceps acts as sling to stabilise fragments.
 Displacement → MUA + fixation with K-wires +
collar and cuff with arm flexed for 3wks.

Femoral and Tibial Fractures Ankle Injuries
Specific Management Ligament Strains
 Resus and Mx life-threatening injuries first.  Typically twisting inversion injury
 X-Match  Strains anterior talofibular part of lateral collateral
 Tibial #: 2 units ligament
 Femoral #: 4 units  Medial deltoid ligament strains are rare.
 Assess neurovascular status: esp. distal pulses  May be assoc. c̄ malleolar avulsion #s
 If open
 Abx and ATT
 Take to theatre urgently for debridement, Ankle Fracture
washout and stabilisation
 Fixation methods Ottowa Ankle Rules
 Intramedullary nail  X-ray ankle if pain in malleolar zone + in any of:
 Ex-fix  Tenderness along distal 6cm of posterior tib / fib
 Plates and screws including posterior tip of the malleoli.
 MUA c̄ fixed traction for 3-4mo  Inability to bear weight both immediately and in
ED
Specific Complications
 Hypovolaemic shock Weber Classification
 Neurovascular  Relation of fibula # to joint line
 SFA: swelling and check pulses  A: below joint line
 Sciatic nerve  B: at joint line
 Compartment syndrome  C: above joint line
 Respiratory complications  Weber’s B and C represent possible injury to the
 Fat embolism syndesmotic ligaments between tib and fib → instability
 ARDS
 Pneumonia Mx
 Weber A
 Boot or below-knee POP
 Non-displaced Weber B/C
 Below-knee POP
 Displaced Weber B/C
 Closed reduction and POP if anatomical
reduction achieved
 ORIF if closed reduction fails

Knee Injuries
History Arthroscopy
 Mechanism  Direct vision of inside of knee joint by arthroscope
 Swelling  Can examine knee under anaesthesia (↓ muscle tone)
 Immediate = haemarthrosis = # or torn cruciates  Meniscal tears can be trimmed or repaired.
 Overnight = effusion = meniscus or other lgt
 Pain / tenderness Mx of Ruptured ACL
 Joint line = meniscal
 Med/lateral margins = collateral lgts. Conservative
 Locking: meniscal tear → mechanical obstruction  Rest
 Giving way: instability following lgt. injury  Physio to strengthen quads and hamstrings
 Not enough stability for many sports
Knee Haemarthrosis Surgical

 1O: spontaneous bleeding  Gold-standard is autograft repair
 Coagulopathy: warfarin, haemophilia  Usually semitendinosus ± gracilis (can use patella
 2O: trauma tendon)
 ACL injury: 80%  Tendon threaded through heads of tibia and femur and
 Patella dislocation: 10% held using screws.
 Meniscal injury: 10%
 Outer third where its vascularised
 Osteophyte #
Unhappy Triad of O’Donoghue

 ACL
 MCL
 Medial Meniscus
Mx of acutely injured knee

 Full examination of acutely swollen knee after injury is
difficult.
 Take x-ray to ensure no #s
 Fluid level indicates a lipohaemarthrosis and
indicates either a # or torn cruciate.
 If no # → RICE + later re-examination for pathology
 If meniscal or cruciate injury suspected → MRI

Osteoarthritis
Definition Pathophysiology
 Degenerative joint disorder in which there is  Softening of articular cartilage → fraying and fissuring
progressive loss of hyaline cartilage and new bone of smooth surface → underlying bone exposure.
formation at the joint surface and its margin.  Subchondral bone becomes sclerotic c̄ cysts.
 Proliferation and ossification of cartilage in unstressed
Aetiology / Risk Factors areas → osteophytes.
 Age (80% > 75yrs)  Capsular fibrosis → stiff joints.
 Obesity
 Joint abnormality Differential
 Septic
Classification  Crystal
 Primary: no underlying cause  Trauma
 Secondary: obesity, joint abnormality
X-ray Changes
Symptoms  Loss of joint space
 Affects: knees, hips, DIPs, PIPs, thumb CMC  Osteophytes
 Pain: worse c̄ movement, background rest/night pain,  Subchondral cysts
worse @ end of day.  Subchondral sclerosis
 Stiffness: especially after rest, lasts ~30min (e.g. AM)  Deformity
 Deformity
 ↓ ROM Bloods
 CRP may be mildly elevated
Signs  Ca, PO4 and ALP all normal
 Pouchards (prox), Heberdips (dist.)
 Thumb CMC squaring
 Fixed flexion deformity
Rx
MDT: GP, physio, OT, dietician, orthopod
History
 Pain severity, night pain Conservative
 Walking distance Lifestyle: ↓ wt., ↑ exercise
 Analgesic requirements Physio: muscle strengthening
 ADLs and social circumstances OT: walking aids, supportive footwear, home mods
 Co-morbidities
 Underlying causes: trauma, infection, congenital Medical
Analgesia
Paracetamol
NSAIDs: e.g. arthrotec (diclofenac + misoprostol)
Tramol
Joint injection: local anaesthetic and steroids
Surgical
Arthroscopic Washout
Mainly knees
Trim cartilage
Remove loose bodies.
Realignment Osteotomy
Small area of bone cut out
Useful in younger (<50yrs) pts. c̄ medial knee OA
High tibial valgus osteotomy redistributes wt. to
lateral part of joint.
Arthroplasty: replacement (or excision)
Arthrodesis: last resort for pain management
Novel Techniques
Microfracture: stem cell release → fibro-cartilage
formation
Autologous chondrocyte implantation

Back Pain
Mechanical Pain Spondylolisthesis
 Soft tissue injury → dysfunction of whole spine → muscle  Displacement of one lumbar vertebra on another
spasm → pain.  Usually forward
 May have inciting event: e.g. lifting  Usually L5 on S1
 Younger pts. c̄ no sinister features  May be palpable
Mx Causes
 Conservative  Congenital malformation
 Max 2d bed rest  Spondylosis
 Education: keep active, how to lift / stoop  Osteoarthritis
 Physiotherapy
 Psychosocial issues re. chronic pain and disability Presentation
 Warmth: e.g. swimming in a warm pool  Onset of pain usually in adolescence or early adulthood
 Medical  Worse on standing
 Analgesia: paracetamol ± NSAIDs ± codeine  ± sciatica, hamstring tightness, abnormal gait
 Muscle relaxant: low-dose diazepam (short-term)
Dx
Disc Prolapse  Plain radiography
 Herniation of nucleus pulposus through annulus fibrosus
Rx
Presentation  Corset
 L5 and S1 roots most commonly compressed by prolapse  Nerve release
of L4/5 and L5/S1 discs.  Spinal fusion
 May present as severe pain on sneezing, coughing or
twisting a few days after low back strain Spinal Stenosis
 Lumbago: low back pain  Developmental predisposition ± facet joint osteoarthritis
 Sciatica: shooting radicular pain down buttock and thigh → generalized narrowing of lumbar spinal canal.
Signs Presentation
 Limited spinal flexion and extension  Spinal claudication
 Free lateral flexion  Aching or heavy buttock and lower limb pain on
 Pain on straight-leg raise: Lesague’s Sign walking
 Lateral herniation → radiculopathy  Rapid onset
 Central herniation → corda equina syndrome  May c/o paraesthesiae/numbness
 Pain eased by leaning forward (e.g. on bike)
L4/5 → L5 Root Compression  Pain on spine extension
 Weak hallux extension ± foot drop
 In foot drop due to L5 radiculopathy, weak Ix
inversion (tib. post.) helps distinguish from  MRI
peroneal N. palsy.
 ↓ sensation on inner dorsum of foot Rx
 Corsets
L5/S1 → S1 Root Compression  NSAIDs
 Weak foot plantarflexion and eversion  Epidural steroid injection
 Loss of ankle-jerk  Canal decompression surgery
 Calf pain
 ↓ sensation over sole of foot and back of calf Neurosurgical Emergencies
Ix: MRI (emergency if cauda equina) Acute Cord Compression
 Bilateral pain: back and radicular
Rx  LMN signs at compression level
 Brief rest, analgesia and mobilisation effective in ≥90%  UMN signs and sensory level below compression
 Conservative: brief rest, mobilisation/physio  Sphincter disturbance
 Medical: analgesia, transforaminal steroid injection
 Surgical: discectomy or laminectomy may be needed in Acute Cauda Equina Compression
cauda-equina syndrome, continuing pain or muscle  Alternating or bilateral radicular pain in the legs
weakness.  Saddle anaesthesia
 Loss of anal tone
Lumbar Microdiscectomy  Bladder ± bowel incontinence
 Commonest procedure for disc prolapse
 Microscopic resection of the protruding nucleus pulposus Rx
 Posterior approach c̄ pt. in prone position.  Large prolapse: laminectomy / discectomy
 May be performed endoscopically  Tumours: radiotherapy and steroids
 Abscesses: decompression

Osteochondritis Traction Apophysitis
 Idiopathic condition in which bony centres of
children/adolescents become temporarily softened due Osgood-Shlatter’s
to osteonecrosis.  Tibial tuberosity apophysitis + patellar tendonitis
 Pressure → deformation  Children 10-14yrs, M>F=3:1
 Bone hardens in new, deformed position  Assoc. c̄ physical activity
 Symptoms: pain below knee, esp c̄ quads contraction
Radiography  X-ray: tuberosity enlargement ± fragmentation
 Initially: ↑ density / sclerosis  Rx: rest, consider POP
 Then: patchy appearance
Sinding Larsen’s Disease
Scheuermann’s Disease  Tranction tendinopathy with calcification of proximal
 Vertebral ring epiphyses attachment of patellar tendon
 Auto dom  Children 8-10yrs
 Vertebral tenderness and kyphosis
 X-ray: wedge-shaped thoracic vertebra Sever’s Disease
 Calcaneal apophysitis
Kohler’s Disease  8-13yrs
 Navicular bone  Symptoms: pain behind heal + limping
 Children 3-5yrs  Rx: physio
 Pain in mid-tarsal region → limp
Kienbochs Disease Osteochondritis Dissecans

 Lunate bone
 Piece of bone and overlying cartilage dissects off into
 Adults joint space.
 Pain over lunate, esp. on active movement  Commonly knee (med. fem. condyle), also elbow, hip
 Impaired grip and ankle.
 Young adult / adolescent
Friedberg’s Disease  Symptoms: pain, swelling, locking, ↓ ROM
 2nd/3rd metatarsal heads  X-ray: loose bodies, lucent crater
 Around puberty  Mx: arthroscopic removal
 Forefoot pain worse c̄ pressure
Panner’s Disease Avascular Necrosis

 Capitulum of humerus
Causes
Perthes’ Disease  # or dislocation
 Hip  SCD, thalassaemia
 SLE
 Gaucher’s
 Drugs: steroids, NSAIDs

The Limping Child
Aetiology Perthes’ Disease
 DDH  Osteochondritis of the femoral head 2O to AVN.
 Transient synovitis
 Septic arthritis Epidemiology
 Perthes’  4-10yrs
 Slipped Capital Femoral Epiphyses  M>F=5:1
 JIA / Still’s Disease
Presentation
 Insidious onset
 Hip pain initially, then painless
DDH  10-20% bilateral
 Congenital hip joint deformity in which the femoral head
is or can be completely / partially displaced. Ix
 X-rays normal initially
Epidemiology  ↑ density of femoral head
 Incidence: 1/1000  Becomes fragmented and irregular
 Sex: F>M  Flattening and sclerosis
 Bone scan is useful
Predisposing Factors
 FH Mx
 Breach presentation  Detected early and < half femoral head affected
 Oligohydramnios  Bed rest and traction
 More severe
Presentation  Maintain hip in abduction c̄ plaster
 Screening  Femoral or pelvic osteotomy
 Asymmetric skin folds
 Limp / abnormal gait
Slipped Capital Femoral Epiphysis
Ix  Postero-inferior displacement of femoral head epiphysis
 US is v. specific  10-15yrs
 Two main groups
Mx: maintain abduction  Fat and sexually underdeveloped
 Double nappies  Tall and thin
 Pavlik harness
 Plaster hip spica Presentation
 Open reduction: derotation varus osteotomy  Slip may be acute, chronic or acute-on-chronic
 Acute
 Groin pain
Transient Synovitis: Irritable Hip  Shortened, externally rotated leg
 Commonest cause of acute hip pain in children  All movements painful
 20% bilateral
Presentation
 2-12yrs Ix
 Sudden onset hip pain / limp  Confirm Dx by x-ray
 Often following or with viral infection
 Not systemically unwell Mx
 Acute: reduce and pin epiphysis
Ix  Chronic: in situ pinning
 PMN and ESR/CRP are normal  Epiphyseal reduction risks AVN
 -ve blood cultures
 May need joint aspiration and culture Complications
 Chondrolysis: breakdown of articular cartilage
Mx  ↑ risk c̄ surgery
 Rest and analgesia
 Settles over 2-3d

Acute Osteomyelitis Septic Arthritis
Pathophysiology Pathophysiology
 Source: local or haematogenous.  Source: local or haematogenous.
 Organisms  Organisms
 Staph  Staph: 60%
 Strep  Streps
 E. coli  Gonococcus
 Pseudomonas  Gm-ve bacilli
 Salmonella (in SCD)  RFs
 RFs  Joint disease (e.g. RA)
 Vascular disease  CRF
 Trauma  Immunosuppression (e.g. DM)
 SCD  Prosthetic joints
 Immunosuppression (e.g. DM)
 Children Symptoms
 Rich blood supply to growth plate  Acutely inflamed tender, swollen joint.
  usually affects metaphysis  ↓ROM
 Systemically unwell
Symptoms and Signs
 Pain, tenderness, erythema, warmth, ↓ROM Investigations
 Effusion in neighbouring joints  Joint aspiration for MCS
 Signs of systemic infection  ↑↑ WCC (e.g. >50,000/mm3) : mostly PMN
 ↑ESR/CRP, ↑WCC, Blood cultures
Investigations  X-ray
 ↑ESR/CRP, ↑WCC
 +ve blood cultures in 60% Management
 X-ray:  IV Abx: vanc + cefotaxime
 Changes take 10-14d  Consider joint washout under GA
 Haziness + ↓ bone density  Splint joint
 Sub-periosteal reaction  Physiotherapy after infection resolved
 Sequestrum and involucrum
 MRI is sensitive and specific Complications
 Osteomyelitis
Management  Arthritis
 IV Abx: Vanc + cefotaxime until MCS known  Ankylosis: fusion
 Drain abscess and remove sequestra
 Analgesia Differential
 Crystal arthropathy
 Reactive arthritis

Bone Tumours
Bony Mets
 Commonest bone tumours
 Bronchus, thyroid, breast, kidney and prostate
 Usually radiolucent (except prostate which is sclerotic)
 Usually axial skeleton (contains red marrow)
 Present with pain or pathological #
 Path # → internal fixation
 Pain → radiotherapy
Tumour-like Non-neoplastic Conditions
Lesion Clinical Features Location X-ray

Fibrous Dysplasia 0-30 Long bones “Ground Glass” lytic lesion
F>M Ribs
↑ # risk Skull Shepherds crook deformity of prox. femur
McCune Albright’s Usually mono-ostotic

- Polyostotic fibrous dysplasia
- Precocious puberty (females)
- Café-au-lait spots
Simple bone cyst <20 Prox metaphysis of Well-defined lytic lesion
Lump migrates down shaft humerus or femur Cortex can fall into cyst → “fallen
from original growth plate site. fragment”
Aneurysmal bone cyst <30yrs MRI shows multiple fluid levels
Pain
Fibrous cortical defect Children Dist femur
and non-ossifying Non-painful, benign Prox tibia
fibroma Spontaneously regress Often multiple
Benign Cartilaginous Neoplasms

Osteochondroma 10-20 Knee Cartilage-capped bony outgrowth
(exostosis) M>F = 3:1
Commonest benign bone tumour
May be related to previous trauma
Enchondroma / 10-40 Hands O sign
Chondromas M=F Feet - Oval lucencies c̄ radiodense rim
Ollier Disease = multiple enchondromas Endosteal scalloping
Maffucci Syn = Enchondromatosis + multiple

soft-tissue haemangiomas
Multiple enchondromas have risk of malignant

transformation
Chondroblastoma 10-20 Epiphysis Radiolucent with sclerotic border
M>F = 2:1 Knee
Malignant Cartilaginous Neoplasms

Chondrosarcoma >40 Pelvis Lytic lesion
Pain + lump Axial skeleton Fluffy “popcorn calcification”
Arise de novo or from chondromas
70% 5ys

Benign Bone-forming Neoplasms

Osteoma Lump Skull
Usually solitary Facial bones
Multiple in Gardner syn
Osteoid osteoma M>F = 2:1 Lower limb Lytic lesion c̄ central nidus and sclerotic rim
Teens and 20s Diaphyseal cortex
Severe nocturnal pain
relieved by aspirin
Hot on bone scan
Osteoblastoma Pain unresponsive to aspirin Spine
Giant Cell Tumour 20-40 Knee Soap bubble appearance
/ Osteoclastoma (After fusion of growth plate) Abut joint surface Solitary, expansile, lytic lesion
F>M
Malignant Bone-forming Neoplasms

Osteosarcoma Adolescents Knee Periosteal Elevation:
M>F = 2:1 Metaphysis - Sunburst appearance
Commonest 1O bone tumour - Codman’s triangle
Pain, warm, bruit
May arise 2o to Paget’s or irradiation
Ewing’s Sarcoma <20 Long bone diaphysis Lytic tumour
Painful, warm, enlarging mass Onion-skin periosteal reaction
Systemic: fever, ↑ESR, anaemia, ↑WCC

Brachial Plexus Injuries Other Nerve Injuries
Anatomy Radial Nerve (C5-T1)
 C5-T1
 Roots leave vertebral column between scalenus Low Lesions: posterior interosseous nerve
anterior and medius.  Site: # around elbow or forearm
 Divisions occur under the clavicle, medial to coracoid  E.g. # head of radius
process.  Loss of extension of CMC joints (finger drop)
 Plexus has intimate relationship c̄ subclavian and  No sensory loss
brachial arteries. Median N. is formed anterior to
brachial artery. High Lesions
 Site: # shaft of humerus where N. is in radial groove.
C5  Wrist drop
Lat  Loss of sensation to dorsum of thumb root (snuff box)
MC
 Triceps functions normally
C6
Post Axillary Median Very High Lesions
C7
Radial  Site: axilla – e.g. crutches or Sat night palsy
C8  Paralysis of triceps and wrist drop
Med Ulnar
T1
Roots (5) Divisions (6)
Ulnar Nerve (C8-T1)
Trunks (3) Cords (3)
Site
 Elbow: cubital tunnel
Causes  Wrist: in Guyon’s Canal
 Direct: e.g. shoulder girdle #, penetrating or iatrogenic
injury Effects
 Indirect: e.g. avulsion or traction injuries  Intrinsic hand muscle paralysis → claw hand
 Ulnar paradox: lesion at elbow has less clawing as
Leffert Classification FDP is paralysed, decreasing flexion of 4th/5th digits.
1. Open  Weakness of finger ad/abduction (interossei)
2. Closed  Sensory loss over little finger
a. Supraclavicular
b. Infraclavicular Tests
3. Radiation-induced  Can’t cross fingers for luck
4. Obstetric  Froment’s Sign: flexion of thumb IPJ when trying to
a. Upper hold onto paper held between thumb and finger.
b. Lower  Indicates weak adductor policis.
c. Mixed
High (C5/6): Erb’s Palsy Median Nerve (C5-T1)

 Abductors and external rotators paralysed
 Waiter’s tip position Injury Above the Antecubital Fossa
 Loss of sensation in C5/6 dermatomes  Can’t flex index finger IPJs (e.g. on clasping hands)
 Can’t flex terminal thumb phalanx (FPL)
Low (C8/T1): Klumpke’s Paralysis  Loss of sensation in median distribution
 Paralysis of small hand muscles
 Claw hand Injury at the Wrist
 Loss of sensation in C8/T1 dermatomes  Typically affects abductor pollicis brevis
Carpal Tunnel Syndrome

Carpal Tunnel Syndrome
Anatomy Ix
 Carpal tunnel formed by flexor retinaculum and carpal  Not usually performed
bones.  Nerve conduction studies
 Contains  US
 4 tendons of FDS
 4 tendons of FDP Non-surgical Mx
 1 tendon of FPL
 Mx of underlying cause
 Median N.
 Wrist splints
 Median N. supplies LLOAF (aBductor pollicis brevis)
 Neutral position
 Palmer cutaneous branch travels superficial to flexor
 Esp. @ night
retinaculum → spares sensation over thenar area.
 Local steroid injections
Surgical Mx
Causes  Carpal tunnel decompression by division of the flexor
 F>M retinaculum
 Primary / idiopathic
 Secondary Complications
 Water: pregnancy, hypothyroidism  Scar formation: high risk for hypertrophic or keloid
 Radial #  Scar tenderness: up to 40%
 Inflammation: RA, gout  Nerve injury
 Soft tissue swelling: lipomas, acromegaly,  Palmar cutaneous branch of the median nerve
amyloidosis  Motor branch to the thenar muscles
 Toxic: DM, EtOH  Failure to relieve symptoms
Symptoms Other Locations of Median Nerve Entrapment

 Tingling / pain in thumb, index and middle fingers  Pronator syndrome
 Pain worse @ night or after repetitive actions  Entrapment between two heads of pronator
 Relieved by shaking / flicking teres
 Clumsiness  Anterior interroseous syndrome
 Compression of the anterior interosseous
branch by the deep head of pronator teres
Signs  Muscle weakness only
 ↓ sensation over lateral 3½ fingers  Pronator quadratus
 ↓ 2-point touch discrimination  FPL
 Early sign of irreversible damage  Radial half of FDP
 Wasting of thenar eminence
 Late sign of irreversible damage
 Phalen’s flexing and Tinel’s tapping

Minor Hand Conditions
Dupuytren’s Contracture Trigger Finger
 Progressive, painless fibrotic thickening of palmar  Tendon nodule which catches on proximal side of
fascia. tendon sheath → triggering on forced extension.
 → Fixed flexion deformity
The Patient  Usually ring and middle fingers
 M>F  Assoc. c̄ RA
 Middle age / elderly  Rx: steroid injection (high recurrence) or surgery
 Skin puckering and tethering
 Fixed flexion contracture of ring and little fingers
 Often bilateral and symmetrical
 MCP and IP joint flexion
Ganglion
 Smooth, multilocular cystic swellings
 Mucoid degeneration of joint capsule or tendon sheath
Associations: BAD FIBERS
 May be in communication c̄ joint capsules / tendons
 Bent penis: Peyronies (3%)
 AIDS
Presentation
 DM
 90% located on dorsum of wrist.
 FH: AD
 Subdermal, fixed to deeper structures.
 Idiopathic: commonest
 Limits planes of movement
 Booze: ALD
 May cause pain or nerve pressure symptoms
 Epilepsy and epilepsy meds (phenytoin)
 Reidel’s thyroiditis and other fibromatoses Management
 Ledderhose disease  50% disappear spontaneously
 Fibrosis of plantar aponeurosis  Aspiration ± steroid and hyaluronidase injection
 5% c̄ dupuytren’s  Surgical excision
 Retroperitoneal fibrosis
 Smoking Differential
 Lipoma
Management  Fibroma
 Conservative: e.g. physio / exercises  Sebaceous cyst
 Fasciectomy
 e.g. when hand can’t be placed flat on the table.
 Z-shaped scars: prevent contracture
 Can damage ulnar nerve
 Usually recurs
Differential
 Skin contracture: old laceration or burn
 Tendon fibrosis, trigger finger
 Ulnar N. palsy

Minor Leg and Foot Conditions
Meralgia Paraesthetica Hallux Valgus
 Entrapment of lat. cutaneous nerve of thigh  Great toe deviates laterally @ MTP joint
 Between ASIS and inguinal ligament  Pressure of MTP against shoe → bunion
 Pain ± paraesthesia on the lateral thigh  ↑ wt. bearing @ 2nd metatarsal head
 No motor deficit  → pain: “Transfer metatarsalgia”
 ↑ risk c̄ obesity: compression by belts, underwear  → hammer toe
 Relieved by sitting down
 Can occasionally be damaged in lap hernia repair Aetiology
 Pointed shoes
 Wearing high heals
Chondromalacia Patellae Mx
 Predominantly young women  Conservative: bunion pads, plastic wedge between
 Patellar aching after prolonged sitting or climbing stairs great and second toes.
 Pain on patellofemoral compression: Clarke’s test  Surgical: metatarsal osteotomy
 Ix: no abnormality on X-ray
 Rx: vastus medialis strengthening
Lesser Toe Deformities
Baker’s Cyst
 Popliteal swelling arising between the medial head of
gastrocnemius and semimembranosus muscle
 Herniation from joint synovium
 Usually 2O to OA
 Rupture: acute calf pain and swelling
 DVT differential
Morton’s Metatarsalgia / Neuroma

 Pain from pressure on an interdigital neuroma between
the metatarsals.
 Pain radiates to medial side of one toe and lateral side
of another.
 Rx: neuroma excision

Ear, Nose and Throat
Contents
Audiometry ........................................................................................................................................................................... 132
Otalgia .................................................................................................................................................................................. 132
Otitis Media ........................................................................................................................................................................... 133
Cholesteatoma ..................................................................................................................................................................... 134
Tinnitus ................................................................................................................................................................................. 134
Vertigo .................................................................................................................................................................................. 135
Adult Hearing Loss ............................................................................................................................................................... 136
Hearing Loss in Children ...................................................................................................................................................... 137
Miscellaneous Ear Conditions .............................................................................................................................................. 137
Allergic Rhinosinusitis........................................................................................................................................................... 138
Sinusitis ................................................................................................................................................................................ 138
Nasal Polyps......................................................................................................................................................................... 139
Fractured Nose ..................................................................................................................................................................... 139
Epistaxis ............................................................................................................................................................................... 140
Tonsillitis ............................................................................................................................................................................... 141
The Larynx ............................................................................................................................................................................ 142
Paediatric Airway Issues ...................................................................................................................................................... 142
Facial Nerve Palsy................................................................................................................................................................ 143

Audiometry Otalgia
 Quantify loss and determine its nature.
Otitis Externa
Pure tone audiometry (PTA) Presentation
 Headphones deliver tones at different frequencies  Watery discharge
and strengths in a sound-proofed room.  Itch
 Pt. indicates when sound appears and disappears.  Pain and tragal tenderness
 Mastoid vibrator → bone conduction threshold.
 Threshold at different frequencies are plotted to Causes
give an audiogram.  Moisture: e.g. swimming
 Trauma: e.g. fingernails
 Absence of wax
Tympanometry  Hearing aid
 Measures stiffness of ear drum
 Evaluates middle ear function Organisms
 Flat tympanogram: mid ear fluid or perforation  Mainly pseudomonas
 Shifted tympanogram: +/- mid ear pressure  Staph aureus
Management
Evoked response audiometry  Aural toilet c̄ drops
 Auditory stimulus c̄ measurement of elicited brain  Betamethasone for non-infected eczematous OE
response by surface electrode.  Betamethasone c̄ neomycin
 Used for neonatal screening (if otoacoustic emission  Hydrocortisone c̄ gentamicin
testing negative)  Acidifying drops
Malignant Otitis Externa

 Life-threatening infection which can → skull osteomyelitis
 90% of pts. are diabetic (or other immune compromise)
 Presentation
 Severe otalgia which is worse @ night
 Copious otorrhoea
 Granulation tissue in the canal
 Rx
 Surgical debrdement
 Systemic Abx
Bullous Myringitis
 Painful haemorrhagic blisters on deep meatal skin and TM.
 Assoc. c̄ influenza infection
TMJ Dysfunction
Symptoms
 Earache (referred pain from auriculotemporal N.)
 Facial pain
 Joint clicking/popping
 Teeth-grinding (bruxism)
 Stress (assoc. c̄ depression)
Signs
 Joint tenderness exacerbated by lateral movements of an
open jaw.
Investigation
 MRI
Management
 NSAIDs
 Stabilising orthodontic occlusal prostheses

Otitis Media
Classification Chronic Suppurative OM
 Acute: acute phase
 Glue ear / OME: effusion after symptom regression Presentation
 Chronic: effusion > 3mo if bilat or > 6mo if unilat  Painless discharge and hearing loss
 Chronic suppurative OM: Ear discharge c̄ hearing
loss and evidence of central drum perforation. o/e
 TM perforation
Organisms
Rx
 Viral
 Aural toilet
 Pneumococcus
 Abx / Steroid ear drops
 Haemophilus
 Moraxella
Complications
 Cholesteatoma
Acute OM
Presentation
Mastoiditis
 Middle-ear inflam → destruction of mastoid air cells
 Usually children post viral URTI
and abscess formation.
 Rapid onset ear pain, tugging @ ear.
 Irritability, anorexia, vomiting Presentation
 Purulent discharge if drum perforates  Fever
 Mastoid tenderness
o/e
 Protruding auricle
 Bulging, red TM
 Fever Imaging: CT
Rx Rx
 Paracetamol: 15mg/kg  IV Abx
 Amoxicillin: may use delayed prescription  Myringotomy ± mastoidectomy
Complications
 Intratemporal
 OME
 Perforation of TM
 Mastoiditis
 Facial N. palsy
 Intracranial
 Meningitis / encephalitis
 Brain abscess
 Sub- / epi-dural abscess
 Systemic
 Bacteraemia
 Septic arthritis
 IE
OME
Presentation
 Inattention at school
 Poor speech development
 Hearing impairment
o/e
 Retracted dull TM
 Fluid level
Ix
 Audiometry: flat tympanogram
Rx
 Usually resolves spontaneously,
 Consider grommets if persistent hearing loss
 SE: infections and tympanosclerosis

Cholesteatoma Tinnitus
 Sensation of sound w/o external sound stimulation
Definition
 Locally destructive expansion of stratified squamous Causes
epithelium within the middle ear.  Specific
 Meniere’s
Classification  Acoustic neuroma
 Congenital  Otosclerosis
 Acquired: 2O to attic perforation in chronic suppurative  Noise-induced
OM  Head injury
 Hearing loss: e.g. presbyacusis
Presentation  General
 ↑BP
 Foul smelling white discharge
 ↓Hb
 Headache, pain
 Drugs
 CN Involvement
 Aspirin
 Vertigo
 Aminoglycosides
 Deafness
 Loop diuretics
 Facial paralysis
 EtOH
o/e Hx
 Appears pearly white c̄ surrounding inflammation
 Character: constant, pulsatile
 Unilateral: acoustic neuroma
Complications  FH: otosclerosis
 Deafness (ossicle destruction)  Alleviating/exacerbating factors: worse @ night?
 Meningitis  Associations
 Cerebral abscess  Vertigo: Meniere’s, acoustic neuroma
 Deafness: Meniere’s, acoustic neuroma
Mx  Cause: head injury, noise, drugs, FH
 Surgery
Examination
 Otoscopy
 Tuning fork tests
 Pulse and BP
Ix
 Audiometry and tympanogram
 MRI if unilateral to exclude acoustic neuroma
Mx
 Treat any underlying causes
 Psych support: tinnitus retraining therapy
 Hypnotics @ night may help

Vertigo
Definition Ménière’s Disease
 The illusion of movement
Pathology
 Dilatation of endolymph spaces of membranous
Causes labyrinth (endolymphatic oedema)
Peripheral / Vestibular Central Presentation

 Meniere’s  Acoustic neuroma  Attacks occur in clusters and last up to 12h.
 BPV  MS  Progressive SNHL
 Labyrinthitis  Vertebrobasilar  Vertigo and n/v
insufficiency / stroke  Tinnitus
Head injury  Aural fullness
 Inner ear syphilis
Ix
Drugs (central/ototoxic)  Audiometry shows low-freq SNHL which fluctuates
 Gentamicin
 Loop diuretics Rx
 Metronidazole  Medical
 Co-trimoxazole  Vertigo: cyclizine, betahistine
 Surgical
 Gentamicin instillation via grommets
 Saccus decompression
Hx
 Is it true vertigo or just light-headedness?
 Which way are things moving?
Vestibular Neuronitis / Viral Labyrinthitis
 Timespan
 Assoc. symptoms: n/v, hearing loss, tinnitus, Presentation
nystagmus
 Follows febrile illness (e.g. URTI)
 Sudden vomiting
 Severe vertigo exacerbated by head movement
Examination and Tests
 Hearing Rx
 Cranial nerves  Cyclizine
 Cerebellum and gait  Improvement in days
 Romberg’s +ve = vestibular or proprioception
 Hallpike manouvre
 Audiometry, calorimetry, LP, MRI Benign Positional Vertigo: BPV
Pathology
 Displacement of otoliths in semicircular canals
 Common after head injury.
Presentation
 Sudden rotational vertigo for <30s
 Provoked by head turning
 Nystagmus
Causes
 Idiopathic
 Head injury
 Otosclerosis
 Post-viral
Dx
 Hallpike manoeuvre → upbeat-torsional nystagmus
Rx
 Self-limiting
 Epley manoeuvre
 Betahistine: histamine analogue

Adult Hearing Loss
Conductive Acoustic Neuroma / Vestibular Schwannoma
 Impaired conduction anywhere between auricle and
round window. Pathology
 Benign, slow-growing tumour of superior vestibular N.
External canal obstruction  Acts as SOL → CPA syndrome
 Wax  80% of CPA tumours
 Pus  Assoc. c̄ NF2
 Foreign body
Presentation
TM perforation  Slow onset, unilat SNHL, tinnitus ± vertigo
 Trauma  Headache (↑ICP)
 Infection  CN palsies: 5,7 and 8
 Cerebellar signs
Ossicle defects
 Otosclerosis Ix
 Infection  MRI of cerebellopontine angle
 Trauma  MRI all pts. c̄ unilateral tinnitus / deafness
 PTA
Inadequate eustachian tube ventilation of middle ear
Differential
 Meningioma
Sensorineural  Cerebellar astrocytoma
 Defects of cochlea, cohlear N. or brain.  Mets
Drugs Rx
 Aminoglycosides  Gamma knife
 Vancomycin  Surgery (risk of hearing loss)
Post-infective
 Meningitis Otosclerosis
 Measles  AD condition characterised by fixation of stapes at the
 Mumps oval window.
 Herpes  F>M=2:1
Misc. Presentation
 Meniere’s  Begins in early adult life
 Trauma  Bilateral conductive deafness + tinnitus
 MS  HL improved in noisy places: Willis’ paracousis
 CPA lesion (e.g. acoustic neuroma)  Worsened by pregnancy/ menstruation/ menopause
 ↓B12
Ix
 PTA shows dip (Caharts notch) @ 2kHz
Rx
 Hearing aid or stapes implant
Presbyacussis
 Age-related hearing loss
Presentation
 >65yrs
 Bilateral
 Slow onset
 ± tinnitus
Ix: PTA
Rx: hearing aid

Hearing Loss in Children Miscellaneous Ear Conditions
Congenital Causes Congenital Anomalies
 1st and 2nd branchial arches form auricle while 1st
Conductive branchial groove forms external auditory canal.
 Anomalies of pinna, external auditory canal, TM or  Malfusion → accessory tags/auricles and preauricular
ossicles. pits, fistulae or sinuses.
 Congenital cholesteatoma  Sinuses may get infected, mimicking a sebaceous
 Pierre-Robin cyst.
SNHL Pinna Haematoma

 AD  Blunt trauma → subperichondrial haematoma.
 Waardenburgs: SNHL, heterochromia +
 Can → ischaemic necrosis of cartilage and
telecanthus
subsequent fibrosis to “cauliflower ears”.
 AR
 Mx: aspiration + firm packing to auricle contour.
 Alport’s: SNHL + haematuria
 Jewell-Lange-Nielson: SNHL + long QT
 X-linked
 Alport’s Exostoses
 Infections: CMV, rubella, HSV, toxo, GBS  Smooth, symmetrical bony narrowing of external
 Ototoxic drugs canals.
Path
Perinatal  Bony hypertrophy due to cold exposure
 Anoxia  e.g. from swimming / surfing
 Cerebral palsy
Symptoms
 Kernicterus
 Asympto unless narrowing occludes → conductive
 Infection: meningitis
deafness.
Rx: conservative or surgical widening

Acquired Causes
 OM/OME
 Infection: meningitis, measels Wax: Cerumen Auris
 Head injury  Secreted in outer 3rd of canal to prevent maceration
 Wax accumulation can → conductive deafness.
 Mx
Universal Neonatal Hearing Tests  Suction under direct vision c̄ microscope
 Detection and Mx of hearing loss before 6mo improves  Syringing after 1wk softening with olive oil
language.
 Tests
 Otoacoustic emissions
 Audiological brainstem responses. TM Perforation
Causes
 OM
 Foreign body
 Barotrauma
 Trauma

Allergic Rhinosinusitis Sinusitis
Classification Pathophysiology
 Seasonal: hay-fever (prev = 2%)  Viruses → mucosal oedema and ↓ mucosal ciliary
 Perennial actions → mucus retention ± 2O bacterial infection
 Acute: Pneumococcus, Haemophilus, Moraxella
Pathology  Chronic: S. aureus, anaerobes
 T1HS IgE-mediated inflam from allergen exposure →
mediator release from mast cells. Causes
 Allergens: pollen, house dust mites (perennial)  Majority are bacterial infection 2O to viral
 5% 2O to dental root infections
Symptoms  Diving / swimming in infected water
 Sneezing  Anatomical susceptibility: deviated septum, polyps
 Pruritus  Systemic Disease
 Rhinorrhoea  PCD / Kartagener’s
 Immunodeficiency
Signs
 Swollen, pale and boggy turbinates Symptoms
 Nasal polyps  Pain
 Maxillary (cheek/teeth)
Ix  Ethmoidal (between eyes)
 ↑ on bending / straining
 Skin-prick testing to find allergens
 Don’t perform if prone to eczema  Discharge: from nose → post-nasal drip c̄ foul taste
 RAST tests  Nasal obstruction / congestion
 Anosmia or cacosmia (bad smell w/o external source)
Mx  Systemic symptoms: e.g. fever
Allergen Avoidance Imaging

 Regularly washing bedding (inc. toys) on high heat or  Nasendoscopy ± CT
use acaricides.
 Avoid going outside when pollen count high. Mx
1st Line Acute / Single Episode
 Anti-histamines: cetirazine, desloratidine  Bed-rest, decongestants, analgesia
 Or, beclometasone nasal spray  Nasal douching and topical steroids
 Or, chromoglycate nasal spray (children)  Abx (e.g. clarithro) of uncertain benefit
2nd Line: intranasal steroids + anti-histamines Chronic / recurrent

 Usually a structural or drainage problem.
3rd Line: Zafirlukast  Stop smoking + fluticasone nasal spray
 Functional Endoscopic Sinus Surgery
4rd Line: Immunotherapy  If failed medical therapy
 Aim to induce desensitisation to allergen
 OD SL grass-pollen tablets → ↑ QOL in hay-fever Complications (rare)
 Injection immunotherapy  Mucoceles → pyoceles
 Orbital cellulits / abscess
Adjuvants
 Osteomyelits – e.g. Staph in frontal bone
 Nasal decongestants: Pseudoephedrine, Otrivine
 Intracranial infection
 Meningitis, encephalitis
 Abscess
 Cavernous sinus thrombosis.

Nasal Polyps Fractured Nose
The Patient Anatomy
 Male, > 40yrs  Upper 3rd of nose has bony support
 Lower 2/3 and septum are cartilaginous.
Sites
 Middle turbinates Hx
 Middle meatus  Time of injury
 Ethmoids  LOC
 CSF rhinorrhoea
Symptoms  Epistaxis
 Watery, anterior rhinorrhoea  Previous nose injury
 Purulent post-nasal drip  Obstruction
 Nasal obstruction  Consider facial #, check for
 Sinusitis  Teeth malocclusion
 Headaches  Piplopia (orbital floor #)
 Snoring
Ix
Signs  Cartilaginous injury won’t show and radiographs don’t
 Mobile, pale, insensitive alter Mx.
Associations Mx
 Allergic / non-allergic rhinitis  Exclude septal haematoma
 CF  Re-examine after 1wk (↓ swelling)
 Aspirin hypersensitivity  Reduction under GA c̄ post-op splinting best w/i 2wks
 Asthma
Septal haematoma
Single Unilateral Polyp  Septal necrosis + nasal collapse if untreated
 May be sign of rare but sinister pathology  Cartilage blood supply comes from mucosa
 Nasopharyngeal Ca  Boggy swelling and nasal obstruction
 Glioma  Needs evacuation under GA c̄ packing ± suturing.
 Lymphoma
 Neuroblastoma
 Sarcoma
 Do CT and get histology
Nasal Polyps in Children

 Rare <10yrs old
 Must consider neoplasms and CF
Mx
 Drugs
 Betamathasone drops for 2/7
 Short course of oral steroids
 Endoscopic Polypectomy

Epistaxis
Causes Posterior / Major Epistaxis
 80% unknown  Posterior packing (+ anterior pack)
 Trauma: nose-picking / #s  Pass 18/18G Foley catheter through the nose
 Local infection: URTI into nasopharynx, inflate c̄ 10ml water and pull
 Pyogenic granuloma forward until it lodges.
 Overgrowth of tissue on Little’s area due to  Admit pt. and leave pack for ~48hrs.
irritation or hormonal factors.  Gold standard is endoscopic visualisation and direct
 Osler-Weber-Rendu / HHT control: e.g. by cautery or ligation.
 Coagulopathy: Warfarin, NSAIDs, haemophilia, ↓plats,
vWD, ↑EtOH After the Bleed
 Neoplasm  Don’t pick nose
 Sit upright, out of the sun
Classification  Avoid bending, lifting or straining
 Anterior  Sneeze through mouth
 Posterior  No hot food or drink
 Avoid EtOH and tobacco
Initial Mx
 Wear PPE
 Assess for shock and manage accordingly
 If not shocked Osler-Weber-Rendu / HHT
 Sit up, head tilted down  Autosomal dominant
 Compress nasal cartilage for 15min.  5 genetic subtypes
 If bleeding not controlled remove clots c̄ suction or by
blowing and try to visualise bleed by rhinoscopy Features
 Telangiectasias in mucosae
Anterior Epistaxis  Recurrent spontaneous epistaxis
 Usually septal haemorrhage: Little’s area /  GI bleed (usually painless)
Kisselbach’s plexus  Internal telangiectasias and AVMs
 Ant. Ethmoidal A.  Lungs
 Sphenopalatine A.  Liver
 Facial A.  Brain
 Insert gauze soaked in vasoconstrictor + LA  Rarely
 Xylometazoline + 2% lignocaine  Pulmonary HTN
 5min  Colon polyps: may → CRC
 Bleeds can be cauterised c̄ silver nitrate sticks
 Persistent bleeds should be packed with Mericel pack
 Refer to ENT if this fails or if you can’t visualise
the bleeding point.
 They may insert a posterior pack or take pt. to
theatre for endoscopic control.

Tonsillitis
Symptoms Strep Throat Complications
 Sore throat
 Fever, malaise Peritonsillar Abscess (Quinsy)
 Typically occurs in adults
Signs  Symptoms
 Lymphadenopathy: esp. jugulodigastric node  Trismus
 Inflamed tonsils and oropharynx  Odonophagia: unable to swallow saliva
 Exudates  Halitosis
 Signs
 Tonsillitis
Organisms  Unilateral tonsillar enlargement
 Viruses are most common (consider EBV)  Contralateral uvula displacement
 GAS: Pyogenes  Cervical lymphadenopathy
 Staphs  Rx
 Moraxella  Admit
 IV Abx
Mx  I&D under LA or tonsillectomy under GA
 Swabbing superficial bacteria is irrelevant and can →
overdiagnosis.
 Analgesia: Ibuprofen / Paracetamol ± Difflam gargle Retropharyngeal Abscess
 Consider Abx only if ill: use Centor Criteria  Rare
 Pen V 250mg PO QDS (125mg TDS in  Presentation
children) or erythromycin for 5/7  Unwell child c̄ stiff, extended neck who refuses
 NOT AMOXICILLIN → MACPAP RASH IN EBV to eat or drink
 Fails to improve c̄ IV Abx
Centor Criteria  Unilateral swelling of tonsil and neck
 Guideline for admin of Abx in acute sore throat /  Ix
tonsillitis / pharyngitis  Lat. neck x-rays show soft tissue swelling
 CT from skull-base to diaphragm.
1 Point for Each of  Rx
1. Hx of fever  IV Abx
2. Tonsillar exudates  I&D
3. Tender anterior cervical adenopathy
4. No cough
Lemierre’s Syndrome
Mx  IJV thrombophlebitis c̄ septic embolization most
 0-1: no Abx (risk of strep infection <10%) commonly affecting the lungs.
 2: consider rapid Ag test + Rx if +ve  Organism: Fusobacterium necrophorum
 ≥3: Abx  Rx
 IV Abx: pen G, clinda, metro
Tonsillectomy
Scarlet Fever
Indications  “Sandpaper”-like rash on chest, axillae or behind ears
 Recurrent tonsillitis if all the below criteria are met 12-48h after pharyngotonsillitis.
 Caused by tonsillitis  Circumoral pallor
 5+ episodes/yr  Strawberry tongue
 Symptoms for >1yr  Rx
 Episodes are disabling and prevent normal  Start Pen V/G and notify HPA.
functioning
 Airway obstruction: e.g. OSA in children
 Quinsy Rheumatic Fever
 Suspicion of Ca: unilateral enlargement or ulceration  Carditis
 Arthritis
Methods  Subcutaneous nodules
 Cold steel  Erythema marginatum
 Cautery  Sydenham’s chorea
Complications
 Reactive haemorrhage Post-streptococcal Glomerulonephritis
 Tonsillar gag may damage teeth, TMJ or posterior  Malaise and smoky urine 1-2wks after a pharyngitis
pharyngeal wall.
 Mortality is 1/30,000

The Larynx Paediatric Airway Issues
Functions Laryngomalacia
 Phonation  Immature and floppy aryepiglottic folds and glottis →
 Positive thoracic pressure: inc. auto-PEEP laryngeal collapse on inspiration
 Respiration
 Prevention of aspiration Presentation
 Stridor: commonest cause in children
Laryngitis Presents w/i first wks of life.
 Usually viral and self-limiting  Noticeable @ certain times
 2O bacterial infection may develop  Lying on back,
 Symptoms: pain hoarseness and fever  Feeding
 Excited/upset
 o/e: redness and swelling of the vocal cords
 Problems can occur c̄ concurrent laryngeal infections
 Rx: Supportive, Pen V if necessary
or c̄ feeding.
Laryngeal Papilloma Mx
 Pedunculated vocal cord swellings caused by HPV
 Usually no Rx required but severe cases may warrant
 Present c̄ hoarseness surgery.
 Usually occur in children
 Rx: laser removal
Epiglottitis
Recurrent Laryngeal N. Palsy
 Supplies all intrinsic muscles of the larynx except for Symptoms
cricothyroideus.  Sudden onset
 Ext. branch of sup laryngeal N.  Continuous stridor
 Responsible for ab- and ad-uction of vocal folds  Drooling
 Toxic
Symptoms
 Hoarseness Pathogens: haemophilus, GAS
 “Breathy” voice c̄ bovine cough
 Repeated coughing from aspiration (↓ supraglottic Rx
sensation)  Don’t examine throat
 Exertional dyspnoea (narrow glottis)  Consult c̄ anaesthetists and ENT surgeons
 O2 + nebulised adrenaline
Causes  IV dexamethasone
 30% are cancers: larynx, thyroid, oesophagus,  Cefotaxime
hypopharynx, bronchus  Take to theatre to secure airway by intubation
 25% iatrogenic: para- / thyroidectomy, carotid
endarterectomy
 Other: aortic aneurysm, bulbar / pseudobulbar palsy
Foreign Body
 Sudden onset stridor in a previously normal child.
Laryngeal SCC  Back slaps and abdominal thrusts.
 Incidence: 2000/yr in uk  Needle cricothyrotomy in children
 Associations: smoking, EtOH  Can only exclude foreign body in bronchus by
bronchoscopy
Presentation
 Male smoker
 Progressive hoarseness → stridor
 Dys-/odono-phagia Subglottic Stenosis
 Wt. loss  Subglottis is narrowest part of respiratory tract in
children.
Ix  Symptoms: stridor, FTT
 Laryngoscopy + biopsy (inc. nodes)  Causes
 MRI staging  Prolonged intubation
 Congenital abnormalities
Mx  Rx
 Based on stage  Mild: conservative
 Severe: Tracheostomy or partial tracheal
 Radiotherapy
resection
 Laryngectomy
After total laryngectomy

 Pts have permanent tracheostomy
 Speech valve
 Electrolarynx
 Oseophageal speech (swallowed air)
 Regular f/up for recurrence
Facial Nerve Palsy
Bell’s Palsy Other Causes of Facial Palsy
 Inflammatory oedema from entrapment of CNVII in
narrow facial canal May be suggested by
 Probably of viral origin (HSV1).  Bilateral symptoms (Lyme, GBS, leukaemia,
 75% of facial palsy sarcoid)
 UMN signs: sparing of frontalis and orbicularis oculi
Features  Other CN palsies (but seen in 8% of Bell’s)
 Sudden onset: e.g. overnight  Limb weakness
 Complete, unilateral facial weakness in 24-72h  Rashes
 Failure of eye closure (Bell’s Sign) → dryness
and conjunctivitis Intracranial Lesions
 Drooling, speech difficulty  Vascular, MS, SOL
 Numbness or pain around ear  Motor cortex → UMN signs
 ↓ taste (ageusia)  Brainstem nuclei → LMN signs
 Hyperacusis: stapedius palsy  Cerebello-pontine angle lesion
th th th
 May be accompanied by 5 , 6 , and 8 CN
Ix palsies
 Serology: Borrelia or VZV Abs
 MRI: SOL, stroke, MS Intratemporal Lesions
 LP  Otitis media
 Cholesteatoma
Mx  Ramsay Hunt
 Protect eye
 Dark glasses Infratemporal
 Artificial tears  Parotid tumours
 Tape closed @ night  Trauma
 Give prednisolone w/i 72hrs
 60mg/d PO for 5/7 followed by tapering Systemic
 Valaciclovir if zoster suspected (otherwise antivirals  Peripheral neuropathy
don’t help).  Demyelinating: GBS
 Plastic surgery may help if no recovery  Axonal: DM, Lyme, HIV, Sarcoid
 Pseudopalsy: MG, botulism
Prognosis
 Incomplete paralysis usually recovers completely w/i
wks.
 With complete lesions, 80% get full recovery but the
remainder have delayed recovery or permanent
neurological / cosmetic abnormalities.
Complications: Aberrant Neural Connections

 Synkinesis: e.g. blinking causes up-turning of
mouth
 Crocodile tears: eating stimulates unilateral
lacrimation, not salivation
Ramsay Hunt Syndrome

 American neurologist James Ramsay Hunt in 1907
 Reactivation of VZV in geniculate ganglion of CNVII
Features
 Preceding ear pain or stiff neck
 Vesicular rash in auditory canal ± TM, pinna, tongue,
hard palate (no rash = zoster sine herpete)
 Ipsilateral facial weakness, ageusia, hyperacusis,
 May affect CN7 → vertigo, tinnitus, deafness
Mx
 If Dx suspected give valaciclovir and prednisolone
w/i first 72h
Prognosis
 Rxed w/i 72h: 75% recovery
 Otherwise: 1/3 full recovery, 1/3 partial, 1/3 poor

Ophthalmology
Contents
Pupils ......................................................................................................................................................................................... 145
Optic Atrophy / Optic Neuropathy.............................................................................................................................................. 146
Red Eye: History, Examination and Differential ........................................................................................................................ 147
Visual History............................................................................................................................................................................. 147
Red Eyes: Specific Diseases .................................................................................................................................................... 148
Sudden Loss of Vision ............................................................................................................................................................... 150
Gradual Visual Loss .................................................................................................................................................................. 151
The Eye in DM ........................................................................................................................................................................... 152
Cataracts ................................................................................................................................................................................... 153
The Retina ................................................................................................................................................................................. 153
The External Eye ....................................................................................................................................................................... 154
Orbital Swellings ........................................................................................................................................................................ 154
Refractive Errors........................................................................................................................................................................ 155
Strabismus / Squint / Tropia ...................................................................................................................................................... 155
Eye Trauma ............................................................................................................................................................................... 156
Floaters, Flashes and Haloes .................................................................................................................................................... 156
Allergic Eye Disease.................................................................................................................................................................. 157
Tropical Eye Disease................................................................................................................................................................. 157
Eye Signs in Systemic Conditions ............................................................................................................................................. 158
Ophthalmic Pharmacology ........................................................................................................................................................ 158

Pupils
Afferent Defect Horner’s Syndrome
 Johann Horner (1831-1886), Swiss ophthalmologist
Features
 No direct response but intact consensual response Features: PEAS
 Cannot initiate consensual response in contralateral eye.  Ptosis: partial (superior tarsal muscle)
 Dilatation on moving light from normal to abnormal eye  Enophthalmos
 Anhydrosis
Causes  Small pupil
 Total CN II lesion
Causes
Relative Afferent Pupillary Defect  Central
 = Marcus-Gunn Pupil  MS
 Wallenberg’s Lateral Medullary Syndrome
Features  Pre-ganglionic (neck)
 Minor constriction to direct light  Pancoast’s tumour: T1 nerve root lesion
 Dilatation on moving light from normal to abnormal eye.  Trauma: CVA insertion or CEA
 RAPD = Marcus Gunn Pupil  Post-ganglionic
 Cavernous sinus thrombosis
O
Causes  Usually 2 to spreading facial infection
 Optic neuritis via the ophthalmic veins
 Optic atrophy  CN 3, 4, 5, 6 palsies
 Retinal disease
Efferent Defect Argyll Robertson Pupil

Features
Feature
 Small, irregular pupils
 Dilated pupil does not react to light
 Accommodate but doesn’t react to light
 Initiates consensual response in contralateral pupil
 Atrophied and depigmented iris
 Ophthalmoplegia + ptosis
Cause
Cause
 DM
 3rd nerve palsy
 The pupil is often spared in a vascular lesion (e.g.  Quaternary syphilis
DM) as pupillary fibres run in the periphery.
Differential of a fixed dilated pupil

 Mydriatics: e.g. tropicamide
 Iris trauma
 Acute glaucoma
 CN3 compression: tumour, coning
Holmes-Adie Pupil
Features
 Young woman c̄ sudden blurring of near vision
 Initially unilateral and then bilateral pupil dilatation
 Dilated pupil has no response to light and sluggish
response to accommodation.
 A “tonic” pupil
Ix
 Iris shows spontaneous wormy movements on slit-lamp
examination
 Iris streaming
Cause
 Damage to postganglionic parasympathetic fibres
 Idiopathic: may have viral origin
Holmes-Adie Syndrome
 Tonic pupil + absent knee/ankle jerks + ↓ BP

Optic Atrophy / Optic Neuropathy
Features
 ↓ acuity
 ↓colour vision (esp. red)
 Central scotoma
 Pale optic disc
 RAPD
Causes: CAC VISION

 Commonest: MS and glaucoma
Congenital
 Leber’s hereditary optic neuropathy
 Epi: mitochondrial, onset 20-30s
 PC: attacks of acute visual loss, sequential in
each eye ± ataxia and cardiac defects
 HMSN / CMT
 Friedrich’s ataxia
 DIDMOAD
 Retinitis pigmentosa
Alcohol and Other Toxins

 Ethambutol
 Lead
 B12 deficiency
Compression
 Neoplasia: optic glioma, pituitary adenoma
 Glaucoma
 Paget’s
Vascular: DM, GCA or thromboembolic

Inflammatory: optic neuritis – MS, Devic’s, DM
Sarcoid / other granulomatous
Infection: herpes zoster, TB, syphilis
Oedema: papilloedema
Neoplastic infiltration: lymphoma, leukaemia

Red Eye: History, Examination and Differential
Differential
Visual History
Site Mechanical Inflammation Infection
Vision Lids Ectropion Blepharitis Preseptal cellulitis
 Blurred Entropion Chalazion Orbital cellulitis
 Distorted FB / Trichiasis
 Diplopia Conjunctiva Sub conj haem Allergic conjunct Conjunctivitis
 Field defect / Scotoma Sclera Perforation Chemical burn
 Floaters, Flashes Episcleritis
Scleritis
Sensation Cornea Foreign body Keratitis
 Irritation Abrasion
 Pain Ant Chamber Acute glaucoma Iritis / uveitis Endophthalmitis
 Itching
 Photophobia
 FB Presentation Summary
Appearance Acute Anterior Conjunctivitis

Glaucoma Uveitis
 Red: ?distribution
Pain +++ ++ +/-
 Lump
Photophobia ++ +
 Puffy lids
Acuity ↓ ↓ normal
Cornea hazy/cloudy normal normal
Discharge Pupil large small normal
 Watering IOP ↑↑ normal normal
 Sticky
 Stringy
Key Examination Questions

 Inspect from anterior to posterior
 Is acuity affected?
 Is the globe painful?
 Pupil size and reactivity?
 Cornea: intact, cloudy? Use fluorescein
Signs of Serious Disease

 Photophobia
 Poor vision
 Corneal fluorescein staining
 Abnormal pupil

Red Eyes: Specific Diseases
Acute Closed Angle Glaucoma Anterior Uveitis / Acute Iritis
 Blocked drainage of aqueous from anterior chamber via
the canal of Schlemm. Pathophysiology
 Pupil dilatation (e.g. @ night) worsens the blockage.  Uvea is pigmented part of eye and included: iris, ciliary
 Intraocular pressure rises from 15-20 → >60mmHg body and choroid.
 Iris + ciliary body = anterior uvea
Risk Factors  Iris inflammation involves ciliary body too.
 Hypermetropia
 Shallow ant. chamber Symptoms
 Female  Acute pain and photophobia
 FH  Blurred vision (aqueous precipitates)
 ↑age
 Drugs Examination
 Anti-cholinergics  Small pupil initially, irregular later
 Sympathomimetics  Circumcorneal injection
 TCAs  Hypopyon: pus in anterior chamber
 Anti-histamines  White (keratic) precipitates on back of cornea
 Talbots test: ↑pain on convergence
Symptoms
 Prodrome: rainbow haloes around lights at night-time. Associations (most have no systemic associations)
 Severe pain c̄ n/v  Seronegative arthritis: AS, psoriatic, Reiter’s
 ↓ acuity and blurred vision  Still’s / JIA
 IBD
Examination  Sarcoidosis
 Cloudy cornea c̄ circumcorneal injection  Behcet’s
 Fixed, dilated, irregular pupil  Infections: TB, leprosy, syphilis, HSV, CMV, toxo
 ↑ IOP makes eye feel hard
Mx
Ix  Refer to ophthalmologist
 Tonometry: ↑↑ IOP (usually >40mmHg)  Prednisolone drops
 Cyclopentolate drops: dilates pupil and prevents
Acute Mx: Refer to Ophthalmologist adhesions between iris and lens (synechiae)
 Pilocarpine 2-4% drops stat: miosis opens blockage
 Topical β-B (e.g. timolol): ↓ aqueous formation
 Acetazolamide 500mg IV stat: ↓ aqueous formation
 Analgesia and antiemetics
Subsequent Mx
 Bilat YAG peripheral iridotomy once IOP ↓ medically

Episcleritis Corneal Abrasion
 Inflammation below conjunctiva in the episclera  Epithelial breech w/o keratitis
 Cause: trauma
Presentation
 Localised reddening: can be moved over sclera Symptoms
 Painless / mild discomfort  Pain
 Acuity preserved  Photophobia
 Blurred vision
Causes
 Usually idiopathic Ix
 May complicate RA or SLE  Slit lamp: fluorescein stains defect green
Rx: Topical or systemic NSAIDs Rx

 Chloramphenicol ointment for infection prophylaxis
Scleritis
 Vasculitis of the sclera Corneal Ulcer + Keratitis (corneal inflammation)
Presentation Causes: bacterial, herpetic, fungal, protozoa, vasculitic (RA)
 Severe pain: worse on eye movement  Dendritic ulcer = Herpes simplex
 Generalised scleral inflammation  Acanthamoeba: protazoal infection affecting contact
 Vessels won’t move over sclera lens wearers swimming in pools.
 Conjunctival oedema (chemosis)
Presentation
 Pain, photophobia
Causes  Conjunctival hyperaemia
 Wegener’s  ↓ acuity
 RA  White corneal opacity
 SLE
 Vasculitis Risk factors: contact lens wearers
Mx Ix: green c̄ fluorescein on slit lamp

 Refer to specialist
 most need or corticosteroids or immunosuppressants Rx: refer immediately to specialist who will
 Take smears and cultures
Complications:  Abx drops, oral/topical aciclovir
 Scleromalacia (thinning) → globe perforation  Cycloplegics/mydriatics ease photophobia
 Steroids may worsen symptoms: professionals only
Conjunctivitis Complications
 Scarring and visual loss
Presentation
 Often bilateral c̄ purulent discharge
 Bacterial: sticky (staph, strep, Haemophilus) Ophthalmic Shingles
 Viral: watery  Zoster of CNV1
 Discomfort  20% of all Shingles (only commoner in thoracic
 Conjunctival injection dermatomes)
 Vessels may be moved over the sclera
 Acuity, pupil responses and cornea are unaffected. Presentation
 Pain in CNV1 dermatome precedes blistering rash
Causes  40% → keratitis, iritis
 Viral: adenovirus  Hutchinson’s sign
 Bacterial: staphs, chlamydia, gonococcus  Nose-tip zoster due to involvement of nasociliary
 Allergic branch.
 ↑ chance of globe involvement as nasociliarry
Rx nerve also supplies globe
 Bacterial: chloramphenicol 0.5% ointment  Ophthalmic involvement
 Allergic: anti-histamine drops: e.g. emedastine  Keratitis + corneal ulceration (fluorescein stains)
 ± iritis

Sudden Loss of Vision
Key Questions Central Retinal Artery Occlusion
 Headache associated: GCA
 Eye movements hurt: optic neuritis Presentation
 Lights / flashes preceding visual loss: detached retina  Dramatic unilateral visual loss in seconds
 Like curtain descending: TIA, GCA  Afferent pupil defect (may precede retinal changes)
 Poorly controlled DM: vitreous bleed from new vessels  Pale retina c̄ cherry-red macula
Causes
Anterior Ischaemic Optic Neuropathy (AION)  GCA
 Optic nerve damaged if posterior ciliary arteries blocked  Thromboembolism: clot, infective, tumour
by inflammation or atheroma.
 Pale / swollen optic disc Rx
 If seen w/i 6h aim is to ↑ retinal blood flow by ↓ IOP
Causes  Ocular massage
 Arteritic AION: Giant Cell Arteritis  Surgical removal of aqueous
 Anti-hypertensives (local and systemic)
 Non-arteritic AION: HTN, DM, ↑ lipids, smoking
Optic Neuritis Retinal Vein Occlusion
Symptoms Central
 Unilateral loss of acuity over hrs – days  Commoner than arterial occlusion
 ↓ colour discrimination (dyschromatopsia)  Causes: arteriosclerosis, ↑BP, DM, polycythaemia
 Eye movements may hurt  Pres: sudden unilat visual loss c̄ RAPD
 Fundus: Stormy Sunset Appearance
Signs  Tortuous dilated vessels
 ↓ acuity  Haemorrhages
 ↓ colour vision  Cotton wool spots
 Enlarged blind-spot  Complications
 Optic disc may be: normal, swollen, blurred  Glaucoma
 Afferent defect  Neovascularisation
 Prognosis: possible improvement for 6mo-1yr
Causes
 Multiple sclerosis (45-80% over 15yrs) Branch
 DM  Presentation: unilateral visual loss
 Drugs: ethambutol, chloamphenicol  Fundus: segmental fundal changes
 Vitamin deficiency  Comps: retinal ischaemia → VEGF release and
 Infection: zoster, Lyme disease neovascularisation (Rx: laser photocoagulation)
Rx
 High-dose methyl-pred IV for 72h Retinal Detachment
 Then oral pred for 11/7  Holes/tears in retina allow fluid to separate sensory
retina from retinal pigmented epithelium
 May be 2O to cataract surgery, trauma, DM
Vitreous Haemorrhage
Presentation: 4 F’s
Source  Floaters: numerous, acute onset, “spiders-web”
 New vessels: DM  Flashes
 Retinal tears / detachment / trauma  Field loss
 Fall in acuity
Presentation  Painless
 Small bleeds → small black dots / ring floaters
 Large bleed can obscure vision → no red reflex, retina Fundus: grey, opalescent retina, ballooning forwards
can’t be visualised
Rx
Ix  Urgent surgery
 May use B scan US to identify cause  Vitrectomy + gas tamponade c̄ laser coagulation to
secure the retina.
Mx
 VH undergoes spontaneous absorption
Causes of transient visual loss
 Vitrectomy may be performed in dense VH
 Vascular: TIA, migraine
 MS
 Subacute glaucoma
 Papilloedema
Gradual Visual Loss
Causes Chronic Simple (Open-Angle) Glaucoma
Common Pathogenesis
 Diabetic retinopathy  Depends on susceptibility of pt’s. retina and optic nerve
 ARMD to ↑ IOP damage.
 Cataracts  IOP >21mmHg → ↓blood flow and damage to optic
 Open-angle Glaucoma nerve → optic disc atrophy (pale) + cupping
Rarer Presentation
 Genetic retinal disease: retinitis pigmentosa  Peripheral visual field defect: superior nasal first
 Hypertension  Central field is intact  acuity maintained until late
 Optic atrophy  Presentation delayed until optic N. damage is
irreversible
Screen if High Risk

Age-Related Macular Degeneration (ARMD)
 >35yrs
 Commonest cause of blindness >60yrs
 Afro-Caribbean
 30% of >75yrs will have dry AMD
 FH
 Drugs: steroids
Risk Factors
 Co-morbidities: DM, HTN, migraines
 Smoking
 Myopia
 ↑ age
 Genetic factors
Ix
 Tonometry: IOP ≥21mmHg
Presentation
 Fundoscopy: cupping of optic disc
 Elderly pts.
 Visual field assessment: peripheral loss
 Central visual loss
Mx
Dry ARMD: Geographic Atrophy
 Life-long f/up
 Drusen: fluffy white spots around macula
 Degeneration of macula
Eye-drops to ↓ IOP to baseline
 Slow visual decline over 1-2yrs st
 1 line: β-blockers
 Timolol, betaxolol
Wet ARMD: Subretinal Neovascularisation
 ↓ aqueous production
 Aberrant vessels grow into retina from choroid and →  Caution in asthma, heart failure
haemorrhage
 Prostaglandin analogues
 Rapid visual decline (sudden / days / wks) c̄ distortion  Latanoprost, travoprost
 Fundoscopy shows macular haemorrhage → scarring  ↑ uveoscleral outflow
 Amsler grid detects distortion  α-agonists
 Brimonidine, apraclonidine
Ix  ↓ aqueous production and ↑ uveoscleral outflow
 OCT: optical coherence tomography  Carbonic anhydrase inhibitors
 Gives high resolution images of the retina  Dorzolamide drops, acetazolamide PO
 Miotics
Mx for Wet AMRD  Pilocarpine
 Photodynamic therapy
 Intravitreal VEGF inhibitors Non-medical Options
 Bevacizumab (Avastin)  Laser trabeculoplasty
 Ranibizumab (Lucentis)  Surgery (trabeculectomy) is used if drugs fail
 Antioxidant vitamins (C,E) + zinc may help early ARMD  New channel allows aqueous to flow into
conjunctival bleb
Tobacco-Alcohol Amblyopia
 Due to toxic effects of cyanide radicals when combined
with thiamine deficiency. Commonest Causes of Blindness Worldwide
 Pres: Optic atrophy, loss of red/green discrimination,  Trachoma
scotomata  Cataracts
 Rx: vitamins may help  Glaucoma
 Keratomalacia: vitamin A deficiency
 Onchocerciasis
 Diabetic Retinopathy

The Eye in DM
The Problem Fundoscopy Findings
 DM is leading cause of blindness up to 60yrs
 30% have ocular problems @ presentation Background Retinopathy: Leakage
 BP < 130/80 and normoglycaemia → ↓ diabetic retinopathy  Dots: microaneurysms
 Blot haemorrhages
Pathogenesis  Hard exudates: yellow lipid patches
Cataract Pre-proliferative Retinopathy: Ischaemia

 DM accelerates cataract formation  Cotton-wool spots (infarcts)
 Lens absorbs glucose which is converted to sorbitol by  Venous beading
aldose reductase.  Dark Haemorrhages
 Intra-retinal microvascular abnormalities
Retinopathy
 Microangiopathy → occlusion Proliferative Retinopathy
 Occlusion → ischaemia → new vessel formation in retina  New vessels
 Bleed → vitreous haemorrhage  Pre-retinal or vitreous haemorrhage
 Carry fibrous tissue c̄ them → retinal detachment  Retinal detachment
 Occlusion also → cotton wool spots (ischaemia)
 Vascular leakage → oedema and lipid exudates Maculopathy
 Rupture of microaneurysms → blot haemorrhage  Caused by macular oedema
 ↓ acuity may be only sign
 Hard exudates w/i one disc width of macula
Screening
 All diabetics should be screened annually
 Fundus photography
 Refer those c̄ maculopathy, NPDR and PDR to
ophthalmologist
 30% NPDR develop PDR in 1yr
Ix
 Fluorescein angiography
Mx
 Good BP and glycaemic control
 Rx concurrent disease: HTN, dyslipidaemia, renal disease,
smoking, anaemia
 Laser photocoagulation
 Maculopathy: focal or grid
 Proliferative disease: pan-retinal (macula spared)
CN Palsies
 CNIII and VI palsies may occur
 In diabetic CNIII palsy the pupil may be spared as its nerve
fibres run peripherally and receive blood from pial vessels.

Cataracts The Retina
 Outer pigmented layer in contact c̄ the choroid
Presentation  Inner sensory layer in contact c̄ vitreous
 Increasing myopia  At centre is fovea
 Blurred vision → gradual visual loss
 Dazzling in sunshine / bright lights Optic Disc
 Monocular diplopia
Colour
Causes  Should be pale pink
 ↑Age: 75% of >65s  Paler in optic atrophy
 DM
 Steroids Contour
 Congenital  Margins blurred in papilloedema and optic neuritis
 Idiopathic
 Infection: rubella Cup
 Metabolic: Wilson’s, galactosaemia  Physiological cup lies centrally and should occupy 1/3
 Myotonic dystrophy of disc diameter
 Cup widening and deepening in glaucoma
Ix
 Visual acuity
 Dilated Fundoscopy Retinitis Pigmentosa
 Tonometry  Most prevalent inherited degeneration of the macula
 Blood glucose to exclude DM  Various modes of inheritance
 Mostly AR
Mx  AD has best prognosis
 X-linked has worst prognosis
Conservative  Affects ~ 1/2000
 Glasses
 Mydriatic drops and sunglasses may give some relief Presentation
 Night blindness
Surgery  ↓↓ visual fields → tunnel vision
 Consider if symptoms affect lifestyle or driving (<6/10)  Most are registrable blind (<3/60) by mid 30s
 Day-case surgery under LA
 Phacoemulsion + lens implant Fundoscopy
 1% risk of serious complications  Pale optic disc: optic atrophy
 Anterior uveitis / iritis  Peripheral retina pigmentation: spares the macula
 VH
 Retinal detachment Associations
 Secondary glaucoma  Friedrich’s ataxia
 Endophthalmitis (→ blindness in 0.1%)  Refsum’s disease
 Post-op capsule thickening is common  Kearns-Sayre Syndrome
 Easily Rx c̄ laser capsulotomy.  Usher’s Syndrome
 Post-op eye irritation is common and requires drops
Retinoblastoma
 Commonest intraocular tumour in children
 1:15,000 LBs
Inheritance
 Hereditary type differs from non-hereditary type
 AD mutation of RB gene (a TSG)
 Pts. typically have one mutant allele in every retinal cell;
if the other allele mutates → retinoblastoma.
Associations
 5% occur c̄ pineal or other tumour
 ↑ risk of osteosarcoma and rhabdomyosarcoma
Signs
 Stabismus
 Leukocoria (white pupil) → no red reflex
Rx
 Depends on size
 Options include: chemo, radio, enucleation

The External Eye Orbital Swellings
Inflammatory Lid Swellings Orbital Cellulitis
Stye or hordeolum externum Pathophysiology

 An abscess / infection in a lash follicle which points  Infection spreads locally: e.g. from paranasal sinuses,
outwards. eyelid or external eye.
 Rx: local Abx – e.g. fusidic acid  Staphs, pneumococcus, GAS
Chalazion or hordeolum internum Presentation

 Abscess of the Meibomian glands which points inwards  Usually a child c̄ inflammation of the orbit + lid swelling
onto conjunctiva.  Pain and ↓ range of eye movement
 Sebaceous glands of eyelid  Exophthalmos
 Systemic signs: e.g. fever
Blepharitis  ± tenderness over the sinuses
 Chronic inflammation of eyelid
 Causes: seborrhoeic dermatitis, staphs Rx
 Features  IV Abx: Cefuroxime (20mg/kg/8h IV)
 Red eyes
 Gritty / itchy sensation Complications
 Scales on lashes.  Local extension → meningitis and cavernous sinus
 Often assoc. c̄ rosacea thrombosis.
 Rx  Blindness due to optic N. pressure.
 Clean crusts of lashes c̄ warm soaks
 May need fusidic acid drops
Carotico-cavernous fistula
Entropion  May follow carotid aneurysm rupture c̄ reflux of blood
 Lid inversion → corneal irritation into cavernous sinus.
 Degeneration of lower lid fascia  Causes: spontaneous, trauma
 Presentation
 Engorgement of eye vessels
Ectropion  Lid and conjunctival oedema,
 Low lid eversion → watering and exposure keratitis  Pulsatile exophthalmos
 Assoc. c̄ ageing and facial N. palsy  Eye bruit
Ptosis
 True ptosis is intrinsic LPS weakness
Rx
 Bilateral
 Congenital  Oral antivirals: famciclovir, aciclovir
 Senile
 MG
 Myotonic dystrophy Exophthalmos / Proptosis
 Unilateral  Protrusion of one or both eyes
 3rd Nerve palsy
 Horner’s syndrome (partial) Common Causes
 Mechanical: xanthelasma, trauma  Graves’ Disease
 25-50%
 ↑ risk in smoker’s
Lagophthalmos  Anti-TSH Abs → retro-orbital inflammation and
 Difficulty in lid closure over the globe which may → lymphocyte infiltration → swelling
exposure keratitis  Orbital cellulitis
 Causes: exophthalmos, facial palsy, injury  Trauma
 Rx
 Lubricate eyes c̄ liquid paraffin ointment Other Causes
 Idiopathic orbital inflammatory disease
 Temporary tarsorrhaphy may be needed if
corneal ulcers develop.  Vasculitis: Wegener’s
 Neoplasm
 Lymphoma
Pinguecula  Optic glioma: assoc. c̄ NF-1
 Yellow vascular nodules either side of the cornea
 Capillary haemangioma
 Mets
Pterygium  Carotico-cavernous fistula
 Similar to pinguecula but grows over the cornea → ↓
vision.
 Benign growth of conjunctiva
 Assoc. c̄ dusty, wind-blown life-styles, sun exposure

Refractive Errors Strabismus / Squint / Tropia
Refractive errors arise from disorders of the size and shape Esotropia = convergent squint
of the eye.  Commonest type in children
 May be idiopathic or due to hypermetropia
Myopia: Short-sightedness Exotropia = divergent squint

 Older children
The Problem  Often intermittent
 The eye is too long
 Distant objects are focussed too far forward.
Non-Paralytic Squint
Causes
 Genetic Diagnosis
 Excessive close work in the early decades  Corneal reflection: should fall centrally and symmetrically
on each cornea.
The Solution  Cover test: movement of uncovered eye to take up
 Concave lenses fixation demonstrates manifest squint.
Management: 3 O’s
Astigmatism  Optical: correct refractive errors
 Orthoptic: patching good eye encourages use of squinting
The Problem eye.
 Cornea or lens doesn’t have same degree of  Operations: e.g. resection and recession of rectus
curvature in horizontal and vertical planes. muscles – help alignment and cosmesis.
 Image of object is distorted longitudinally or vertically
The Solution Paralytic Squint

 Correcting lenses  Diplopia is most on looking in direction of pull of paralysed
muscle.
 Eye won’t fixate on covering.
Hypermetropia: long-sightedness  Cover each eye in turn: which ever eye sees the outer
image is malfunctioning
The Problem
 Eye is too short CNIII
 When eye is relaxed and not accommodating, objects  Ptosis (LPS)
are focussed behind the retina.  Fixed dilated pupil (no parasympathetic)
 Contraction of ciliary muscles to focus image →  Eye looking down and out
tiredness of gaze and possibly a convergent squint in  Causes
children.  Medical: DM, MS, infarction
 Surgical: ↑ ICP, cavernous sinus thrombosis,
The Solution posterior communicating artery aneurysm
 Convex lenses
CNIV
 Diplopia especially on going down stairs
Presbyopia  Head tilt
 With age, lens becomes stiff and less easy to deform.  Test: can’t depress in adduction
 Start at about 40yrs and are complete by 60yrs.  Causes
 Use convex lenses.  Peripheral: DM (30%), trauma (30%), compression
 Central: MS, vascular, SOL
CNVI
 Eye is medially deviated and cannot abduct
 Diplopia in the horizontal plane.
 Causes
 Peripheral: DM, compression, trauma
 Central: MS, vascular, SOL
 Rx: botulinum toxin can eliminate need for surgery

Eye Trauma Floaters, Flashes and Haloes
 Record acuity of both eyes
 Take detailed Hx of event Floaters
 If unable to open injured eye, instil LA (e.g. tetracaine  Small dark spots in the visual field
1%)  Sudden showers of floaters in one eye may be due to
blood or retinal detachment
Foreign Bodies Causes

 X-ray orbit if metal FB suspected  Retinal detachment
 Fluorescein may show corneal abrasions  VH
 Diabetic retinopathy / Hypertension
Mx  Old retinal branch vein occlusion
 Chloramphenicol drops 0.5% prevent infection  Syneresis (degenerative opacities in the vitreous)
 Usually coagulase-negative Staphylococcus
 Eye patch
 Cycloplegic drops may ↓ pain Flashes (Photopsia)
 Tropicamide, cyclopentolate  Either from intraocular or intracerebral pathology
 Headache, n/v: migraine
 Flashes and floater: retinal detachment
Intra-ocular Haemorrhage
 Blood in anterior chamber = hyphaema
 Small amounts clear spontaneously, but some may Haloes
need evacuation.  Usually just diffractive phenomena
 Complicated by corneal staining and glaucoma (pain)  May be caused by hazy ocular media – cataract,
 Keep IOP↓ and monitor corneal oedema, acute glaucoma
 Haloes + eye pain = acute glaucoma
 Jagged haloes which change shape are usually
Orbital Blowout Fracture migrainous.
 Blunt injury → sudden ↑ in orbital pressure c̄ herniation
of orbital contents into maxillary sinus.
Presentation
 Ophthalmoplegia + Diplopia
 Tethering of inferior rectus and inferior oblique
 Loss of sensation to lower lid skin
 Infraorbital nerve injury
 Ipsilateral epistaxis
 Damage to anterior ethmoidal artery
 ↓ acuity
 Irregular pupil that reacts slowly to light
Mx
 Fracture reduction and muscle release necessary.
Chemical Injury
 Alkaline solutions are particularly damaging
 Mx
 Copious irrigation
 Specialist referral

Allergic Eye Disease Tropical Eye Disease
Seasonal Allergic Conjunctivitis (SAC) Trachoma
 50% of allergic eye disease
 Small papillae on tarsal conjunctivae Pathophysiology
 Rx  Caused by Chlamydia trachomatis (A,B,C)
 Antazoline: antihistamine drops:  Spread by flies
 Cromoglycate: inhibits mast cell degranulation  Inflammatory reaction under lids → scarring → lid
distortion → entropion → eyelashes scratch cornea →
Perennial Allergic Conjunctivitis (PAC) ulceration → blindness
 Symptoms all year c̄ seasonal exacerbations
 Small papillae on tarsal conjunctivae Rx
 Rx: olopatadine (antihistamine and mast-cell stabiliser)  Tetracycline 1% ointment ± PO
Prevention
Giant Papillary Conjunctivitis  Good sanitation
 Iatrogenic FBs: contact lenses, prostheses, sutures
 Face washing
 Giant papillae on tarsal conjunctivae
 Rx: removal of FB, mast cell stabilisers
Onchocerciasis (River Blindness)
Pathophysiology
Management of Allergic Eye Disorders  Caused by microfilariae of nematode Onchocerca
volvulus
1. Remove the allergen responsible where possible
 Spread by flies
 Fly bites → microfilariae infection → invade the eye →
2. General measures
inflammation → fibrosis → corneal opacities and
 Cold compress
synechiae
 Artificial tears
 Oral antihistamines: loratadine 10mg/d PO Rx
 Ivermectin
3. Eye drops
 Antihistamines: antazoline, azelastine
 Mast cell stabilizers: cromoglycate, lodoxamide
Xerophthalmia and Keratomalacia
 Steroids: dexamethasone
 Manifestations of vitamin A deficiency
 Beware of inducing glaucoma
 NSAIDs: diclofenac Presentation
 Night blindness and dry conjunctivae (xerosis)
 Corneal ulceration and perforation
Rx
 Vitamin A / palmitate reverses early corneal changes

Eye Signs in Systemic Conditions Ophthalmic Pharmacology
Hypertensive Retinopathy Mydriatics
 Keith-Wagener Classification
1. Tortuosity and silver wiring Anti-Muscarinics
2. AV nipping  Tropicamide
3. Flame haemorrhages and soft / cotton wool spots  Duration: 3h
4. Papilloedema  Cyclopentolate
 Grades 3 and 4 = malignant hypertension  Duration: 24h
 Preferred for paediatric use
Granulomatous Disorders  Pupil dilatation + loss of light reflex
 TB, sarcoid, toxo, leprosy, brucella  Cycloplegia (ciliary paralysis) → blurred vision
 Uveitis (ant/post) and choroidoretinitis
Sympathomimetics
 Para-hydroxyamphetamine, phenylephrine
Systemic Inflammatory Disease
 May be used c̄ tropicamide
 Conjunctivitis: SLE, reactive arthritis, IBD
 Don’t affect the light reflex or accommodation
 Scleritis / episcleritis: RA, vasculitis, SLE, IBD
 Iritis : ank spond, IBD, sarcoid
Indications
 Retinopathy: dermatomyositis
 Eye examination
 Prevention of synechiae in ant. uveitis / iritis
Keratoconjunctivitis Sicca / Sjogren’s
 ↓ tear production (Schirmer’s: <5mm in 5min) Caution
 Dry eyes and dry mouth  May → acute glaucoma if shallow anterior chamber
 1O or 2O: SLE, RA, sarcoid
 Rx: artificial tears or saliva
Miotics
Vascular Occlusion
 Emboli → amaurosis fugax: GCA, carotid atheroemboli Effect
 Microemboli → Roth spots: infective endocarditis  Constrict the pupil
 Boat-shaped haemorrhage c̄ pale centre
Pilocarpine
Metabolic  Muscarinic agonist
 Kayser-Fleischer Rings: Wilson’s
 Exophthalmos: Graves’ Use
 Corneal calcification: HPT  Acute closed-angle glaucoma
HIV/AIDS
 CMV retinitis: pizza-pie fundus + flames Other
 HIV retinopathy: cotton wool spots
Tetracaine
 Anaesthetic used to permit examination of a painful eye
Lubricants
 Hypomellose
 Carbomer (viscotears)
Topical Anti-histamine
 Emedastine
 Antazoline
Chronic Open-Angle Glaucoma

st
 1 line: β-blockers
 Timolol, betaxolol
 ↓ aqueous production
 Caution in asthma, heart failure
 Prostaglandin Analogues
 Latanoprost, travoprost
 ↑ uveoscleral outflow
 α-agonists
 Brimonidine, apraclonidine
 ↓ aqueous production and ↑ uveoscleral outflow
 Carbonic anhydrase inhibitors
 Dorzolamide drops, acetazolamide PO
 Miotics
 Pilocarpine

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Surgery

© Alasdair Scott, 2012 1

© Alasdair Scott, 2012 2

Regional Anaesthesia 1. Non-opioid ± adjuvants

2. Weak opioid + non-opioid ± adjuvants

© Alasdair Scott, 2012 4

Intra-op: ↓ physical stress

Post-op: early return to function and mobilisation

© Alasdair Scott, 2012 5

Haemorrhage Classification Wound Infection

Pulmonary Atelectasis Risk Factors

© Alasdair Scott, 2012 6

Cholecystectomy Arterial Surgery

Small Bowel Surgery Hip Replacement

Early: 0-5d post-op Cause

Cause: β-haemolytic Streps + staph. aureus

© Alasdair Scott, 2012 8

Graduated Compression Stockings

© Alasdair Scott, 2012 9

© Alasdair Scott, 2012 10

© Alasdair Scott, 2012 11

Hydrostatic Pressure Daily Requirements

Replace other losses

© Alasdair Scott, 2012 12

Hartmann’s / Ringer’s Lactate

© Alasdair Scott, 2012 13

Suspect Catheter Problem

© Alasdair Scott, 2012 16

© Alasdair Scott, 2012 17

REPEAT 1O SURVEY AGAIN!

© Alasdair Scott, 2012 18

© Alasdair Scott, 2012 19

© Alasdair Scott, 2012 21

NB. may also use Lund and Browder charts

© Alasdair Scott, 2012 23

© Alasdair Scott, 2012 24

© Alasdair Scott, 2012 25

Oesophageal Anatomy Achalasia

© Alasdair Scott, 2012 27

Extra-oesophageal Nissen Fundoplication

© Alasdair Scott, 2012 29

Test and Treat

© Alasdair Scott, 2012 31

© Alasdair Scott, 2012 32

© Alasdair Scott, 2012 33

Laparoscopic Gastric Banding

Roux-en-Y Gastric Bypass

© Alasdair Scott, 2012 34

© Alasdair Scott, 2012 35

© Alasdair Scott, 2012 36

© Alasdair Scott, 2012 37

Modified Glasgow Criteria Interventional Mx: ERCP

© Alasdair Scott, 2012 40

Insulinoma Pancreas Divisium

VIPoma / Verner-Morrison / WDHA Syn.

© Alasdair Scott, 2012 41

Risk Factors Presentation

© Alasdair Scott, 2012 42

© Alasdair Scott, 2012 43

© Alasdair Scott, 2012 44

Carcinoid Syndrome: FIVE HT

© Alasdair Scott, 2012 45

© Alasdair Scott, 2012 46