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									                       SURGICAL FACTS FOR THE EXAM
                         (Derived mostly from past exam questions)

How do you examine a path pot?
 What is the organ?
 Where is the pathological process?
 What is the pathological process?
      o Use pathology terms & definitions
      o Mechanisms – cellular, tissue, organ or systemic
 Aetiologic clues
 Sequelae & complications
 Misc processes  related and incidental
 Differential diagnoses

How do you describe a lump?

1. Size
 ↑ size  more likely it is to be malignant
 Multiple bony lumps is suggestive of multiple hereditary exostosis & ollier‟s disease

2. Site
 Describe precisely in exact anatomical terms, measuring distances from bony points
 Closer to joint (ie metaphysis)  more likely to be a tumour (benign or malignant)

3. Shape
 Remember it is 3-Dimensional

4. Surface
 May be smooth or irregular, or a mixture of surfaces

5. Margin/edges
 Well defined margin  likely to be benign
 Irregular margin  likely to be malignant tumour, fracture callus or inflammatory new bone

6. Tenderness
 Suggestive of active inflammation, recent callus, rapidly growing sarcoma or tumour
    impinging on surrounding structures

7. Composition

7a. Consistency
 Stony hard : not indentable
 Rubbery : hard to firm, but slightly squashable
 Spongy : soft & very squashable
 Soft : squashable & no resilienc
7b. Fluctuation (fluid-filled)
 Can only be elicited by feeling at least two other areas of the lump whilst pressing on a third
    – if 2 areas on opposite aspects of the lump bulge when a 3rd area is pressed in, the lump
    fluctuates & contains fluid

7c. Fluid thrill
 Detected by tapping one side of the lump & feeling the transmitted vibration when it reaches
    the other side
 Place patient‟s/assistant‟s hand on lump midway between your percussing & palpating hands

7d. Transillumination (fluid-filled)
 Light will pass easily thru clear fluid (water, serum, lymph, plasma), but not thru solid tissues
    or opaque fluids (eg blood)
 Place small torch behind lump in dark room & shine towards tour eye. If it glows red it

7e. Resonance
 Solid & fluid-filled lumps are dull to percussion
 Gas-filled lumps are resonant

7f. Pulsatility
 Pulsation can be caused by the lump itself (true expansile pulsation, eg aneurysm or vascular
    tumour) or by transmitted to lump from elsewhere
 Place a finger of each hand on opposite sides of the lump :
           o Fingers being pushed apart  true expansile pulsation
           o Fingers being pushed in same direction (upwards)  transmitted pulsation
 Listen for bruits – vascular lumps may have a systolic bruit
 Check neurovasculature of limb distal to the lump

8. Reducibility
 Compress lump to see if reducible, a feature of herniae
 If patient coughs, the lump may return &/or expand (cough impulse)

7. Mobility/fixation of lump & its tissue layer
 Skin  lump moves when skin moves (eg sebaceous cyst, epidermoid cyst or papilloma)
 Subcutaneous tissue  skin can be moved over the lump (eg neurofibroma, lipoma)
 Muscle/tendon  contraction of muscle limits the lump‟s mobility (eg tumour, haematoma)
 Nerve  pressing on the lump may elicit pins and needles in nerve distribution; Lump cannot
    be moved in the longitudinal axis but it can be moved in the transverse axis
 Bone  lump is immobile, tethered (eg callus, subperiosteal haematoma, 20 ossification
    centre, tumour)

10. Overlying skin
 Signs of inflammation : redness (rubor), heat (callor), swelling (tumor), tenderness (dolor)
    Colour & texture, eg smooth & shiny

11. Regional lymph nodes
 Check regional LNs & other major LN groups (cervical, axillary & groin)

12. Other
 Muscle wasting
 Joint movements (eg ↓ ROM due to mass)
 Gait (? Limp)
 General physical examination : cachexia, SOB/cough/haemoptysis etc


How do you report fractures to an orthopaedic registrar?

1.   Name & details of patient & technique (types of views performed & position)
2.   Anatomical site : which side, which bone, where it is (proximal ⅓, mid-shaft or distal ⅓)
3.   Open or closed (gas in soft tissue may indicate open # or infection)
4.   Appearance of fracture line
             a) Transverse/oblique/spiral/comminuted/greenstick
             b) Complete or incomplete
5.   Degree of displacement or angulation of the distal segment
             o Undisplaced = fragments in  anatomical position, reduction not required
             o Displacement is due to traumatic force, gravity &/or muscle pull
             a) Displacement/apposition :What % of bone ends remain in contact (eg
                 undisplaced, ½ a diameter displaced, completely displaced) & in what direction
                 (eg dorsal vs volar, valgus vs varus)
             b) Angulation/tilt : By drawing a line along both major fragments & measuring the
                 angle of intersection (anterior or posterior, medial or lateral)
             c) Rotation : About longitudinal axis, distal fragment cf proximal fragment
             d) Length of bone : distraction (↑ length) or overlap/impaction (↓ length)
6.   Involvement of articulations
             a) Does # line involve a joint or the epiphysis ?
             b) In kids, involvement of epiphyseal plate (Salter-Harris classification)
7.   Bone texture : Does the bone look normal or is there evidence that it is a pathological # ?
8.   Soft tissue : calcification, gas, FBs, etc
9.   Neurovasculature – presence of pulses; motor & sensory function; compartment syndrome

How do you examine a fractured limb?

    Always compare w/ normal side
    Closed vs open # : look for skin openings (need invasive therapy urgently)
    Assess distal neurovascular function
            o Circulatory function : capillary refill, peripheral pulses, skin colour (if blood flow
                is compromised, get urgent orthopaedic consult)
            o Neurology : test motor & sensory function of major peripheral nerves
   Local inspection : swelling, lump, shape, normal anatomy
   Test anatomical structures for tenderness, crepitation, deformity
   Active & passive & stress testing of bone/s & ligaments  ROM, continuity, pain,
    crepitation, stability & motion abnormalities (if –ve X-ray)
   Examine joints above & below (eg # involvement, synovial swelling, fat pad)
   Consider child abuse in infants with #‟s

What are the complications of fractures?

             Immediate (hrs)                 Early (hrs-wks)             Late (months-yrs)
Local        - Haemorrhage                   - Infection (Clostridia)    - Deformity – malunion or
             - Damage to arteries/nerves     - Compartment syndrome*     non-union; growth probs
             - Damage to surrounding         - Implant failure           - 20 OA; joint stiffness
             structures/viscera (eg spine)   - Fracture blisters         - Avascular necrosis*
Systemic     - Hypovolaemic shock            - Fat embolism (< 48h)      - Osteomyelitis
                                             - DVT/PE                    - RSD (Sudeck‟s atrophy)
                                             - Septicaemia, pneumonia    - Myositis ossificans
                                             - ARDS                      - Tendon/muscle damage
                                             - DIC                       - Ischaemic contracture
                                             - Crush syndrome  ARF

Describe compartment syndrome, its clinical features & management

   Soft tissue swelling (oedema) & bleeding into tight osteofascial compartment  ↑
    compartment pressure (non-expansile)  impaired venous drainage (if pressure > 40mmHg)
     ultimately, occlusion of arterial input  ischaemic necrosis of contained muscles & nerves
    (within 12hrs)  later muscle fibrosis
   Major causes : # of forearm, elbow or upper tibia; vascular compromise, reperfusion injury,
    compressive dressings, any MSK injury
         o Most commonly involves anterior compartment of calf following closed tibial #
   Complcn :  fibrotic contractions of muscle (eg Volkmann‟s ischaemic contracture of
    forearm flexors); nerve damage; myoglobinuria
   Early S&S – diagnosis is made almost solely on the clinical findings
         o Swollen & tense limb – palpation of firm, tender compartments
         o Unrelenting pain out of proportion to the injury which is not relieved by opiates
         o Passive hyperextension of toes or fingers will ↑↑ pain in calf or forearm
         o Loss of sharp sensation
   6 P‟s : pain, pallor, pulselessness, perishing cold, paraesthesia, paralysis
   Ix : measure intracompartmental pressure ( urgent Tx if > 40mmHg) – normal is 0-
   Mx if > 30mmHg : elevate & ice limb; hyperbaric therapy  some advocate fasciotomy !
   Mx if > 40mmHg : decompression of skin & fascial compartments (open fasciotomy) within
    4hrs  wound left open until swelling has subsided
         o Monitor UO for signs of myoglobinuria & ARF

Describe the parts of a normal bone
   Diaphysis : shaft or long, main portion
   Epiphysis : Extremity or end of bone
   Metaphysis : Region where diaphysis joins epiphysis – in growing bone includes the
    epiphyseal plate or physis (hyaline cartilage)
   Articular cartilage : Thin layer of hyaline cartilage covering epiphysis where bone forms
    articulation with another bone

   Medullary (marrow) cavity : Central part – houses bone marrow & trabeculae
   Periosteum : External covering of bone (except articular surface)
           o Outer fibrous layer – dense fibrous CT (with BV‟s, lymph V‟s, nerves)
           o Inner osteogenic layer – mesenchymal osteoprogenitor cells (can become
              osteoblasts or osteoclasts)  bone growth in diameter, repair
   Endosteum : Internal covering – CT monolayer of osteoprogenitor cells

Describe the 2 types of bone growth

Intramembranous ossification               (ALK p131)
 Occurs within a membrane (eg flat bones of skull, mandible) w/o a cartilage intermediate
1. Mesenchymal cell aggregate (TGF-β, FGF etc)  osteoprogenitor cells  osteoblasts
2. Bone deposition (osteoblasts) & remodelling (osteoclasts) forms trabecular bone
3. ↑ bone formation on outer & inner surfaces forms cortical plates of bone
4. Residual mesenchymal tissue becomes haemopoeitic bone marrow (medulla)

Endochondral ossification             (ALK p 133-134)
 Occurs in most bones, eg long bones
1. Hyaline cartilage model from mesenchymal tissue
2. Outer layer of mesenchymal cells, chondroblasts & osteoprogenitor cells form perichondrium
3. BVs enter diaphysis, with chondrocyte proliferation (↑ length/width) & osteoblasts beginning
   osteoid formation  primary ossification centre
4. Continued osteoid formation & remodelling forms central network of trabecular bone
5. After birth, BV‟s invade the epiphysis & bring osteoprogenitor cells, which convert the
   cartilage model into trabecular bone, forming the secondary ossification centre
6. Remaining hyaline cartilage forms epiphyseal plate in the metaphysis & articular cartilage
7. Epiphyseal plate allows for growth of bone in length  Growth of cartilage on epiphyseal
   side of epiphyseal plate & its subsequent replacement with bone on the diaphyseal side
8. Puberty  ↑↑ hormones  ↑↑ bone growth > cartilage proliferation  epiphyseal plate
   narrows & disappears  epiphyseal line
 Bone can grow in diameter/width throughout life by appositional growth : As bone is being
   laid down from the periosteum by osteoblasts, osteoclasts remove bone matrix on the inner
   (endosteal) surface  Enlarges marrow cavity while retaining cortical thickness

What are the layers of the epiphyseal plate?         (ALK p139/135)

   Involves growth of cartilage on the epiphyseal side of the epiphyseal plate and its subsequent
    replacement with bone on the diaphyseal side
1. Zone of resting cartilage (reserve zone) – hyaline cartilage, w/ continuous cell division
2. Zone of proliferation (epiphyseal side of plate) – active proliferation (hyperplasia) of
   chondrocytes which ↑↑ the length of the bone
3. Epiphyseal growth plate (hyaline cartilage)
4. Zone of hypertrophy (diaphyseal side of plate) – Chondrocytes enlarge (hypertrophy) –
   salter-harris fractures affect this part
5. Zone of calcifying cartilage : calcification of the matrix (via alkaline phosphatase 
   calcium salts), which eventually cuts off nutrient supply & prevents waste removal
6. Zone of cartilage cell death (vascular invasion) – Imprisoned chondrocytes die (lack of
   blood supply). BV‟s invade this zone.
7. Zone of ossification & bone reabsorption – Osteoblasts invade (via BV‟s) & lay down
   osteoid on the calcified cartilaginous matrix. Deposited bone is remodelled by osteoclasts as
   it gets incorporated into the diaphysis.
 NB Cell stays at same point in bone & goes thru the various stages  zone migrates, not the
   cells  forcing plates away from each other  ↑ length

Describe Salter-Harris fractures using a diagram

   Epiphyseal plate (physis) injuries – usually affects the zone of hypertrophy (diaphyseal side
    of growth plate)
   Most commonly occur in children aged 10-15 years
   Make up ≈ 1/3rd of all skeletal injuries in children
   Can cause severe deformity in later life if a bony bridge forms across the # site & prevents
    growth on one side of the bone.
   Type I : # line extends thru the epiphyseal line (horizontal shearing force) - not visible on x-
   Type II : Separation of epiphysis w/ triangular fragment of metaphyseal shaft attached to it
    (lateral displacement force) – most common type !!
   Type III : Vertical # thru epiphysis extending into epiphyseal plate
   Type IV : # line passes thru both epiphysis, physis & metaphysis – may cause growth arrest
    & joint deformities.
   Type V : Compression of epiphyseal plate. Commonly assoc/ w/ growth arrest.
See radiology recall p638
               Separated (type I)
               Above (type II)
               Lower (type III)
               Through (type IV)
               Ruined (type V)

What are the orthopaedic emergencies?

   Open fracture/dislocation (OT within 6hrs)
   Vascular injuries
   Compartment syndrome
   Neural compromise, esp. spinal injury
   Acute septic arthritis or osteomyelitis
   Exsanguinating pelvic #
   Hip dislocation

What are the indications for open reduction of fractures?

   N - Non-union, failure of closed reduction or unstable fractures prone to redisplacement after
   O - Open # (needs ex fix)
   C – Compromise of neurovasculature; Compartment syndrome; Co-morbidities, eg elderly,
   A – Articular surface malalignment (intra-articular #, requires anatomic reduction)
   S – Salter-Harris III or IV
   T – Trauma patient‟s – earlier mobilisation & ↓ risk of ARDS
   Pathological #‟s

Principles of fracture management
   1. Reduction of the fracture – open or closed
   2. Immobilisation of # fragments – relieve pain & prevent mal-union
   3. Rehabilitation of the soft tissues & joints (early mobilisation)

What is external fixation? Why is it used? What are the complications?

   A scaffold or gantry attached to threaded pins set in the bone fragments (eg ring fixator)
   Reasons for using external fixation – see NO CAST above
       o Open fractures
       o Fractures with skin loss or infection
       o Able to easily adjust position of fragments
       o Non-union or malunion
   Complications
       o Non-union (if hold fracture fragments too tight)
       o Pin-track infection
       o Neurovascular damage
       o Refracture when Ex Fix is removed

What is a Colles #? What are the complications? Why use external fixation?

Colle’s fracture
 FOOSH in older women
 Fracture of distal radius, with dorsal angulation & displacement of distal fragment, often w/
   associated # of ulnar styloid
 „Dinner fork‟ deformity : dorsal angulation & displacement, radial deviation, supination &
   proximal impaction
 Mx controversial : if displaced, reduce & apply cast from elbow to MCPJs (with wrist in
   flexion & ulnar deviation); Cast worn for 4 weeks, check at 1 week

 Median N damage/compression – runs right across site of Colles‟ fracture
 Rupture of EPL tendon – EPL runs across # site on dorsum of wrist
 Sudeck‟s atrophy (reflex sympathetic dystrophy, RSD) – disturbance of sensory & autonomic
  innervation of bone/BVs – hand becomes stiff, blotchy & cold)
 Malunion – fracture is unstable & bone is crushed – may require operative intervention

External fixation
 Primary external fixation (possible including percutaneous pin fixation) should be considered
   for intra-articular, displaced fractures

How do you manage open fractures?
1. An open fracture is suspected if there is : wound at # site, ooze from puncture wound (leaking
   haematoma) or protruding bone fragments
2. Emergency management & assessment
      a. ABCs
      b. Assess entire limb, esp neurovasculature
      c. Assess wound : state of skin around wound, does wound communicate with # ?
      d. Assume contaminated – remove gross debris, clean wound w/ sterile saline,
          chlorhexidine & cetrimide; cover wound w/ sterile dressing
      e. Reduce # & place in backslab, keep NBM
3. Give antibacterial prophylaxis – antibiotics (IV fluclox + benzylpen +/- gent/Flagyl) &
   Tetanus toxoid/Ig
4. OT within 6hrs for debridement – extend wound, thoroughly irrigate, remove dead tissue,
   pack wound & leave open for DPC in 3-5 days
5. OT to treat the fracture – Grade III requires Ex Fix

What is neurapraxia?
 Neurapraxia** = minimal nerve damage (localised demyelination or compression) – axons
  intact, but conduction ceases transiently
          o Spontaneous recovery in days or weeks
   Axonotmesis (axonal separation) = severe axon damage by compression or traction
          o Distal portions degenerate, but investing sheath remains intact  usually get
             delayed recovery (1-2mm/day)
   Neurotmesis = complete severance of a peripheral nerve
          o Spontaneous recovery does not occur  needs surgical repair
          o Assoc/ w/ degeneration of the nerve fibre distal to the point of severance

Clinical features
 Symptoms : numbness, sensory alterations (eg paraesthesia), weakness
 Inspection : skin smooth & shiny; muscle wasting
 Palpation : ↓ power, ↓ sensation, Tinel‟s sign
 Tinel sign : A sensation of tingling felt at the lesion site or more distally along the course of a
   nerve when the latter is percussed; indicates a partial lesion or early regeneration in the nerve

What nerve would you use for a graft? Why?
 Open injuries – explore at primary operation – if cleanly divided repair immediately,
  otherwise leave alone & re-explore at 2-3 weeks
 Closed injuries – usually nerve sheath is intact, so repair will occur – if healing does not
  occur, a nerve graft (eg Sural nerve) can be used, followed by splintage
 Only thin nerves are useful, as thick nerves undergo central necrosis after grafting

What are the signs of facial nerve palsy? How do you tell if it is UMN or LMN?

Relevant anatomy
 The facial nerve provides motor function to the muscles of facial expression, as well as taste
   via the chorda tympani
 Motor course –lateral surface of pons  thru internal acoustic canals  internal auditory
   meatus  exits skull at stylomastoid foramen  thru parotid gland  splits into its 5
 The UMN from the motor homunculus innervates the facial nerve nucleus in the brainstem
 Facial nucleus receives crossed & uncrossed fibres by way of the corticobulbar tract
 The UMN from the right innervates the whole right nucleus as well as the forehead area of
   the left nucleus. Conversely, the left UMN innervates the whole left nucleus and the forehead
   area of the right nucleus.
  Facial muscles below the forehead receive contralateral cortical innervation, while those
   muscles of the forehead receive bilateral innervation (NB Skin of forehead via CNV1)

Facial nerve lesion
  A LMN lesion of the facial nerve will cause ipsilateral complete paralysis of that side of
   the face including the forehead
       o May be pontine, posterior fossa, petrous temporal bone, #, viral infection
       o If before chorda tympani branches off, will also have taste loss
 An UMN lesion will cause contralateral paralysis of the facial muscles below the level of
   the forehead, with the frontalis & orbicularis oris spared (bilateral cortical innervation)
Examination of CNVII
 Facial asymmetry – During conversation may see unilateral drooping of corner of mouth,
   smoothing of wrinkled forehead (may be symmetrical if bilateral)
 Look up & wrinkle forehead  look for loss of wrinkling (frontalis – LMN lesion) & feel
   muscle strength by pushing down against corrugation either side
 Shut eyes tightly – compare how deeply the eyelashes are buried on the 2 sides & then try to
   force open each eye (if LMN palsy, will get upward mov‟t of eyeball & incomplete closure of
   eyelid on ipsilateral side)
 Grin & compare nasolabial grooves (smooth on the weak side)
 Taste on anterior 2/3 of tongue – distinct substances placed separately each side

Causes of facial weakness
 Pons : MS, vascular lesions,
 Cerebellopontine angle : acoustic neuroma, meningioma, basal meningitis
 Petrous temporal bone : Bell‟s palsy (idiopathic inflammation of CNVII within petrous
   temporal bone – LMN palsy, usually temp), middle ear infection, trauma, HZV, tumours
           o Chorda tympani joins facial N here
 Within the face : parotid gland tumours, mumps, sarcoidosis
 Other (often bilateral) causes : GBS, MND, myasthenia gravis, myotonic dystrophy

Ulnar nerve palsy: what are the causes & clinical features?

 Ulnar nerve entrapment at cubital tunnel : mechanical trauma (eg overhead throwing
   athletes), osteophytes, loose bodies, synovitis, thickened fascia
 Elbow fracture

 Medial side of arm (medial to brachial A)  superficial course thru ulnar groove (cubital
   tunnel) next to medial epicondyle of the ulna (vulnerable to injury = funny bone)  medial to
   ulna in forearm
 Motor : FCU & medial ½ FDP & the intrinsic muscles of the hand (interossei, lumbricals 3
   & 4, adductor pollicis, hypothenar)  fine motor control of the hand
 Myotome : Finger abduction; Fromet’s sign (paper b/w thumb & II finger)
 Sensory : Skin of medial 1/3 of hand, little finger (V) & medial ½ of ring (IV) finger (palmar
   & dorsal surface)

Clinical features
 Impaired adduction & abduction (interosseus 1-4)
 Flexion of wrist moves radially (by FCR)
 Hypothenar muscle wasting
 Ulnar claw hand when attempt to straighten fingers
       o Hyperextension of MCPJ 4&5 (lumbricals gone)
       o Unable to flex 4th and 5th fingers at DIPJ‟s, PIPJ‟s bent
       o Abducted thumb (adductor pollicis)
CNXI (accessory nerve) injury: what are the causes & clinical features?

   The spinal branch of CNXI provides motor innervation to the SCM & trapezius muscles
    (cranial branch assists in swallowing)
   Test by getting patient to shrug the shoulders & turn head against resistance
        o NB R sternocleidomastoid turn head to L  inability to rotate head to contralateral
            side of lesion, but lack of trapezoidal shrug on ipsilateral side
        o Look for a torticollis – overactivity of SCM – head appears turned to one side

Causes of palsy
 Trauma to neck or base of skull
 Poliomyelitis
 Syringomyelia
 Tumours near jugular foramen

What are the causes of LBP? List > 6 pathological conditions

Classification of LBP
 LBP can be classified into mechanical, non-mechanical & non-spinal back pain by history &
 In > 90% of patients, no precise anatomical cause of LBP is found, although  70% are
   presumed to be caused by intervertebral dysfunction. < 10% have structural lesions.

Pathological causes of LBP**
Vascular                Aortic aneurysm
                        Acute aortic dissection
Infective               Osteomyelitis
Inflammatory            Ankylosing spondylitis
                        Rheumatology disorders
Neoplastic              Primary tumours (rare)
                        Metastases – breast, prostate, bronchus
Degenerative/MSK        Spondylogenic (simple mechanical) – vertebral dysfunction
                        (IV discs &/or facet joints)
                        Prolapsed IV disc
                         Sacro-iliac dysfunction
Idiopathic               Paget‟s disease
                         Scheuermann‟s disease
Congenital               Kyphoscoliosis
                         Spina bifida
Traumatic                Vertebral fractures
                         Ligamentous injury
                         Muscle tears
Endocrine/metabolic      Cushing‟s syndrome
Psychogenic              Depression
                         Psychosomatic backache
Visceral                 GIT – penetrating peptic ulcer, Ca rectum
                         Pancreatic Ca
                         Biliary disorders
                         Renal disorders – Ca, renal calculus, inflammatory disease
                         OBGYN – uterine tumours, PID, endometriosis

List > 8 red flag signs for LBP indicating radiologic investigation

   Age : < 20 or > 50
   Significant trauma
   Hx of malignancy, corticosteroid use, diabetes, drug or alcohol abuse, or HIV
   Constitutional symptoms: malaise, febrile, weight loss
   Pain worse at night; constant pain not relieved when supine
   Widespread neurological signs or symptoms
   No improvement > 1 month
   Bowel/bladder dysfunction &/or perianal anaesthesia (cauda equina syndrome)
   Deformity
   ↑ ESR

List > 5 conditions in which bone scan investigation of LBP would help

   Metastases or primary malignancy – 90% positive
   Infections
   Fractures
   Osteomalacia/osteodystrophy
   Spondyloarthropathies (ankylosing spondylitis, psoriasis, IBD, reactive arthritis) – SI joints
   Hyperparathyroidism – 50% positive
   Paget’s disease
 Plain x-rays are only 70% sensitive & give the diagnosis only 33% of the time.

Disk prolapse

    L4/5 & L5/S1 in 90% of cases
    Back pain exacerbated by sitting and bending
    Lasegue’s test (straight leg raise): raise leg to 90 deg. Normally, only min tension
   Disk prolapse  severe pain
    Level affected
      L1-2-3: iliopsoas (pain on hip flexion)
      L2-3-4: quads (loss of reflex, weak leg extension)
      L4: tibialis anterior (loss of heel walking)
      L5: loss of dorsiflexion, numbness
      S1: loss of plantarflexion, absent Achilles tendon reflex


What is scoliosis?
 Abnormal lateral curvature &/or twisting of the spine – seen from behind & accentuated by
  bending forwards

What are the causes & classification of scoliosis?
 Postural (non-structural) scoliosis – compensatory to some condition outside the skin, eg
  short leg, pelvic tilt or prolapsed IV disc
      o Disappears on sitting and bending forward
 Structural scoliosis – caused by bony abnormality or vertebral rotation – secondary curves
  nearly always develop to counterbalance the primary deformity
      o Deformity is fixed & does not disappear with changes in posture
      o Major types
              1. Adolescent idiopathic scoliosis** - usually thoracic curve convex to the right
                  – presents before puberty & progresses until skeletal growth ceases
              2. Infantile (congenital) scoliosis – may regress
              3. Neuromuscular scoliosis, eg polio, cerebral palsy
              4. Osteopathic scoliosis – due to congenital vertebral abnormalities

What are the clinical signs?
 Curved spine, accentuated by bending forwards – postural curves disappear
 Shoulders & waist are asymmetrical
 Thoracic scoliosis – rib angles protrude (posterior hump), breasts asymmetrical

What are the radiological signs & angles of importance?
 Full length erect views of the spine & pelvis – identify primary curves clinically or by lateral
  flexion radiographs
 Cobb’s angle : measures the angle of curvature
      o Find upper & lower limits of primary curve by drawing tangents to the bodies (where
          disc spaces begin to become widened on concavity of curve)
        o Draw perpendiculars from these vertebrae
        o Note the angle between them
   Risser’s sign : x-ray of pelvis shows when the iliac apophysis has ossified & fused, a sign of
    skeletal maturity after which progression of the curve is minimal

What is the treatment? Who should be treated?
 Observation – involves 4-monthly examination, photography & radiography
 Braces – may stop progression in some curves (eg Milwaukee brace)
 Operation – curve can be corrected by instrumentation to the back or front of the spine &
  held with internal fixation devices (eg Harrington rod) or fuse permanently (via bone graft) in
  the corrected position.
      o Indications : respiratory compromise; rapid progression; curves > 400; failure of brace

    Treatment recommendations in adolescent scoliosis
    Curvature (Cobb’s angle)        Treatment
    < 20                            Observe
    20-40                           Brace
    > 400                           Operative intervention

What are the causes of a painful hip?

Causes of painful hip                       Hip diagnostic calendar
Referred pain                               0 (birth)              CDH/DDH
 Discogenic disease                        0-5                    Infections
Joint disorders                             5-10                   Perthes‟ disease or TS
 Infection                                 10-20                  SCFE
 Perthes‟ disease                          Adults                 OA
 Slipped epiphysis                                                Avascular necrosis
 RA                                                               RA
 OA                                                               Prolapsed disc
 Osteonecrosis
Periarticular disorders
 Hernia
 Tendinitis
 Bursitis

Trendelenburg test

What is the Trendelenburg test? What indicates a positive Trendelenburg sign?
 Patient asked to stand, unassisted, on each leg in turn – lift other leg by bending knee (not
 Normally the weight-bearing hip is held stable by the abductors & the pelvis rises on the
  unsupported side (negative Trendelenburg test)
 If the hip is unstable, or very painful, the pelvis drops on the unsupported side (positive
  Trendelenberg sign)

What may cause a positive Trendelenburg sign? Give ≥ 4 causes
1. Dislocation or subluxation of hip (eg CDH)
2. Weakness of the ABductors : gluteus medius & minimus via superior gluteal N
3. Shortening of the femoral neck
4. Any painful disorder of the hip (causes gluteal inhibition)

What is Perthes disease? What are the classic radiologic findings?

   Idiopathic avascular necrosis of the femoral head – precipitating factor is probably a joint
    effusion following trauma or non-specific synovitis.
   Causes hip or knee pain, limp & ↓ ROM in 3-8 year olds (♂ > ♀)
   DDx = transient synovitis (irritable hip)

Radiological signs (Dandy p316; Dixon p180) – Frogleg view
1. Initially normal (cold on bone scan) – bone necrosis
2. ↑ density of epiphysis & widening of the joint space – revascularisation & repair
3. Fragmentation of the epiphysis (collapse & remodelling)
4. Epiphysis flattened & enlarged (coxa plana & coxa magna)

 Containment of femoral head within acetabulum ( more likely to retain normal shape) by
  abduction & internal rotation using „broomstick‟ plaster or a removable splint
 Alternative is osteotomy (late Dx)

What is SCFE? What are the classic radiologic findings?

   Slipped upper/capital femoral epiphysis caused by fracture thru the physis – related to
    hormonal imbalances
   Occurs during pubertal growth spurt; esp in fat ♂‟s
   Causes pain in hip or knee &/or limp – O/E leg is shortened & externally rotated; ↓ ROM in
    abduction & internal rotation

Radiologic findings (Dixon p173)
1. Epiphysis for head of femur is displaced posteriorly &/or medially
2. Widening of the physis
3. Trethowan’s sign - line drawn along superior surface of neck remains superior to head
   instead of passing thru it

 Mild displacement – fix epiphysis with 2 threaded pins
 Severe displacement - 2 threaded pins, followed by compensatory osteotomy

 Recurrent subluxation or dislocation of the hip secondary to acetabular dysplasia, abnormal
  ligamentous laxity or both
 More common in ♀‟s (oestrogen ↑ laxity); L hip > R hip; related to breech delivery or FHx

List ≥ 4 clinical features suggesting CDH

Routine post-natal exam
 Ortolani‟s test – baby‟s thighs are held b/w thumb & forefingers w/ hips flexed to 900 – hip is
   slowly abducted – if a hip is dislocated, as full abduction is approached femoral head will be
   felt slipping into acetabulum +/- an audible „click‟
 Bartlow‟s test – fix pelvis b/w symphysis & sacrum – then attempt to dislocate the hip by
   gentle backward pressure during abduction & adduction
   (Remember Ortolani‟s is outwards, Bartlows is backwards)

Late features
 Asymmetrical skin creases (unilateral DDH)
 ↓ hip abduction (tested at 900 hip flexion)
 Leg is shortened & rotated externally
 Trendelenburg test is positive
 Gait – dip on affected side, or waddling gait if bilateral

What investigations are necessary? What are the radiographic signs?
 Ultrasound – essential for all babies with Ortolani click, family Hx or predisposing factor
      o Decisions on treatment based on U/S findings
 X-ray: AP pelvis may be helpful after 6 months (Dandy 340), Putti‟s triad
      1. Acetabular dysplasia : shallow acetabular socket & ↑ acetabular angle
      2. Small upper femoral epiphysis
      3. Delayed ossification of femoral head
      4. Superolateral displacement of femoral head – loss of Shenton‟s line, movement lateral
         to Perkin‟s line (lateral margin of acetabulum) & movement superior to Hilgenreiner‟s
         line (tri-radiate cartilage of acetabulum)
What is the initial management (after USS)?
 At birth : Nurse baby in double nappies or abduction pillow for 1st 6 weeks
 6 weeks : re-examine – if hips stable, observation only for 6 months. Babies with persistent
  instability need formal abduction splinting until radiological confirmation of acetabular
  development (usually 3-6 months).
      o Splintage : Ensure the hips are reduced first (confirm by U/S). Apply splintage to
          hold hips at 1000 flexion & somewhat abducted. Infants will require a Von Rosen’s
          splint, Pavlik harness or Cambridge splint.
 6 months – 6 years : gradual closed reduction (over 3 weeks by traction) followed by plaster
  spica (hips flexed, abducted & internally rotated) for 6 weeks
 > 6 years : Operative reduction +/- osteotomy

What are the risks of management?
 Avascular necrosis of femoral head
 Incomplete healing may predispose the child to secondary OA in later life.
 Splinting without first ensuring that the hip is satisfactorily reduced – poor position.
 Unnecessary treatment – most dislocatable hips self-stabilise within a few days of birth.

What is acetabular dysplasia?
 Consists of
      o ↑ acetabular angle (steeply sloping roof), &
      o Shallow acetabular fossa
 Predisposes to spontaneous dislocation or subluxation

How can acetabular dysplasia be reversed?
 Abduction splinting in neonates, as per DDH
 In older children, surgery may be necessary: an osteotomy of the femur to restore joint
  alignment, or osteotomy of the pelvis to restore correct acetabulum shape.

What are the pathological causes of limp in a child?

   Vascular (ischaemia) – Perthes‟ disease
   Infection – septic arthritis, osteomyelitis
   Inflammation – transient synovitis, juvenile RA
   Neoplastic – tumour, leukaemia
   Congenital/developmental – CDH/DDH, SUFE
   Trauma – SUFE, fracture
   Neuromuscular – cerebral palsy

Acute                         Subacute                       Chronic
Fracture                      Juvenile RA                    Cerebral palsy
Transient synovitis           Tumour/leukaemia               CDH/DDH
Septic arthritis              Acute on chronic SUFE          Perthes‟ disease
Osteomyelitis                                                Chronic SUFE
Hip timeline
0 (birth)                             CDH
0-5                                   Infections
5-10                                  Perthes‟ disease; Transient synovitis
10-20                                 SUFE
Adults                                OA, RA, avascular necrosis

Elbow dislocation

What neurovascular structures are in danger?
 90% are posterior dislocations
 Median nerve injury – test by touching thumb to 5th finger
 Ulnar nerve injury – test by spreading fingers apart
 Radial nerve injury – extend thumb, fingers & wrist
 Brachial artery injury – palpate brachial artery at elbow & palpate ulnar & radial arteries
  – compare to other side

How do you manage a dislocated elbow?
1. Analgesia
2. Check neurovasculature
3. Obtain x-ray promptly to exclude fracture-dislocation
4. Reduce dislocation ASAP under regional (eg Bier‟s block) or general anaesthesia
      a. Apply traction to forearm, with countertraction applied to distal aspect of humerus –
          also correct any medio-lateral displacement with counterforce simultaneously
      b. Gently flex the elbow to accomplish the reduction – often hear/feel clunk
5. Reassess neurovascular function & flex/extend elbow to check reduction
6. Apply posterior splint with elbow at 900 flexion
7. Obtain post-reduction x-rays

What is a Dupuytren’s contracture? What are the causes?

   Contracture of the palmar fascia which can involve the skin  flexion deformity
   May only affect 1 finger (usually the little finger) or entire hand (Dandy p367)
   Often symmetrical, commoner in ♂, may run in families

 Idiopathic
 Familial
 Liver disease
 Alcoholism
 Diabetes
 Epilepsy

 Slight deformities are best left untreated
   Surgical correction involves excising the contracted tissue
   Severe, uncorrectable deformity may require amputation of the affected digit


Colorectal neoplasia

Identify the lesion on the above pictures?

   Left : pedunculated polyp
   Right : sessile polyp

What types of polyps are there (ie classify large bowel polyps)?

Shape (Robbins p827)
 Sessile – small, flat projection into lumen (more likely to be villous architecture)
 Pedunculated – contains a stalk (more likely to be tubular architecture)

 Neoplastic (adenomatous polyp) – result of epithelial proliferative dysplasia –
    adenocarcinoma generally arises from adenomas
        o > 100 are present in FAP (familial adenomatous polyposis – defect in APC gene) &
            Gardner‟s syndrome
 Hyperplastic polyp : composed of well formed, mature glands & scant lamina propria – result
    from delayed shedding of surface epithelial cells – usually found in distal colon
        o Histology – hyperplastic crypts have a serrated or saw-tooth outline
 Inflammatory polyps : found in IBD (Crohn‟s &/or ulcerative colitis)
 Hamartomatous polyps : normal tissue in abnormal configuration – sporadic & usually found
    in kids – also seen in Peutz-Jegher‟s syndrome

Adenomatous polyps
 Tubular adenoma : tubular glands; smooth surface; usually pedunculated; most common
   Villous adenoma : villous frondlike projections (look like broccoli heads); usually sessile;
    greatest risk of malignancy (villous = villain)
   Tubulovillous adenoma : mixture

Risk of malignancy (ie. progression to adenocarcinoma)
 Polyp size : adenomas > 2cm have 50% risk of carcinoma
 Architectural type : villous 40%, tubulovillous 20%, tubular 5%
 Severity of epithelial dysplasia

What are the risk factors for CRC?
 ↑ age (incidence raises sharply after 50yrs)
 Family Hx (20% occur in setting of FHx, esp. if 1st degree relative < 50yrs at Dx)
 Presence of FAP, HNPCC or adenomatous polyps
 Low dietary fibre intake
 Excess intake of dietary fat, refined carbohydrates & red meat
 Ulcerative colitis (long-standing)
 Physical inactivity & obesity
 Alcohol & tobacco
 Irradiation

What is the adenoma-carcinoma sequence? What is the evidence to support it?

   Most colorectal carcinomas arise from, or within, pre-existing benign adenomas – a process
    that evolves over 5-15 years
   Ca develops from progressive accumulation of multiple genetic mutations – there is
    progressive increases in size, level of dysplasia & invasive potential
   Normal colonic epithelium  Hyperproliferative epithelium  Early adenoma  Late
    adenoma  Carcinoma
   Most sporadic cancers develop via the chromosomal instability pathway (A), due to
    inactivation of tumour suppressor genes (eg APC, p53, LOH) & activation of oncogenes (eg
   All HNPCC & some sporadic cancers follow the microsatellite instability pathway (B),
    beginning with APC mutation, then defect/s in DNA mismatch repair genes, hMLH1 or
Evidence for the adenoma-carcinoma progression = HI TEC
 Histology : adenomas commonly harbour carcinoma
 Intervention : screening programmes for adenomas ↓ incidence of CRC
 Topology : colorectal distributions are similar to that of adenomas
 Epidemiology : populations with high prevalence of adenomas also have high risk of CRC
 Chronology : peak incidence of adenomas antedates peak incidence of CRC

Genetic factors
 20% of colorectal Ca occurs in setting of a FHx; 5% due to HNPCC; <1% FAP
 FAP patients exhibit a somatic mutation in the tumour-suppressor APC gene – mutations in
   this gene also occur in sporadic cancers
 Hereditary mutations in DNA mismatch repair genes occur in hereditary non-polyposis
   colorectal cancer (HNPCC), aka Lynch’s syndrome – sporadic cancers can exhibit the same
           o Autosomal dominant mutation in hMLH1 or hMSH2
           o Diagnosis requires > 3 relatives with CRC spanning 2 generations
           o 80% lifetime risk of colorectal Ca – also ↑ risk of gynaecological tumours
           o Requires 2nd yearly colonoscopy from 25 yrs & gynaecological screening

What treatment is used for CRC?

   Aim is to excise the cancer with an adequate margin of surrounding tissue (usually 2cm, some
    say 5cm but ? effect on survival) & lymphovascular clearance
            o A large segment of colon (up to 15cm) is usually resected because of the extent of
                 lymphovascular clearance
   Usually results in an anastomosis via staples or sutures
   Procedure may be open or laparoscopic
   Surgical resection : attempts to remove area of bowel containing tumour complete with its
    lymphatic drainage (pericolic LNs) – as lymphatic drainage follows arterial supply, the axial
    artery is ligated at its origin, creating an ischaemic segment of bowel for excision
   Chemotherapy – 5-Fluorouracil + levamisole (or folinic acid) is used
        o To ↑ survival in Stage C cancers
       o In advanced disease as palliation (↑ survival 6 months)
   Radiotherapy – may be used pre- or post-op for T3-T4 rectal cancers to ↓ local recurrence
   Metastases may be treated by resection, embolisation, chemotherapy &/or XRT
       o Liver mets can be resected with a 1-2cm margin + adjuvant chemoRx
   FOLLOW-UP is essential to detect recurrence (most occur in 1st 3 years) – colonoscopy &
    CEA (at 1 year, then every 3-5 years)

What is the treatment for a Ca at the hepatic flexure?
 Right hemicolectomy (Clunie p184)
      o Laparotomy or laparoscopic approach
      o Excision of caecum, ascending colon & part of transverse colon & overlying
      o Division of ileocolic, R colic & R branch of middle colic vessels (SMA)
      o Anastomosis of ileum to transverse colon


What are the features of UC vs CD on contrast examinations?

Crohn’s disease                                               Ulcerative colitis
- SBS/SBE :  oedema & separation of bowel loops;             - AXR : thumb-printing (mucosal oedema); dilatation
   skip lesions;  string sign (terminal ileal stricture);   - SBS/SBE : normal (or backwash ileitis)
   deep rose-thorn ulcers;  cobblestone appearance;         - Ba Enema : rectum always involved
   fistulas                                                    Acute : granular colonic margin w/ thumbprinting
- Ba Enema : patchy involvement of colon. Rectum                Subacute : pseudopolyposis & superficial ulcerations
  may or may not be involved                                    Chronic : pipe-stem colon – smooth, narrowed &
                                                                shortened colon with lack of haustrations

Eisenberg p149, Dixon p115

What are the perianal features of CD?

   Present in ≈ 50% of CD patients
   Perianal skin tags
   Fissures
   Perianal sepsis
   Anorectal strictures

Compare UC vs CD

                                    Ulcerative Colitis                     Crohn’s Disease
Macro pathology
Bowel region                        Colon only                           Mouth  Anus
Rectal involvement                  Always – involvement proximally      Rectum often spared (50%)
                                    from rectum up
Distribution of lesions             Continuous                           Skip lesions / cobblestone
Mucosal appearance           Friable, purulent, diffusely        Patchy ulceration, fissured &
                             involved; may be atrophy            cobblestoned
Associated ileal disease     Only in „backwash ileitis‟          50% have combined ileal and colonic
Creeping mesenteric fat      Not seen                            Common
Serosa                       Normal                              Granular, fibrous or „flared‟
Micro pathology
Depth of inflammation        Mucosal (submucosal rarely)         Transmural (full thickness)
Wall thickening              Not seen (minimal fibrosis)         Common (“lead pipe”), often fibrosis
Crypt abscesses              Common                              Common
Pseudopolyps                 Marked                              Not uncommon in colonic CD
Granulomas (noncaseating)    Not seen                            Granulomas common (> 50%)
Ulcers / fissures            Superficial (no fissures)           Deep, linear  fissures
Lymphoid reaction            Mild                                Marked

Clinical features
Symptomatology               Diarrhoea w/ blood & mucus;         Diarrhoea (watery or bloody); Abdo
                             Cramping abdo discomfort;           pain (obstructions)
Abdominal O/E                Tenderness over colon or NAD        Tenderness; RIF mass;
Perianal abscess/fistulas    Rare (< 25%)                        Yes (75%)
Fat/vitamin malabsorption    No                                  Yes (ileal disease) – wt loss
Response to surgery          Good (colectomy = cure)             Poor-fair (recurrence !)
Intestinal obstruction       Late / rare                         Common
Intestinal fistulas          Not seen                            Common, 80%
Intestinal perforation       Occasionally                        Rare
Intestinal haemorrhage       Common                              Rare
Toxic megacolon              Occurs rarely                       Very rare
Colorectal carcinoma         10% (dysplasia common)              Rare
Extraintestinal manifestations
Sclerosing pericholangitis   Common                              Rare
Uveitis or arthritis         Common                              Common
Pyoderma gangrenosum         Rare                                Not seen

Bowel obstruction

What are the causes of SBO & LBO?

SBO (remember HANS had an SBO)                          LBO
 Hernia                                                 Neoplasia
 Adhesions***                                           Diverticular disease
 Neoplasia                                              Volvulus
 Stricture                                              In lumen : faeces, FB, bezoar, barium
 Intussusception                                        In wall : stricture, Hirschsprung‟s
 Volvulus, gallstone, bezoar, CF, abscess               Outside wall : tumour, hernia, adhesions

What are the S&S?

    1.   Colicky abdominal pain
    2.   Vomiting (provides relief) – early in high SBO, late or absent in LBO
    3.   Abdominal distension – epigastric or hypogastric in SBO, generalised in LBO
    4.   Absolute constipation – failure to pass flatus (obstipation) & faeces – occurs early with
         LBO, late in SBO

 Look for cause – scars, hernias, abdominal mass etc
 Inspection – abdominal distension, visible peristalsis
 Palpation – tenderness
 Percussion – hyper-resonant
 Auscultation – bowel sounds louder, more frequent & high pitched („tinkling‟)
 PR exam – faeces, blood or mucus

What investigations should be performed? What are the radiological features?

   Supine & erect AXR, erect CXR
   FBC, U&Es
   SBS or abdominal CT to determine level & extent of obstruction

Radiologic signs of obstruction
 Supine : gas-distended loops of bowel – level of obstruction determined by number of loops
   & amount of plicae (jejunum has multiple plicae, ileum has minimal)
          o Bowel distal to obstruction will be devoid of gas (the „cut-off‟)
          o String of beads sign – as bowel progressively fills with fluid, get ↓ gas – some gas
               remains trapped b/w adjacent plicae forming small beads of gas in a line
 Erect : air-fluid levels
 Volvulus: huge, distended gas-filled loop of sigmoid/caecum with a long-fluid level on erect
   film. Sigmoid volvulus presents „bent inner tube sign‟. Caecal distension > 10cm suggests
   imminent perforation.

SBO vs LBO on plain radiographs***
                     Small bowel obstruction                    Large bowel obstruction
Luminal folds        Plicae circulares extend across width of   Haustra (plicae semicirculares) extend only
                     lumen (step-ladder appearance)             partway across the lumen
Position             Central                                    Peripheral
Fluid levels         Short (3-5cm), but more numerous           Long fluid levels, but less numerous
Colonic/rectal gas   Absence of colonic gas                     Absence of rectal gas
Other                String of beads sign (fluid-filling)       May be huge distended loops

What is the management of SBO?

   Conservative – „Drip & suck‟ used if incomplete/uncomplicated obstruction or paralytic ileus
    – monitor closely, operate if persists
   Surgical – if complete/complicated – LOA or herniorrhaphy

Haemorrhagic loop of bowel caused by adhesions  SBO
   Adhesion  internal herniation of bowel contents  bowel obstruction & ↓ venous drainage
     engorgement & haemorrhage  ↓ arterial inflow  infarction


What is a stoma ?

   Ostomy : operation that connects the GI tract to the abdominal wall skin, or the lumen of
    another hollow organ (man-made fistula)
   Stoma : the opening of the ostomy
   Epithelialisation (mucosa to skin) prevents closure

What is the difference b/w a temporary & a permanent stoma ?
 Temporary stomas are usually loop ileostomy/colostomy & can be removed at a later date by
  a minor operation +/- anastomosis
 Permanent stomas are usually end ileostomy/colostomy & are more difficult to reverse

When is a stoma indicated ?
 Temporary
      o To protect a distal anastomosis & allow healing, eg ileal pouch-anal anastomosis, low
          colorectal anastomosis
      o To divert stool from the distal anorectum, eg perianal Crohn‟s disease, anorectal Ca,
          severe perineal sepsis, faecal incontinence
      o Caecal volvulus: decompression of colon
 Permanent
      o Following colectomy if cannot anastomose, eg insufficient bowel remaining to
          anastomose, risks of anastomosis
      o Following removal of anorectum, eg APR
      o Severe faecal incontinence

What is the pre- & post-op stomal care ?

   Pre-operative stoma siting, counselling & stoma eduction are important
   Viability of stoma is examined periodically in the post-op period
   Defer oral feeding until intestinal peristalsis recommences & ileostomy has passed gas &
    effluent, usually 2-5 days after surgery
   Normal output ranges 500-1000mL/day – higher outputs may cause dehydration, while lower
    outputs indicate obstruction. Also higher Na & K losses than in pts w/ intact colon
   Stomal education commences pre-op & continues post-op using stomal therapist
        o ↑ psychological adjustment
        o Fitting & changing of appliance
        o Warning signs to look for, eg infection, ischaemia
   Stoma is remeasured for new appliances at 4 weeks (after oedema resolves) – proper fitting
    essential to avoid leakage & skin excoriation
   Dietician advice
        o Initially low-residue diet
       o After 3 weeks introduce food, but must avoid foods that affect the stoma, eg nuts,
           popcorn, corn, string vegetables, fruit peels
       o High H20 & salt intake
   Option for stomal irrigation, whereby patient can irrigate & empty the stoma every few days.
    This removes the need to wear a bag appliance, and a cap over the stoma can be worn instead.

What are potential complications of a stoma ?

   High output causing dehydration/salt & H20 depletion: anorexia, fatigue, muscle cramps,
    thirst. Avoid situations where H20/salt is unavailable.
   Ischaemia – may require urgent laparotomy & refashioning of the stoma
   Stricture – due to ischaemia, parastomal sepsis, recurrent CD, etc
   Bleeding
   Fistula
   Parastomal abscess
   Parastomal ulcer
   Parastomal hernia
   Ileostomy retraction – may require surgical revision
   Small bowel obstruction – due to adhesions, volvulus or internal herniation
   Skin irritation

Meckel’s diverticulum

What is a Meckel’s diverticulum & what is its embryological origin ?

   Solitary true diverticulum on the anti-mesenteric side of the terminal ileum, within 2 feet of
    the ileocaecal valve
   Caused by failure of involution of vitelline duct (connects lumen of primitive midgut gut to
    yolk sac)

What are its complications & resultant symptoms ?
 Ulceration (ectopic gastric mucosa)  bleeding (red blood PR) or perforation
 Meckel‟s diverticulitis – resembles appendicitis
 Obstruction – as volvulus or intussusception

Meckel‟s “rule of 2’s”
       Found in 2% of populati
       2% are symptomatic
       Found ≈ 2 feet from the ileocaecal valve
       Most are 2 inches long
       Most symptoms occur < 2 years
       One in 2 will have ectopic tissue


- linear tears in anal canal
- diagnostic triad:
        i. external skin tag (“sentinel pile”)
        ii. fissure, exposing int sphincter fiber
        iii. hypertrophied anal papilla
- acquired: secondary to passage of hard stool
 consequence, not cause of constipation
- S&S: painful BM and bright-red blood PR
- may undergo malignant change (SCC or BCC)
- post midline – MC site
Complication: sphincter spasm
i. Conservative: mild analgesia, laxatives, Sitz baths, botulinum toxin injection
ii. Surg: lat int sphincterotomy (relieves anal spasm)


- infection of glands, located between int & ext sphincters, when the crypts get occluded
Types: intersphincteric, pararectal, ischiorectal, supralevator
DDx: Crohn‟s, pilonidal dx, TB, actinomycosis, trauma, Cx, radiation injury…
Rx: drainage
         if above levator: inside the anal canal
         if below levator: outside through the skin
Complication: fistula-in-ano


Goodsall’s rule:
if external opening is anterior to a transverse line (ie imaginary line, traversing anus in the
middle) = fistula has straight radial tract
if external opening is posterior = curved fistulous tract
        1. Fistulotomy
        - pass the probe
        - skin, subcutaneous tissue, and internal sphincter muscle are divided to open tract
        - healing by 2nd intention
Complication: incontinence
        2. Seton stitch
        - tighten seton every visit for 6-8 wks. With time, fibrosis occurs above the seton as it
        gradually cuts through the sphincter muscles and exteriorizes the tract.
        3. Mucosal advancement flap (deep complicated fistula, eg rectovaginal)

Haemorrhoids           (Browse p430)

What is the cause of haemorrhoids ?

   Haemorrhoids are submucosal vascular „cushions‟ within the anal canal that represent dilated
    submucosal veins of the internal haemorrhoidal plexus
   Occur 20 to persistently ↑ venous pressure within haemorrhoidal plexus  constipation;
    pregnancy (venous stasis); collaterals in portal HT
   Classically they are situated at 3, 7 & 11 o’clock when the surgeon is looking at the patient in
    the lithotomy position = left lateral, right anterior & right posterior positions

What are the clinical features ?

   Intermittent, bright red bleeding after defaecation – on toilet paper or dripping into bowl
   Palpable lump after defaecation
   Perianal discomfort & pruritus
   PR mucus discharge
    Uncomplicated piles do not cause pain – but thrombosis/strangulation cause severe pain

How are haemorrhoids described & graded ?

 External haemorrhoids : develop in inferior haemorrhoidal plexus  located below dentate
   line (skin tags)
 Internal haemorrhoids : dilation of superior haemorrhoidal plexus, above dentate line

Degree of internal haemorrhoids
 10 haemorrhoids : small haemorrhoids that bleed, but remain in the rectum
 20 haemorrhoids : prolapse on defaecation (or Valsalva) & retract spontaneously
 30 haemorrhoids : prolapse on defaecation (or Valsalva), but require manual replacement
 40 haemorrhoids : prolapse from anus & despite attempts to replace them fall out again

                                                                            Common sites :
                                                                            3, 7 & 11 O‟clock

In a 55 yo patient with PR bleeding & obvious haemorrhoids, what else must be excluded ?

   Haemorrhoids & CRC may co-exist in the same patient
   Any doubt, especially in pt‟s > 50, altered bowel habit or sigmoidoscopic appearances of
    altered blood present  colonoscopy is essential
   Haemorrhoids usually don‟t cause anaemia – look for CRC !!

What does haemorrhoid banding do ?

   Used to treat 20 & 30 internal haemorrhoids
   Performed thru a lubricated proctoscope
   Haemorrhoidal tissues are drawn by a pair of forceps into the barrel of a special band ligator –
    upon release of the trigger, the elastic band is released to encompass the haemorrhoidal tissue
    at the level of the anorectal ring
   This draws the prolapsing haemorrhoid back up into the anal canal & may lead to its
    destruction (via necrosis)
   Complc‟n : haemorrhage, sepsis, pain (due to thrombosis)

What are the other treatment options for haemorrhoids ?

 Dietary fibre, eg psyllium
 Local hydrocortisone & analgesia – topical or suppositories
 If symptoms persist for 4-6 weeks, surgery is recommended

 Injection sclerotherapy (eg 5% phenol in almond or arachis oil) by proctoscopy
 Infrared photocoagulation
 Haemorrhoidectomy – suture apex of haemorrhoid & excise – complications incl
   haemorrhage, infection, anal stenosis & faecal incontinence

What are the complications of hemorrhoids?

- bleeding
- mucus discharge/itchiness
- thrombosis
- strangulation
- septicemia
- pilephlebitis

Rectal prolapse

- thin, asthenic women with poor pelvic floor musculature
Delorme operation
Well‟s op‟n
Tietz‟s procedure

Incisional hernia

Identify from this picture (Browse p338). What is an incisional hernia ?

   Iatrogenic: after 10% of abdo sxs
   A protrusion of the peritoneum (the sac) & abdominal contents into the subcutaneous plane
    thru a defect at the site of a scar following an abdominal operation
   Patients present with an obvious bulge & often c/o nagging discomfort
   Signs – reducible lump with an expansile cough impulse underneath an old scar – tend to be
    accentuated by tensing the recti

What are the risk factors & predisposing factors ?

   Occurs in fibrous scars that become weakened
   Surgical technique & post-op care : factors incl
       o Incision – angulated incisions, incision parallel to previous incisions, T- & V-shaped
           incisions, location (midline wound > paramedian wound; upper > lower wound)
       o Ragged or devitalised tissue left in wounds (predisposes to infection)
       o Strength & type of suture material – sutures should be non-absorbable or should last
           9-12 months until healing process is complete
       o Wound infection – most common cause
   Patient characteristics
       o ↑ age
       o Obesity – causes ↑ intra-abdominal pressure & ↓ muscle tone
       o General factors – corticosteroids, DM, malnutrition
       o Local factors – foreign body, haematoma, movement

How do you treat an incisional hernia ?

   All incisional hernias should be surgically repaired – they ↑ in size over time & ↑ risk of
    complications (irreducibility, obstruction & strangulation)
   Pre-operative weight reduction, physiotherapy & smoking cessation is recommended
   Repair technique
        1. Define the sac & neck – if hernia is irreducible, open sac & mobilise contents by
            dissection. Omentum within the sac should be excised.
        2. If edges of defect can be apposed it can be closed directly with strong non-absorbable
        3. If edges of defect cannot be brought together, the defect is covered by placing a
            prosthetic mesh either beneath the muscle layer in the extraperitoneal plane or on top
            of the muscle layer in the subcutaneous plane.
        4. Prophylactic AB‟s are used & wound is drained with suction drain for short time.

List > 3 differentials for circular lesions in the liver at USS

   Metastases
   HCC (multi-focal)
   Nodular regenerative hyperplasia
   Lymphoma
   Sarcoidosis
   Hydatid cysts
   Multiple abscesses
   Fatty infiltration
   Cirrhotic (regenerating nodules)

CBD obstruction

Describe the anatomic & metabolic pathways by which bilirubin is conveyed from its site of
production until its excretion from the body.

   RBC degradation occurs in reticuloendothelial cells (macrophages) in the spleen (also liver
    & bone marrow)  old or defective RBCs removed from circulation
   The globin portion is degraded to ‟s which are recycled
   Haem ring ( 250mg/day) is opened via haem oxygenase into linear biliverdin (green)
        o By products : carbon monoxide & Fe3+
   Biliverdin converted to bilirubin (yellow) by biliverdin reductase
        o Lipophilic  bound to albumin in plasma (unconjugated – cannot enter urine)
        o Excess unconjugated bilirubin pools in sclera, fat & skin

   Unconjugated bilirubin taken up by hepatocytes from plasma ( 40% refluxes back into
    blood) [NB “free” bilirubin w/o albumin is neurotoxic]
   Bilirubin binds to glutathione S-transferase & Z-protein
   Conjugated with glucuronide twice in ER, via bilirubin UDP-glucuronyl transferase to
    bilirubin diglucuronide (conjugated bilirubin)  water soluble

   Conjugated bilirubin excreted into biliary canaliculi & flows with bile into duodenum &
    colon (some bile reabsorbed in terminal ileum)
   Bacterial action in colon deconjugates & modifies bile  colourless urobilinogen &
    stercobilinogen, then yellow urobilin & dark red-brown stercobilin (gives stool its colour)
    & excreted in faeces
   Some urobilinogen (water soluble) reabsorbed from intestine into portal blood
        o Taken up by liver & re-excreted, or
        o Excreted by kidneys into urine (small amt)  slowly becomes urobilin on exposure
           to air
What imaging investigation would you use to confirm extrahepatic biliary obstruction ?
What are the advantages of this ?

   Ultrasound is the modality of choice – can easily diagnose acute cholecystitis, gallstones &
    other causes of RUQ pain unrelated to the GB
   US can demonstrate :
            o Dilated extrahepatic & intrahepatic bile ducts suggestive of obstruction
            o Gallbladder stones
            o CBD stones (33% of time – often obscured by duodenal gas)
            o Exclude cholangitis & cholecystitis (wall thickening > 3mm)
   Advantages
            o Non-invasive & relatively painless
            o Quick & cheap
            o No ionising radiation
   ERCP or PTC can be used to assess degree of dilatation & site of stone/s & may also allow
    stone removal
   Other Ix : FBC, E/LFTs, blood cultures

List ≥ 3 important causes of extrahepatic biliary obstruction.

   Choledocholithiasis
   Tumour : pancreatic head, ampulla, bile duct (cholangioCa) or duodenum
   Strictures : post-surgical, post-inflammatory
   Pancreatitis or pancreatic pseudocyst
   Lymphadenopathy
   Ampulla of Vater dysfunction
   Parasites

Identify the picture – what is it & where is it inserted ?

   T-tube – inserted into CBD following choledochotomy – T part in CBD, long part goes out
    thru the skin
Give 3 reasons for placing a T-tube in the CBD ?

   To avoid leakage from choledochotomy
   To enable later (7-10 day) T-tube cholangiogram to ensure no residual stones in CBD or
    hepatic radicles
   Post-CBD trauma to prevent bile leakage

When would you remove T-tube ? What precautions would you take before removing it ?

   Usually removed after 7-10 days post-op
   Patient must be in a satisfactory state (eg not toxic, not too unwell)
   Bile drainage must be clear & non-infected
   Perform T-tube cholangiogram prior to removing to ensure no residual stones


What is Charcot’s triad ? What is Reynold’s pentad ?

   Charcot’s triad indicates cholangitis
          o RUQ pain (& tenderness to palpation)
          o Jaundice
          o Fever/rigors – usually intermittent & occurring every few days with exacerbation
               of pain & jaundice (ball-valve mechanism)
   Reynold’s pentad : severe cholangitis may cause septicaemia resulting in
          o Altered mental status
          o Hypotension/shock (due to vomiting & dehydration)

What is the diagnosis ? What may be the underlying cause ?

   Cholangitis
Causes of cholangitis
 Choledocholithiasis – most common cause
 Stricture
 Extrinsic compression – tumours, pancreatic pseudocyst, pancreatitis
 Instrumentation of bile ducts, eg PTC, ERCP
 Biliary stent

What is the pathophysiology of this sign ?

   Blockage of CBD  build-up of pressure within the biliary tree (RUQ pain) & obstructive
    jaundice  overgrowth of gut flora (retrograde via sphincter of Oddi)  may lead to
    septicaemia and septic shock  fever, tachycardia, hypotension

Laparoscopic cholecystectomy

What do you tell the patient pre-op about the risks ?

   “Key hole” surgery – involves ≈ 4 small incisions 0.5-2.5cm long made in the abdomen used
    to insert the laparoscope & other devices via ports
   Benefits – in most cases will relieve pain & prevent complications of gallstones
   Risks of not having surgery – symptoms continue, potential for complications & sequelae
   May need to convert to open cholecystectomy if not possible to do lap approach (5-10%
    conversion rate)
   May need to insert T-tube or wound drain

General risks/complications
 Reaction to anaesthetic &/or contrast
 Wound haematoma
 Infection
 Atelectasis +/- pneumonia
 Incisional hernia

Specific risks/complications
 Mortality < 1 in 1000
 Gas embolus – heart, lungs or brain
 Collection – bile (biloma), blood or pus
 Bile leaks – caused by injury to CBD, R hepatic duct or cystic duct – causes external biliary
 Bile duct stricture
 Damage to vasculature (eg R hepatic artery) causing haemorrhage
 Damage to nearby structures – liver, colon, porta hepatis, diaphragm
 Adhesions
 Potential for missed stones – may need ERCP or further operation
   „Post-cholecystectomy syndrome‟

What length of hospital stay is necessary ? How long till feeling better ?

   Pain, nausea & vomiting may occur
   May need T-tube in-situ
   Usually ambulatory within 24 hrs
   May need narcotics in first 24 hrs, then oral analgesics (panadeine) for ~ 4-5 days
   NBM initially (& IV fluids), then sips of water (~ 24 hours, due to ileus), then normal diet
   Usually discharged after 1-2 days (compared with 5 days for an open procedure) – avoid
    strenuous exercise & heavy lifting for > 2 weeks
   Recovery time frames
        o Drive after ≈ 7 days
        o Return to normal activity after ~ 2 weeks (c/w 4 weeks for open procedure)

Acute pancreatitis

What are the above sign’s called ?

Left = Cullen‟s sign ; Right = Grey-Turner‟s sign

What is the underlying pathogenesis & cause ?

   Haemorrhagic acute pancreatitis – bleeding into parenchyma & retroperitoneal structures with
    extensive pancreatic necrosis – indicates severe pancreatitis has been present for several days
   Cullen’s sign : bluish discolouration of the periumbilical area – caused by retroperitoneal
    haemorrhage tracking around to the anterior abdominal wall thru fascial planes (think –
    cUllen‟s sign = Umbilicus)
   Grey-Turners sign : ecchymosis or discolouration of the flank – caused by retroperitoneal
    haemorrhage (think – Grey-Turner = turn on side to see it)
   Fox’s sign : ecchymosis of the inguinal ligament
List ≥ 6 causes of pancreatitis

 Gallstones**
 Ethanol**
 Trauma
 Steroids
 Mumps, Mycoplasma
 Autoimmune : PAN, SLE
 Scorpion stings
 Hyperlipidemia/ Hypercalcemia
 Drugs, eg azathioprine, didanosine

What are the other causes of this sign ?

   Other causes of retroperitoneal bleeding may produce these signs – ruptured AAA,
    malignancy, coagulopathy

What are the other clinical features of acute pancreatitis ?

 Severe constant epigastric pain that often radiates to the back
         o Acute onset – builds up over 15-60 min
 Nausea & vomiting

 Sepsis : tachycardia, hypotension, pyrexia, jaundice
 Epigastric tenderness (or diffuse abdominal tenderness)
 ↓ bowel sounds due to paralytic ileus
 Large pseudocyst  constant abdo pain, palpable abdo mass
 Severe  hypoxaemia, hypovolaemic shock

What is the biochemical investigation of choice ?

   Serum amylase > 1000U/L (also do serum lipase FBC, E/LFTs, glucose, calcium, ABGs,
    USS, plain CXR & AXR)
   Damage to pancreas  release of amylase into bloodstream  rapid rise in serum level (it is
    also rapidly cleared within 24hrs)

What criteria are used to assess the severity of pancreatitis ?

   Ranson‟s criteria (2 or more signs assoc/ w/ ↑ incidence of haemorrhagic pancreatitis &
   Imrie (Glasgow) scores
   The more criteria present, the more severe the illness

List ≥ 2 criteria which indicate a worser prognosis.

   On admission : GA LAW
            o Glucose > 10 mmol/l
            o Age > 55 yrs
            o LDH > 600 U/L
            o AST >120 U/L
            o WCC > 16,000
   Within 48 hours : Calvin & HOBBS
            o Calcium < 2 mmol
            o Haematocrit fall >10%
            o Oxygen - pO2 < 60 mmHg
            o Base deficit > 4
            o BUN rise >0.9 mmol/L
            o Sequestration of fluid > 6L
   ↑ number of positive criteria  ↑ mortality (7-8 criteria = 100% mortality)
   In addition, serial assessment of CRP is a useful indicator of progress & severity

What is the management of pancreatitis ?

Medical management
 Supportive therapy & intensive monitoring (T/P/R, BP, O2 sats, urine output) : often in ICU
 Regular assessment of U&Es, Ca2+, blood sugar & LFTs – correct abnormalities
 IV fluid resuscitation with both colloid & crystalloid
 Correct hypoxia  O2 &/or ETT
 Opioid analgesia (meperidine, not morphine)
 Nutrition – pancreatitis is hypercatabolic – often require NG tube &/or TPN
 Antibiotic prophylaxis (eg imipenem, cefuroxime)
 H2-blocker

Surgical management
 Complications such as pseudocyst necessitate surgical management
 Drainage essential for pseudocyst – may be percutaneous, endoscopic or surgical (drainage
   into stomach/duodenum – cystgastrostomy)
 ERCP – performed to clear CBD of gallstones if this is the cause
 Laproscopic cholecystectomy – if caused by gallstones to prevent recurrence


Peripheral vascular disease
What are the major RF’s for atherosclerosis ?

   Non-modifiable RF‟s
           o ↑ age & sex (♂ & postmenopausal ♀)
           o FHx/genetics
           o PHx IHD/CVA
   Modifiable RF‟s :
           o Hypercholesterolaemia & hyperlipidaemia
           o Smoking
           o Hypertension
           o Diabetes mellitus
           o Obesity, physical inactivity & poor diet
           o Hyperhomocysteinaemia, excess alcohol, stress/personality, haemostatic factors

In what ways can lower limb occlusive disease present ?

   Asymptomatic
   Intermittent claudication
   Rest pain (critical limb ischaemia)
   Acute occlusion

What are the common sites of involvement ?

   Superficial femoral artery (SFA) – most common site of arterial occlusion is in the adductor
    (Hunter‟s) canal, 15cm below the inguinal ligament
           o  Calf pain
   Aorto-iliac region
           o  Buttock &/or thigh &/or calf pain
   Popliteal artery

Describe differences b/w intermittent claudication & rest pain ? How do you assess it ?

Intermittent claudication
 Ischaemic pain of the leg that is precipitated by ambulation & relieved by rest
           o Typically a cramp-like pain & varies from an ache to acute severe pain
           o Cyclical pattern of exacerbation & resolution due to progression of disease &
                subsequent dev‟t of collaterals
 Location of pain depends on arteries affected
           o SFA (most common) = calf pain
           o Iliac A = calf, thigh &/or buttock pain
 Other useful information
           o Claudication distance – distance travelled before pain occurs – usually reasonably
                constant, but will be reduced when walking uphill
           o Relief – pain will be relieved by rest, often after a reasonably constant time-period
           o Duration of symptoms
           o Severity of symptoms – does the claudication force patient to stop walking ?
   5% limb loss at 5 years
   DDx : neurogenic claudication, sciatica, OA

Rest pain (critical limb ischaemia)
 Pain in the foot or toes that arises at rest
 Classically occurs at night – will wake from sleep & requires opiate analgesia to enable sleep
 Resolved by hanging the foot over the side of bed or standing/walking – gravity affords some
   extra flow to the ischaemic areas
 Ulceration & gangrene may be present
  Indicates threatened loss of limb (critical limb ischaemia) – more than 50% of patients will
   have amputation of the limb at some point

What are the signs of lower limb ischaemia (see Browse p170 – describe the features seen in
this foot ? what is the underlying pathology ?)

 Thin, shiny, atrophic & pale skin
 Loss of hair
 Muscle atrophy
 Dry, thin & brittle nails
 Ulceration (usually on toes/feet), infection &/or gangrene
 Venous „guttering‟ – veins empty due to inadequate circulation

 ↓ skin temperature
 Capillary return (> 3 seconds is abnormal)
 ↓ or absent peripheral pulses – femoral, popliteal, dorsalis pedis & posterior tibial pulses
 Occasionally can detect palpable collateral vessels (eg medial side of knee joint)
 Buerger’s sign – elevation of leg causes pallor – on dependency affected limb will regain its
   colour more slowly than the healthy limb, followed by a rubor due to reactive hyperaemia

 Auscultate the main vessels – systolic bruit indicates stenosis at that level or higher up

Ankle-brachial index (ABI) = ankle pressure/systolic pressure in the arm
- estimates extent of stenosis
<.8 – claudication
<.4 – rest pain

Gangrene    (Browse p171)
 Gangrene : necrosis due to obstruction, loss, or diminution of blood supply
 Dry gangrene : dry necrosis of tissue without signs of infection („mummified tissue‟)
 Wet gangrene : moist necrotic tissue with signs of infection
 May be a clear demarcation b/w dead & living tissue
   Dead tissue is brown or black & gradually contracts into a crinkled, withered, hard mass –
    infection causes the dead tissue to become soft & boggy, with pus at line of demarcation
   Extent of necrosis varies from a black patch to extensive gangrene of the foot – it starts
    distally on the toes & extends proximally
   Dead part is senseless & not painful

 Ischaemic ulceration usually begins in a pressure area, usually on the foot
 Dead tissue is usually present & granulation tissue is absent

What are suitable investigations ?

Assess extent of PVD
 ABI – ratio of systolic BP at ankle to systolic BP at arm : Normal ≥ 1, claudication  0.6-0.9,
   rest pain 0.3-0.6
 Duplex USS with colour Doppler – non-invasive
 DSA= ANGIOGRAM – gold standard but invasive

Look for a cause
 FBC, U&E, lipids, glucose, syphilis serology

What would you warn a patient about to undergo DSA about to obtain consent ?

Pre-procedure preparation
 Ask about allergies (esp iodine) & previous exposures to x-ray contrast
 Determine medications & past history
 Check & document pulses prior to puncture
 Laboratory studies : PT, APTT, U&Es, FBC
 Withhold aspirin, warfarin & metformin prior to procedure
 Correct coagulopathies using FFP

Required preparation
 Shave & prep groin
 Clear liquids ≈ 8 hours prior to procedure
 IV fluids to maintain hydration

 Arterial access via the Seldinger technique (Radiology recall p209), commonly via the
   common femoral artery (below inguinal ligament) or brachial artery
 Guidewire is advanced into vessel under II guidance – catheter is then passed over wire into
   vessel lumen, and guidewire is then removed
 Catheter is then manipulated to desired location & contrast injected

Post-procedure care
   Apply firm manual compression for > 15 minutes
   Patient must lie flat with limb straight for 6-8 hours
   Evaluate distal pulses & regular observations (cardio, neuro, puncture site)

 Mortality < 0.05%
 Contrast
      o Anaphylactoid reaction
      o Nephrotoxicity
 Vascular access
      o Haemorrhage or haematoma (5%)
      o Pseudoaneurysm
      o AV fistula
      o Infection
      o Nerve damage
 Distal vasculature
      o Thrombosis
      o Embolism
      o Dissection
      o Perforation
 Potential interventions
      o Surgical
      o Worst case scenario is amputation

Interpreting femoral angiogram


1. Aortic bifurcation
2. Common Iliac Artery
3. Internal Iliac Artery
4. External Iliac Artery

What are the management options ?

 Pentoxifylline (↓ blood viscosity)
 Aspirin or ticlodipine
 Cessation of smoking & treat other RF‟s
 Exercise

 Ischaemic rest pain necessitates urgent surgical intervention
 Angioplasty : radiologically-guided balloon angioplasty +/- stent placement is effective in
   patients who have a short segment of stenosis (usually < 3cm) – most patients have long or
   multiple segments of SFA disease
 Endarterectomy : diseased intima & media are „cored out‟
 Bypass graft : a graft is made to bypass the diseased segments of artery & improve distal
   flow, provided there is minimal arterial disease in the distal vessels – graft can be a synthetic
   PTFE tube graft, dacron graft or a vein graft (veins have a longer patency rate)
       o Fem-pop bypass : bypass SFA occlusion with graft from femoral artery to popliteal
           artery above the knee
       o Fem-distal bypass : bypass from femoral artery to a distal artery (peroneal artery,
           anterior tibial artery or posterior tibial artery)

Acute limb ischaemia

List ≥ 5 causes of acute limb ischaemia

   Embolisation
       o Cardiac – mural thrombi (AF, MI), vegetations (endocarditis)
       o Aneurysms (aorta, femoral or popliteal)
       o Atheroemboli
   Acute thrombosis of an atheromatous lesion
   Vascular trauma – arterial transection, AV fistula, intimal dissection

What are the clinical features

Sudden onset of :
 Pain
 Pallor – fixed mottling heralds the onset of gangrene
 Pulselessness
 Perishing cold (others say poikilothermia or polar)
 Paraesthesia & sensory disturbances – impending irreversible ischaemia
 Paralysis – muscle rigidity implies that the damage is irreversible

List the immediate emergency measures for the treatment of a patient with acute limb
ischaemia. List the initial baseline investigation that you would undertake.
   Anticoagulate with IV heparin – bolus followed by constant infusion – prevents further
   Angiogram
   Also do ECG & echo looking for embolic source

 Unless blood flow is restored within 4-6 hours, irreversible tissue damage will occur, leading
to possible amputation.

Definitive management
 Surgical embolectomy or thrombectomy via arterial cutdown & Fogarty balloon catheter
 Thrombolysis (streptokinase, urokinase, t-PA) may be infused locally to lyse a thrombus

Leg ulcers

Describe the ulcer seen in the photo

Probably a venous ulcer
    Edge is sloping & made of new epithelium
    Base is clean & pink
    Surrounding tissue looks healthy
    Venous ulcer

 Remember SEBS – site/size/shape/severity, edge, base, surrounding tissue/LNs

 Site/position & its anatomic relations

                                               Venous – medial side of lower leg
                                               Arterial – pressure areas of dorsum of feet,
                                               lateral side of lower leg & tips of toes
                                               Neuropathic – weight-bearing areas
                                               Neoplastic – sun-exposed areas

 Size, shape, colour & tenderness

 Edge

                                           Indicates rapid death & minimal healing

                                           Rapid growth of tissue at edge of ulcer = carcinoma

                                           Slow growth of tissue at edge of ulcer (rodent ulcer)

“Sloping” edges indicates healing ( not arterial or neuropathic)

 Base/floor
   Usually consists of slough or granulation tissue
   Contents of floor
       o Ischaemic : dry or extended base or necrotic eschar
       o Venous : superficial with fibrinous exudate & ooze
   Colour :
       o Black = necrosis
       o Yellow = slough
       o Red = granulation
       o Pink = epithelium

 Depth
   Record in millimetres & anatomically (described structures penetrated)

 Discharge
   Quantity & type of discharge – serous, sanguinous or purulent

 Surrounding skin/tissue
   Colour – local blood supply, inflammation
   Sensitivity
   Pulses
   Look for evidence of previous ulcers

 Regional lymph nodes
   May be enlarged &/or tender due to secondary infection or neoplasia

What are the causes of leg ulcers ?

Venous ulcers (75%)                  Varicose veins
                                     Post-thrombophlebitis
Arterial ulcers                      Ischaemic – diabetes, artherosclerosis, embolism
                                     Vasculitic – Buerger‟s disease, SLE, RA, scleroderma
Neuropathic ulcers                   Neuropathic (trophic) – diabetes, alcoholism, syphilis
                                     Spinal cord lesion – spina bifida, tabes dorsalis,
Traumatic                            Pressure sores (decubitus)
                                     Ill-fitting footwear
                                     Traumatic lesions
                                     Self-inflicted
Neoplastic                           SCC
                                     BCC
                                     Malignant melanoma
                                     Kaposi‟s sarcoma
Haematological                       Spherocytosis
                                     Sickle cell anaemia
Infective                            Tropical ulcer
                                     Mycobacteria
                                     Post-cellulitis
                                     Chronic infected sinus
Miscellaneous                        Pyoderma gangrenosum
                                     Spider/insect bites

What questions would you ask the patient to determine a cause ?

   Onset & duration of ulcer
   Has ulcer changed since it first appeared ?
   What do they think caused the ulcer ? – may note precipitating injury
   Pain – ischaemic ulcers are painful, venous ulcers have minimal pain, neuropathic ulcers
   Bleeding/discharge
   PHx :
        o Venous – DVT or PE, varicose veins, previous surgery on leg
        o Arterial – intermittent claudication & rest pain; cardiovascular disease
        o Other – diabetes, RA, vasculitis, IBD, chronic skin ulcers
   Medications : β-blockers, ergotamine, corticosteroids, NSAIDs, nifedipine
   Social Hx : tobacco, alcohol
       How do you differentiate arterial, venous, neuropathic/trophic & pressure ulcers ?

                        Venous ulcers                Ischaemic ulcers               Neuropathic ulcers            Pressure sores
History                 Chronic venous disease       Intermittent claudication or   Walking on cotton wool        Bed bound, immobilised
                                                     rest pain                      Diabetes, et-OH, SpC
                                                     IHD or CVD risk factors
Site                    Medial side of lower leg     Pressure areas, esp dorsum     Pressure areas, esp plantar   Bony prominences – heels,
                                                     of foot & tips toes            foot (ball) & heel            malleoli, sacrum, hips
Pain                    Nil to mild                  Very painful                   Painless                      Painful
Ulcer features          Superficial                  Often very deep                Deep & penetrating
                        Ragged or sloping edge       Punched-out edge               Punched-out edge              Undermined at edges
                        Base of granulation tissue   Base of grey-yellow slough     Prone to 20 infection         Necrotic slough & granul‟n
                        Seropurulent ooze            Usually dry, v. little blood
                        Minimal healing              No healing
Rest of limb
 Sensation             Present                      Present, painful               Impaired or absent            May be impaired
 Pulses                Normal                       Absent or ↓↓; ↓ ABI            Bounding pulses               May be impaired
 Temperature           May be hot & tender          Cold                           Warm                          Variable
 Oedema                Usually present              Usually absent                 Absent                        Variable
Other features          Varicose veins               Thin, dry, pale, shiny skin    High arch & clawing of toes   Preceded by erythema at
                        Lipodermatosclerosis         Loss of hair                   Trophic skin lesions          pressure site
                        Stasis eczema                Fissuring of nails             Charcot‟s joints
                        Atrophie blanche                                            Neuro exam
Diabetic foot

What is the underlying pathophysiology & clinical sequelae ?

   Influencing factors
        o Atherosclerosis affecting large vessels
        o Microangiopathy (thickening of BM in arterioles & capillaries)
        o Neuropathy – sensory, motor & autonomic
        o Increased risk of infection (glucose-rich environment for bacteria)
   Resultant lesions
        o Food ulcers
        o Gangrene
        o Infections – cellulitis, abscess & osteomyelitis
        o Charcot joints – painless neuropathic arthropathy
   Peripheral neuropathy  lack of sensation  increased mechanical stress under metatarsal
    heads & heels  intermittent or continuous ischaemia  pressure ulceration  angiopathy
    & intercurrent infection interferes with the healing response

Ischaemia vs neuropathy

                         Ischaemia                              Neuropathy
Symptoms                 Claudication                           Usually painless
                         Rest pain                              Sometimes painful neuropathy
Inspection               Dependent rubor                        High arch
                         Trophic changes                        Clawing of toes
                                                                No trophic changes
Palpation                Cold                                   Warm (ANS neuropathy)
                         Pulseless                              Bounding pulses
Ulceration               Painful, punched-out ulcers            Painless, punched-out ulcers
                         Dorsum of foot & toes                  Plantar foot & heel


List ≥ 4 risk factors for DVT.

   Prior DVT/PE
   Thrombophilia
   Malignancy
   Immobility
   Major medical illness
   Age> 60yrs
   Recent fracture or major surgery (orthopaedic, pelvic, general, urologic) – highest risk is hip
    & knee surgery
   Pregnancy, OCP/HRT
List ≥ 4 methods of preventing DVT formation ?

   Stop OCP > 6 weeks pre-op
   Early mobilisation post-op (even if bed bound do leg exercises)
   Aspirin for 3 weeks
   Mechanical support (aims to ↓ stasis)
           o Elevate foot of bed
           o Graduated compression stockings
           o SCD (sequential compression device)
           o AV foot impulses
   Anti-coagulants : SC Heparin, starting 2hrs pre-op & continuing for 7-10 days
           o High MW, eg 5000U/12hr SC – want INR of 2-3 to prevent DVT
           o Low MW, eg enoxaparin, clexane 20mg/24hr SC
           o Warfarin in patients undergoing major joint replacement

List ≥ 6 clinical features of DVT/

   Swelling of the calf & leg (unilateral oedema) +/- pitting oedema
   Tenderness (squeeze calf to determine)
   Homan‟s sign : pain in calf on dorsiflexion of foot
   Warmth & erythema
   Dilated superficial veins (may be acting as collaterals)
   Phlegmasia cerulea dolens (painful, swollen, cyanotic leg)
   Fever & tachycardia
   Examine chest for signs of PE/MI etc (eg pleural effusion, rub, pulmonary HT)
   Examine abdomen/pelvis (for tumour/nodes, pregnancy or ascites)

 Duplex ultrasound (95% accuracy) – only 50% DVT detected clinically

How can heparin be administered ? What monitoring is required ?

   Heparin can be administered IV or SC
   It can be unfractionated or low MW (eg enoxaparin)
   It is essential to monitor the APTT (intrinsic pathway, HI) if using unfractionated heparin

Treatment of established DVT
 Unfractionated heparin – 5000-10000U of heparin IV as a „loading‟ dose, followed by a
   continuous IV infusion of heparin at 1000-2000U/hr
          o Check clotting at 6 hours & adjust infusion to maintain APTT ≈ 1.5-2.5x’s
              normal – thereafter APTT is estimated daily
          o Continue heparin for 5-10 days
          o Avoid during pregnancy & active PUD
          o Complication = haemorrhage
   Low MW heparin (enoxaparin, SC) – treatment of choice, safe, no need for monitoring (but
          o 1mg/kg twice daily for > 5 days

Varicose veins

How do you test the superficial veins ?

 Look for visible superficial veins – note their site, size & course (draw diagram)
       o Medial – tortuous, dilated branches of great saphenous vein
       o Posterior calf – varicosities of short saphenous vein
 Venous stars – patches consisting of minute veins radiating from a single feeding vein
 Oedema – compare size of legs at ankle level
 Signs of venous stasis (esp lower medial 1/3 of leg) : induration, pigmentation, eczema &

 Feel along course of veins & feel the tension in the veins – hard leg veins suggest
   thrombosis, while tenderness indicates thrombophlebitis
 Harvey’s test – to elicit direction of flow in a vein – place 2 fingers on the vein, sliding one
   finger along the vein to empty it & then releasing one finger & watching it to see which way
   the empty segment fills
 Test for transmission of a cough impulse at the sapheno-femoral & sapheno-popliteal
   junctions – a strong cough impulse indicates that the valves in the SC veins are incompetent
 Palpate skin of lower leg for pitting oedema & thickening/tenderness of SC tissues

Tourniquet tests        (Browse p182)
 Designed to reveal the presence & site of incompetent valves
 Tourniquet test :
   1. Lie pt down & elevate leg to 900 until all blood has drained from the superficial veins
   2. Place a rubber tourniquet around the upper 1/3 of the thigh, tight enough to occlude the
        superficial veins
   3. Get pt to stand, while keeping tourniquet in place – if the superficial veins above the
        tourniquet fill up but those below it stay collapsed, there must be an incompetent
        communicating vein above the tourniquet. If the veins below the tourniquet fill rapidly
        there must be an incompetent communicating vein below it.
   4. It is possible to move one tourniquet progressively down the leg & so define the segment
        of the limb containing the incompetent communicating vein
 Trendelenburg test : Compress the long saphenous-femoral vein junction with direct digital
   pressure (instead of using a tourniquet) – get pt to stand & see if this prevents retrograde
 Perthes test : repeat above, but when pt stands get them to stand on tip-toes a few times –
   veins will become less tense if perforating calf veins are patent w/ incompetent valves.

Percussion – “tap test”
   Normal mapping – one hand is placed gently on a vein, while the other hand below
    compresses/percusses the vein sharply – if a pressure wave is felt in the upper hand, the 2
    parts of the vein are connected
   Incompetence – place the fingers of one hand on the lower limit of the visible veins & tap
    them at their upper limit – a palpable percussion impulse indicates a dilated incompetent vein
    b/w the sites of palpation & percussion.

 Listen over clusters of veins for AV fistulas

What are the causes of varicose veins ?

   Normally blood only flows from superficial to deep veins via competent valves in the
    perforator veins
   Varicose veins are caused by incompetence of the valves of the perforator veins – muscle
    pump forces blood into the superficial system, causing the superficial veins to become
    engorged & dilated (varicosities)

 Idiopathic – most common cause
 Pregnancy – hormones dilate veins causing incompetence of the valvular mechanisms; also
    get impaired venous return
 Prolonged standing causing venous hypertension
 Congenitally weak or absent valves (eg Klippel-Trelaunay syndrome)
 Thrombosis in the superficial or deep system (SVT/DVT) or the perforators – DVT causes
    blood to return to superficial veins & recanalisation damages valves (post-thrombotic
 Pelvic mass (fibroids, malignancy) – back pressure from venous obstruction
 AV fistula

 Varicose dilation of veins leads to venous stasis, congestion, oedema & thrombosis  ↓
   capillary diffusion, dermatitis & ulcerations
 ↑ hydrostatic pressure in SC venous capillaries  Filtration of water & solutes & ↑
   permeability  Serum containing fibrin & other proteins leak into interstitial space 
   Lymphatics fail to remove these large, osmotically active proteins  Proteins trap water in
   interstitial space  oedema  fibrin + oedema creates diffusion barrier, reducing normal
   exchange of O2 & nutrients  if ↑ venous pressure persists, get fibrosis, skin breakdown &
   chronic ulceration

How would you investigate varicose veins ?

   Directional Doppler US : confirms presence of saphenofemoral & short saphenous
    incompetence by detecting reflux on release of manual compression of the calf. Also
    confirms deep valvular incompetence by demonstrating reflux in the popliteal vein despite
    compression of the short saphenous vein.
   Duplex Doppler US** : accurately assess sites of deep & superficial venous reflux
   Venography : demonstrates site of calf & thigh incompetent perforators & can confirm or
    exclude co-existing occlusion of the deep veins
   Ambulatory venous pressures : needle measurement device in a vein on the foot while
    tourniquet controls the superficial veins – confirms deep venous incompetence & venous


Aneurysm = focal dilation of an artery to >1.5 of its normal diameter
MC sites
- infrarenal aorta (no vasa vasovasorum)
- iliac arteries
- popliteal

               Tangential wall stress = P * r/t

P= intraluminal pressure
r = radius of vessel
t = thickness of vessel wall

High TWS = increased risk of rupture

What are the causes/mechanisms of AAA ? List ≥ 4

   Atherosclerotic (95%)
           o Atherosclerosis  medial destruction  arterial wall thinning & weakening
           o Complications – rupture, impingement on adjacent structures, occlusion of vessel,
               embolism, fistula (eg aortoenteric fistula)
   Congenital – weakness of wall due to CT disorders
           o Marfan‟s syndrome
           o Ehlers-Danlos syndrome
           o Behcet‟s disease
   Inflammatory
           o Mycotic – bacterial infection/suppuration weakens arterial wall – causes saccular
               aneurysm – RF‟s are bacterial endocarditis, IVDU, sepsis & immunocompromise
           o Syphilitic – now uncommon, due to 30 syphilis : endarteritis of the vasa vasorum
                ischaemia  medial scarring & medial destruction  intimal wrinkling &
               predisposes to florid atheroma formation

What triad indicates emergent surgery for ruptured AAA ?

   Abdominal pain
   Pulsatile abdominal mass
   Hypotension
 USS, followed by CT

What are the RF’s for rupture ? At what size should AAA be treated ?

   Size : < 5cm = 4%/yr; 5-7cm = 7%/yr; > 7cm = 20%/yr
            o Larger aneurysms grow faster due to Laplace‟s law
            o AAA > 5cm indicates need for surgical repair to prevent rupture (monitor
               aneurysms < 5cm with USS)
   Type : fusiform more likely to rupture than saccular
   Co-morbidities : hypertension, smoking, COPD
   Rupture has 80-90% mortality

What may cause ↓ UO in a man post-AAA repair ?

   Pre-renal = inadequate blood perfusing kidney
       o Inadequate fluids
       o Dehydration (burns, vomiting, diarrhoea, pancreatitis)
       o Hypotension
       o Pump failure : CCF, cardiogenic shock
       o Continued bleeding (hypovolaemic shock)
       o 3rd spacing
   Renal = kidney parenchyma dysfunction
       o Acute tubular necrosis
       o Nephrotoxic drugs (eg gentamicin, contrast agents)
       o Myoglobinuria (rhabdomyolysis)
   Post-renal = obstruction to outflow of urine from kidney
       o Foley catheter obstruction/blockage
       o Stone
       o Ureteral/urethral injury
       o BPH
       o Bladder dysfunction – medications, spinal anaesthesia

Carotid arterial disease (Cerebrovascular insufficiency)

   15% of CO goes to brain
   Cerebral vessels are auto-regulated
   ATH at carotid bifurcation is MCC of CVA

What is the significance of a carotid bruit ?

   A bruit may be heard on auscultation in the neck over the carotid vessels (angle of the jaw) or
    at the root of the neck = systolic
   Significance of bruit in an asymptomatic person (ie no TIAs or CVAs)
         o 1/3rd are caused by stenosis of the carotid or vertebral arteries
         o 1/3rd will radiate from a more distant site, eg aortic valve
       o 1/3rd are haemodynamically insignificant
   A bruit will not always be heard over a significant carotid stenosis

How should a carotid bruit be investigated ?

   Carotid Doppler USS – gives general location & degree of stenosis
   DSA is the gold standard, but is not always necessary
   Also check RF‟s

What is the management ? When is operation indicated ?

General measures
 Stop smoking
 Control hypertension, DM & hyperlipidaemia
 Antiplatelet drugs – aspirin or ticlodipine

Surgical intervention
 Operation performed if patient is symptomatic & the stenosis is > 70% - there is no agreed
   cut-off in the asymptomatic population
 A carotid endarterectomy is performed to removal the diseased intima & media (excise
   atheromatous plaque) from the ICA, often performed with a shunt in place
       o If bilateral CEA, perform left CEA first if right-handed (protect dominant hemisphere)
       o Complc‟n : death (1%), CVA (1-5%), intracranial bleed, MI (most common cause of
           death), haematoma, wound infection, hypotension/hypertension, thrombosis, vagus N
           injury (voice changes), CNXII injury (tongue deviation towards side of injury)


Breast lump

What is the triple assessment ? What does it involve ?

    1. Clinical examination of breasts & lump
    2. Radiological assessment – mammogram &/or ultrasound
    3. Pathological assessment – FNAC &/or core biopsy

   Achieves a 95-99% sensitivity in diagnosis of breast lumps
   When there is doubt and a preoperative diagnosis cannot be made, excision biopsy is required
    for palpable lesions or needle localisation biopsy for impalpable lesions

What is the DDx for a breast lump ?

   Fibroadenoma
   Fibrocystic change
   Mastitis
   Carcinoma
   Fat necrosis
   Abscess
   Radial scar

What are the clinical features of a malignant breast lump ? What causes the clinical
findings of Peau d’orange & Paget’s disease ?

   Breast lump (50% occur in the upper outer quadrant; must be > 1cm to be palpable)
            o Painless
            o Firm to hard (typically stony hard)
            o Irregular & indistinct edge („cancer‟ = crab)
            o Fixed (invasion thru muscle)
   Skin changes
            o Skin tethering – lump pulls on skin when moved beyond limit of the „string‟
            o Skin dimpling or retraction – local invasion of Cooper‟s ligaments with
               subsequent traction on ligaments pulls skin inwards
            o Skin discolouration (if tumour is close to skin surface) – erythema or yellow
            o Peau d’orange (orange peel skin) – dimpling of the skin – tumour blocks
               lymphatic channels in the fibrous septa, causing oedema of the overlying dermis
               b/w the openings of the hair follicles & sweat glands
            o Ulceration thru the skin – usually has an everted edge
   Nipple changes
            o Nipple retraction or inversion
            o Bloodstained nipple discharge
            o Nipple deviation, displacement or depression
            o Paget's disease – unilateral eczematous rash featuring red, encrusted & oozy skin,
               later progressing to nipple destruction & ulceration – due to infiltration of
               squamous epithelium by malignant cells – often there is an underlying lump
   Inflammatory cancer – hot, oedematous & red breast that does not settle on antibiotics – poor
    prognosis (assoc/ w/ widespread permeation of the sub-dermal lymphatics)
   Lymph node enlargement
            o Axillary & supraclavicular nodes are often enlarged
            o Metastases are usually hard & discrrete – may become matted together
            o May cause lymphoedema of the arm
   Metastases : bone pain, hepatomegaly, jaundice, SOB (lung mets)

Breast cancer management

What are the surgical management options for breast cancer ?

 Mastectomy is the definitive procedure for local surgical control – it is often combined with
  later breast reconstruction
 Simple mastectomy : removal of the entire breast & nipple, while the underlying muscles &
  adjacent LNs are left intact – today rarely used
   Radical (Halsted) mastectomy : removal of the breast & nipple, all axillary LNs & the
    pectoralis muscles – now only used for male breast Ca or Ca that has invaded the pec muscles
   Modified radical (Patey) mastectomy : removal of the breast & nipple, some axillary LNs
    (levels I & II – incontinuity clearance) & part of the pec minor – most common procedure

Breast conservation surgery (lumpectomy; segmental mastectomy)
 Has become standard procedure for most women undergoing breast surgery for cancer –
   predominantly for smaller tumours (stage I & stage II)
 Involves removal of the tumour together with a 1cm rim of normal breast tissue – often
   combined with some form of axillary clearance
 After histological examination, a 2nd excision or conversion to mastectomy may be necessary
   to achieve clear margins
 Increased risk of local relapse (30% within 7 years)  essential to give post-op XRT to
   residual breast tissue (↓ risk to 1-2% per year)
 Better cosmetic result & lesser psychological impact (although may ↑ anxiety re relapse)

What are the potential complications of mastectomy or lumpectomy ?

   Breast haematoma
   Wound infection or breast cellulitis
   Seroma formation
   Skin flap necrosis or nipple necrosis
   Phantom breast syndrome or sensory disturbances (T2-T3 dermatomes)
   Scarring & deformity

When is a hookwire localisation done ? See Scott p215

   In order to remove the correct target zone, a needle should be placed into the area of
    abnormality to facilitate precise surgical removal – this is performed under US or
    mammographic guidance (hookwire localisation or needle localisation biopsy)
   A mammogram is taken with the hookwire in-situ pre-operatively
   Operation can be definitive excision (if pre-operative diagnosis via FNAC or core biopsy) or
    an excision biopsy (necessitates 2nd operation)

Why is the hookwire specimen x-rayed after removal ?

   To make sure that the relevant portion of the breast has been excised with good radiological

Describe the anatomy of the axillary LN’s – name the groups & what they drain ?

   Pectoral (anterior) LNs – drain lymph from outer 2/3 of breast & upper ½ of trunk anteriorly
   Subscapular (posterior) LNs – receive lymph from axillary tail & upper ½ of trunk
   Lateral LNs – receive lymph from the upper limb
   Central LNs – receive lymph from above LNs (pectoral, subscapular, lateral)
   Apical LNs – receive lymph from the central LNs & all above LNs  subclavian lymph trunk
     supraclavicular LNs  thoracic duct or R lymphatic trunk

Remember PCA : pectoral  central  apical  supraclavicular LN‟s

    1.   Central
    2.   Lateral
    3.   Pectoral
    4.   Infraclavicular
    5.   Subscapular

What is an axillary        dissection ? What does it involve ?
   Axillary LNs need pathological assessment in order to stage the tumour & gain prognostic
    information – however, there is no evidence that full axillary clearance improves survival
   Extent of axillary clearance made in reference to pec minor
        o Level I : lower axilla up to lower border of pec minor
        o Level II : axillary contents up to upper border of pec minor
        o Level III : axillary contents extending to the apex of the axilla
   Axillary sampling : removal of any number of nodes extending up to level I – high FN rate in
    detecting nodal mets  has no therapeutic role
   Full axillary clearance : remove all nodes able to be found (usually 15-20 nodes) – harvest
    can be increased by removing the pec minor muscle
   Sentinel node biopsy : instead of removing all the axillary LNs the primary draining or
    “sentinel” lymph node is removed
       o Find sentinel node by injecting blue dye or technetium-labelled sulphur colloid
            around the tumour – follow to draining node
       o If the sentinel node is positive the remaining axillary LNs should be removed
       o If the sentinel node is negative, other nodes are unlikely to be involved

What are the potential complications of axillary dissection ? List ≥ 6

   Infection
   Haematoma
   Seroma formation
   Lymphoedema of the ipsilateral arm – risk is 5%, ↑↑ if also given XRT
   Nerve damage (Surgical recall p378)
        1. Thoracodorsal nerve (lat dorsi)
        2. Long thoracic nerve (winged scapula)
        3. Intercosto-brachial nerve (pain & numbness of upper medial aspect of arm & chest
            wall below axilla)
   Limitation of shoulder movement

What precautions are taken during axillary dissection ?

   Stimulate nerves with resultant muscle contraction to help identify them  don‟t paralyse
    patient (esp long thoracic N & thoracodorsal N)
   Avoid the intercostobrachial nerve – crosses axilla in transverse fashion
   Axillary drains are placed for ≈ 14 days to drain lymph fluid ( prevent seroma)

If a lump is found in the axilla  What are the possible causes  What 5 areas need to be
examined ?

Superficial causes             Abscess
                               Sebaceous cyst
                               Lipoma
Deep causes                    Axillary artery aneurysm
                               Breast lump (in axillary tail)
Lymphadenopathy                Metastases – hard, matted nodes – breast, arm, chest wall
                               Lymphoma – discrete, non-tender nodes
                               Infection – tender, fluctuant nodes – abscess

 Drainage areas for infection or malignancy
      1. Arm
      2. Breast
       3. Chest wall
       4. Abdominal wall as far down as the umbilicus
   Other LNs, eg cervical, supraclavicular, inguinal (lymphoma, mets)
   Hepatosplenomegaly (lymphoma, mets)
   Distal circulation (axillary artery aneurysm)

What must be ruled out in a red breast leaking pus ?

   Inflammatory cancer – hot, oedematous & red breast that does not settle on antibiotics – poor
    prognosis (assoc/ w/ widespread permeation of the sub-dermal lymphatics)

Other causes of breast erythema
 Cellulitis
 Mastitis – acute mastitis or periductal mastitis
 Abscess
 Paget‟s disease (nipple)
 Eczema

Tamoxifen : Discuss its indications, MOA, administration & effectiveness. What are ≥ 2
late complications ?

   Indications :
        o Breast cancer adjuvant Rx – especially in ER+ tumours & in post-menopausal ♀ –
            but is also effective in pre-menopausal women (probably minimal benefit if ER-)
        o ↓ risk of breast cancer in high-risk women (50% ↓ RR)
        o Metastatic male breast cancer
   MOA : non-steroidal anti-oestrogen that has mixed agonist-antagonist effects (antagonist in
    breast; agonist on lipids, endometrium & bone)
        o Competitive inhibitor of oestrogen binding  inhibits transcription of oestrogen-
            responsive genes  ↓ oestrogen-stimulated growth of Ca
        o May inhibit growth messages b/w cancer cells (eg TGF-β)
   Dose : 20-40mg per day PO (tablets) – taken for ≈ 5 years
   Early SE’s : may be troublesome in 5-10% of women
        o Menopausal Sx : nausea, hot flushes, vaginal dryness & pruritus, irregular periods
        o DVT/PE
        o Other : dizziness, skin rash, peripheral oedema
   Late SE’s : endometrial cancer, cataract, retinopathy
   Beneficial SE’s : ↓ incidence of contralateral breast Ca, ↓ risk of MI, ↓ osteoporosis
   Outcomes : 6% improvement in survival at 10 years
   Alternatives : ovarian ablation; aromatase inhibitors


Urinary stones (urolithiasis)

What are the 4 main types of renal calculi ? Which are radio-opaque ?
1. Calcium stones (75%) – calcium oxalate &/or calcium phosphate; radiopaque – RF‟s are
   hypercalciuria & hyperoxaluria
2. Struvite stones (15%) - ammonium magnesium calcium phosphate; radiopaque (+/- staghorn
   calculi) – RF is persistent UTIs producing urease (eg Proteus)
3. Uric acid stones (5-10%) – sodium urate precipitates in acid urine; radiolucent
4. Cystine stones (< 2%) – caused by cystinuria at acid pH

What are the clinical features of urinary stones ?

   Pain – often severe, patient restless & cannot sit still – location of pain suggests location of
            o Kidney stones (PUJ)  continuous, colicky loin pain
            o Ureteric stones (pelvic brim)  pain radiates from loin to groin (ureteric colic)
            o Distal ureter (VUJ)  radiates to the testicles or the tip of the penis
            o Bladder/urethral stones  dysuria, interruption of urine flow, straining
   Infection may be acute, chronic or recurrent
            o Cystitis : frequency, dysuria
            o Pyelonephritis : fever, rigors, loin pain, N&V
   Other : haematuria, pyuria, N&V, calculus anuria, renal impairment

How do you assess a patient with renal colic ?

 Assess diet : protein, sodium, calcium, oxalate, purine, vitamin D
 Assess normal fluid intake & activity (occupation)
 Exclude bowel disease, diarrhoea & use of antacids & diuretics
 Predisposing illness : hypercalciuria, UTI, cystinuria, RTA, gout, aminoacidurias
 Family Hx
 Red flags = obstructive symptoms > 2/52; infection & obstruction; pre-existing impairment

 Restless, sweaty & in pain
 Febrile, rigors (infection)
 Loin tenderness

What is the immediate management ?

   Analgesia : NSAIDs (PR indomethacin) &/or opioids
   IV fluids – if dehydrated give vigorous fluids
   Antibiotics, eg cefuroxime
   Observation

What are the appropriate investigations ?

   Urinalysis – RBCs, WBCs, protein, glucose
           o pH < 5.5 suggests urate stones; pH > 8 suggests infectious stone
   M/C/S – may reveal infection
           o Crystals of uric acid, calcium oxalate or cystine

 U&Es – renal function

 Plain KUB : shows radiopaque stones (> 90%) – imperfect due to phleboliths & calcified
   lymph nodes
 Non-contrast spiral CT urography – initial modality of choice for renal colic – shows all
   calculi, incl radiolucent stones; obstructed ureters
 IVP : radiolucent stones (or tumours) appear as filling defect
           o Early films : dense nephrogram, delayed pyelogram
           o Ureter : dilated & visible to level of obstruction

What are the absolute indications for surgical intervention ?

   Infection
   Obstruction in a solitary kidney
   Impaction
   Colic unresponsive to medication

What are the management options (list ≥ 3) ?

   Depends on composition & position of stone
   90% of stones < 4mm will pass spontaneously, while only 20% of stones > 6mm will pass
   Stones in the proximal ureter are less likely to pass

Management options
 Conservative – stones < 4mm may pass spontaneously. Keep fluids up & provide analgesia.
  Observe for signs of obstruction & inflammation.
 Extra-corporeal shock wave lithotripsy (ESWL) : Aims shock waves at stone thru the skin,
  via U/S guidance, breaking stone into small pieces which can pass down the ureter.
          o Used for stones < 2cm
          o Complic : bleeding, sepsis, difficulty passing fragments
 Percutaneous nephrolithotomy: Needle thru back into kidney to remove stone.
          o Used for larger stones (> 2cm)
          o Complic : renal loss, sepsis, bleeding, colonic perforation, PTX, air emboli
 Ureteric stent – may be inserted to dilate the ureter, enabling passage of stone or for later
  (>24hr) ureteroscopy
 Ureteroscopic removal : Destruction of stone via laser or mechanical methods (lithotrite) +/-
  basket removal of stone/fragments. ↑ complc‟ns.
   Open surgery : Open ureterolithotomy or pyelolithotomy rarely used for large stones.
    Nephrectomy if poor renal function.

What are potential sequelae & complications of urinary stones ?

   Impaction in ureter  renal colic
   Obstructed urinary outflow (at PUJ, pelvic brim or VUJ)  hydroureter & hydronephrosis
   Mucosal injury & obstruction  infection
   Chronic irritation by calculi  SCC

Urinary tract infections

What are the usual causes of UTI’s ? What specific causes apply to post-menopausal
females ?

Predisposing factors
 Females – short urethra, hormones
 Sexual intercourse
 Ureteric stasis :
       o Structural : BPH, pregnancy, urethral stricture, calculi, diverticula, congenital
       o Functional : neurogenic bladder, spina bifida, pregnancy
       o Foreign body : urinary catheter, stent, instrumentation (cystoscope)
 Vesicoureteric reflux
 Immunosuppression, eg DM, immunocompromise

Factors in post-menopausal women
 Oestrogen-deficiency
 Increased residual urine volume
 Atrophic vaginitis
 Need longer course of ABs

 Usually acquired via the ascending route, ie urethra  bladder  ureter (via VUR)  renal
   collecting system  renal parenchyma (via intrarenal reflux)
 Haematogenous spread occurs in the debilitated & immunocompromised

What are the microbiological causes of UTI ?

   Most UTIs are caused by bacteria from intestinal flora
   Community-acquired : mnemonic KEEPS
          K = Klebsiella pneumoniae
          E = **Escherichia coli (70-80%)**
          E = Enterobacter
          P = Proteus mirabilis
          S = Staphylococcus saprophyticus (15%)
   Hospital acquired : Similar to above + Pseudomonas aeruginosa
   Yeasts (eg. candida spp) & protozoa (eg. Trichomonas vaginalis) may also be implicated

What are the symptoms – upper vs lower UTI ?

Lower UTI                                          Upper UTI
 Dysuria (burning/stinging on urination)           Loin pain  may radiate to iliac fossa &
 Frequency, urgency, nocturia                        suprapubic area
 Suprapubic pain, feeling of incomplete            Fever, rigors, malaise, vomiting
   emptying                                         Lower urinary tract symptoms
 Urine may be cloudy & offensive smelling
   +/- haematuria

What investigations are required ?

   MSU – M/C/S
           o Dipstick : +ve for nitrites & leucocyte esterase +/- blood & proteins
           o Micro : WBCs (pyuria > 10/mL) +/- bacteria, red cells & tubular epithelial cells
           o Culture usually positive (> 105 cfu/mL)
   Bloods
           o FBC : neutrophilia
           o U&Es : raised creatinine secondary to dehydration
           o Blood cultures : to exclude bacteraemia (present in 33%)
   Radiology – required for all UTI‟s in ♂ & recurrent/complicated UTI‟s in ♀
           o Renal U/S – 1st line Ix
           o CT scan w/o & w/ contrast
           o MCU – for VUR
           o IVP – delayed nephrogram, SOL, obstruction (needs urgent decompression)

What is the management for lower UTI (cystitis) ?

   Advice/prevention : drink plenty of fluid; urinate frequently & completely; void before &
    after intercourse; ♀ wipe front to back after micturition; Cranberry juice (↓ E. coli adhesion)
   Treat the infection : Any of these regimens, often started empirically while awaiting
    micro/culture results :
             o Trimethoprim : 300mg PO od for 3 days
             o Cephalexin : 500mg PO bd for 5 days
             o Amoxicillin + clavulanate : 500mg + 125mg PO bd for 5 days
             o Men require longer duration, eg 14 days of Rx (may involve prostate &
             o Recurrent infections in ♀ & post-menopausal ♀ : use 10 days Rx, may require
                prophylactic ABs
   Look for a cause & treat it : if UTI occurs in anyone other than a childbearing age ♀, or a ♀
    presents with recurrent UTI
             o Post-menopausal women may need HRT
What is your management of suspected pyelonephritis ?

   Treatment should be given for 7-14 days, with repeated urine cultures during treatment, then
    1 week & 3 weeks after treatment
   Mild-moderate infection : PO alone for 10 days
           o Cephalexin 500mg qid, or
           o Amoxicillin + clavulanate 875mg bd, or
           o Trimethoprim
   Severe infection : sepsis/vomiting  IV therapy initially
           o Amoxy/ampicillin 1g qds plus
           o Gentamicin 4-6g/kg daily
   Rehydration & treatment of septic shock may be needed
   Renal carbuncle or pyonephrosis must be drained under U/S or CT guidance
   Any obstruction must be alleviated – later correct anatomical abnormalities

Haematuria (in a 47 yo ♂)

What are the causes ? List ≥ 4

   Kidney : calculus, renal cell carcinoma, TCC, GN (nephritic syndrome – IgAN), trauma,
    pyelonephritis, polycystic kidney, trauma, TB, embolism, infarct, renal vein thrombosis
   Ureter : stone; TCC
   Bladder : cystitis; TCC; stone; trauma
   Prostate : BPH (varices); prostatitis; carcinoma; trauma
   Urethra : trauma; stone; urethritis; neoplasm
   Bleeding diatheses : anticoagulant Rx ( do not blame this until more sinister causes have
    been excluded); thrombocytopaenia; haemophilia
   Other : malaria; strenuous exercise (fractures GBM); DM; SLE; vasculitis; amyloidosis

How would you proceed ?

   Hx
   Ex
   Ix

What would you ask the patient ?

   Onset & duration – transient or persistent? acute or chronic?
   Colour of urine – upper tract blood is well mixed & is dark or blood-coloured
   Presence of clots ?
           o Spindle-shaped = renal (these can cause „clot colic‟)
           o Large clots = bladder
   Any pain assoc/ w/ haematuria ?
           o  Painless = TCC until proven otherwise – other causes incl drugs, GN, other
            o Loin pain = kidney disease (eg tumour, hydronephrosis, cystic)
            o Loin to groin (colic) = stone or clot passage thru ureter
            o Frequency, urgency, dysuria, suprapubic pain = cystitis
            o Perineum = prostatitis
    At what part of stream does haematuria occur ?
            o Initial = anterior urethra or prostate
            o Total (throughout stream) = upper urinary tract or bladder
            o Terminal = posterior urethra, bladder neck/trigone or prostate
            o Between voidings = urethra
    Fever – suggests pyelonephritis
    Symptoms of prostatism : difficulty starting, poor stream, nocturia
    Bleeding disorders or drugs

What signs would you look for O/E ?

General signs
 Pyrexia – suggests UTI or GN
 Bruising or purpura – bleeding disorder
 Hypertension & oedema – GN
 Signs of anaemia, weight loss & CRF

Abdominal signs
 Bladder – may be palpable 20 to urinary retention (eg infection, clot retention), rarely bladder
 Kidneys – tumours, APCKD or hydronephrosis may be palpable
 PR for prostate
          o Tenderness = prostatitis
          o Smooth, enlarged = BPH
          o Hard, craggy = Ca (feel for bony mets)
 PV – for pelvic mass

What investigations would you perform ?

     In the absence of intrinsic renal disease, urological investigations should come 1st, esp
      in pt‟s > 35 yrs (exclude malignancy)
     Normal urology necessitates referral to nephrologist

 Dipstick : Very sensitive (detects < 5,000 RBC/mL) & can identify all significant bleeding
   (false +ves due to haemoglobinuria & myoglobinuria)
           o Detects proteinuria, leucocytes, nitrites (UTI), etc
 M/C/S of MSU for presence of RBCs, WBCs, clots, casts & crystals
           o RBCs : confirm haematuria (exclude haemoglobinuria) & look at morphology
               (dysmorphic in glomerular bleeds)
           o Red cell casts indicate glomerular bleeding (RBCs leak thru GBM & become
               glued together via mucoproteins)
           o White cells & organisms suggests infection ( tumours & infections can co-exist)
           o Urine culture : identify microbes present
   Cytology – need 3 x 1st morning voids – will detect high-grade TCC‟s
           o +ve in 60-70% of bladder cancers; 15-20% false-positive rate

 FBC, ESR: ↓ Hb in gross haematuria & malignancy. ↑ Hb in polycythaemia (↑ EPO in renal
   Ca). ↑ WCC in infection. ↓ platelets in blood dyscrasias. ↑ ESR in malignancy & TB.
 E/LFTs : renal & liver function; bone parameters (Ca2+, PO42-, Alk Phos) for mets
 Clotting screen : anticoagulant Rx & blood dyscrasias

 IVP –– 1st line investigation for upper urinary tracts
       o Stones - 90% of stones visible on plain KUB
       o Renal lesions
       o Filling defect – TCC or radiolucent stone (uric acid)
       o Delayed excretion & hydronephrosis/hydroureter
 USS – upper renal tracts & bladder
       o Dilatation of collecting system
       o Renal pathology, eg tumour, calculus (solid vs cystic lesion)
 CT with contrast – staging malignancies or in trauma

Cystoscopy +/- ureteroscopy
 1st line Ix for lower urinary tract
 Direct examination of urethra & bladder
           o Bladder lesions
           o Origin of blood, eg prostate, ureter
 RPG/ureteroscopy for ureters, eg TCC

Follow-up for TCC that has been treated
- 3/12 for 2 yrs
- 6/12 for 2 yrs7884
- yearly for rest of life

Acute scrotal pain

What are the causes of acute scrotal pain ? What must be excluded urgently ?

   Testicular torsion (a surgical emergency)
   Torsion of testicular appendage
   Epididymo-orchitis
   Trauma & haematocele
   Testicular tumour
   Strangulated hernia
   Varicocele
   Scrotal skin, eg dermatitis, infected sebaceous cyst, HSV, Behcet‟s disease
   Referred pain (rare), eg renal colic, T10 nerve root compression, ilioinguinal N entrapment,
    groin strain, idiopathic cord neuralgia, spinal nerve irritation

How would you proceed ?

 Sudden onset of pain, redness & swelling  testicular torsion
 Gradual onset of pain, redness & tenderness  epididymo-orchitis
 Symptoms of UTI or STD suggesting epididymo-orchitis
 Trauma suggests haematocele
 Dull, poorly localised ache  varicocele
 PHx of inguinal hernia w/ sudden onset of colicky abdo pain (strangulated hernia)

 If torsion is suspected, surgical exploration is mandatory within 6 hrs of onset of pain as
    the testicle rapidly becomes non viable
 Tests if considered non-urgent include :
             o WCC/ESR
             o U/S for testicular assessment & blood flow (Doppler)
             o MSU for UTI assoc/ w/ epididymo-orchitis

Scrotal lump

What are the causes of a scrotal lump ?

Scrotal swelling that examiner is unable to get above
 Indirect inguino-scrotal hernia
 Varicocele
 Scrotal (infantile/communicating) hydrocele of spermatic cord

True scrotal swelling = examiner able to get above

Cystic swellings
 Spermatocele (epididymal cyst)
 Hydrocele
 Haematocele
 Sebaceous cyst

Solid masses
 Epididymitis* – acute or chronic
 Torsion of hydatid of Morgagni* (appendix testis) or epididymal appendix*
 Testicular tumour
 Torsion of the testis
 Orchitis
 Testicular gumma or TB (rare)
(* = lies separate from the testis; others lie within the testis)

How do you examine a scrotal lump ? What is transillumination & how do you perform it ?

   Examine the scrotum standing & supine
   Can you get above swelling (ie. is lump confined to scrotum) ? Done with pt standing
             o If no upper border is palpable, must be descending down inguinal canal from
                 abdomen (indirect hernia, communicating hydrocele or varicocele)
             o Look for transmission of a cough impulse
   Is the mass separate from or part of the testis ?
             o Separate = spermatocele, epididymitis, torsion of hydatid of Morgagni
             o Testis lies within swelling = hydrocele, haematocele
             o Within testis = tumour, torsion, orchitis, gumma
   Is it cystic or solid, ie does it transilluminate & fluctuate ?
             o Transillumination : with pt in darkened room, a small torch is applied to posterior
                 aspect of swelling by invaginating scrotal wall  cystic mass will light up
                 (transilluminate), while solid/opaque mass remains dark
             o Fluctuation : Can only be elicited by feeling at least two other areas of the lump
                 whilst pressing on a third – if 2 areas on opposite aspects of the lump bulge when
                 a 3rd area is pressed in, the lump fluctuates & contains fluid
   Is the swelling tender ?
             o Indicates torsion (testis/appendix), tumour, epididymo-orchitis, etc
   Look for signs of weight loss, lymphadenopathy, hepatomegaly or pleural effusions


What is the DDx for a lump in the neck ?

Superficial neck lump/s
                                -   Sebaceous cyst
                                -   Lipoma
                                -   Neurofibroma
                                -   Abscess
                                -   Lymph node/s*
Deep neck lump/s
Midline                         Moves on swallowing
                                 Thyroid goitre or nodule
                                 Thyroglossal duct cyst
                                 Dermoid cyst
                                 Subhyoid bursa
Anterior triangle               Moves on swallowing
                                - Thyroid : goitre, nodule
                            - Lymph node*
                            Does not move on swallowing
                            - Submandibular gland stone, sialadenitis or tumour
                            - Parotid tumour
                            - Branchial cyst (anterior border of SCM)
                            - Carotid body tumour
                            - Carotid aneurysm
                            - Sternocleidomastoid tumour
                            - Laryngocele
Posterior triangle          - Lymph node/s*
                            - Cervical rib
                            - Subclavian artery aneurysm
                            - Pharyngeal pouch
                            - Cystic hygroma (cavernous lymphangioma)
Superficial or deep         - Inflammatory (most common) : local, regional or systemic
Anterior triangle or          infection (eg HIV, EBV) or autoimmune disease (eg SLE)
posterior triangle          - Granulomatous – infective (eg TB) or non-infective (eg sarcoid)
                            - Lymphoproliferative malignancy – lymphoma, leukaemia
                            - Secondary malignancy – eg melanoma, carcinoma


List the potential complications of thyroidectomy ?

   Wound complications : infection, hypertrophic scar
   Haematoma (eg damage to superior or inferior thyroid A‟s) – can occur in first few hours
    after operation & may cause laryngeal oedema, stridor & dyspnoea
             Open wound immediately & return to theatre to control haemorrhage
   Nerve damage
            o Recurrent laryngeal N palsy  hoarseness or bovine cough if unilateral; loss of
                speech & airway obstruction if bilateral (may need emergency tracheostomy)
            o Superior laryngeal N (external branch) palsy  loss of vocal pitch
            o Cervical sympathetic chain – rarely at risk – produces a Horner’s syndrome
                (miosis, enophthalmos, partial ptosis & skin sweating loss)
   Hypoparathyroidism causing hypocalcaemia – may be temporary or permanent (eg
    removal of parathyroids)
            o Serum Ca2+ essential 48hrs after thyroid surgery
            o Tx : IV calcium gluconate, followed by PO Ca2+ & vitamin D
   Hypothyroidism (> 10%) – too much thyroid removed
   Thyroid crisis: may be precipitated by other illnesses (eg pneumonia) if the patient is
    thyrotoxic – pyrexia, agitation, confusion, arrhythmias, cardiac failure
   Pneumothorax
   Tracheal collapse

What is the pre-operative preparation ?
   Should be rendered euthyroid
        o Carbimazole or PTU
        o Propanolol
        o Lugol‟s iodine for 10 days to ↓↓ vascularity of the gland
   Inspect vocal cords by direct laryngoscopy to ensure satisfactory functioning
   CXR to assess trachea & any retrosternal extension
   FBC
   Complete bed rest (+/- sedation) to induce sleeping pulse rate of 60-70bpm

What is Chvostek’s sign ? What is the physiological basis ?

   Chvostek sign : spasm of facial muscles after tapping CNVII below zygoma
   Hypocalcaemia  ↓ ECF [Ca2+]  ↑ ion channel permeability to Na+ ions  promotes
    inwards Na+ current  membrane depolarises towards threshold potential  ↑ AP
    production  ↑ excitability of neurons ( spontaneous discharge)


List ≥ 5 causes of hypercalcaemia ? ECF [Ca2+] > 2.65mmol/L (total) or > 1.25mmol/L

   Hyperparathyroidism :
            o Primary : parathyroid adenoma (80%), hyperplasia or carcinoma
            o Tertiary : autonomous PTH secretion due to long standing 20 hyperparathyroidism
                (NB secondary ↑ PTH is due to ↓ Ca2+ levels)
   Malignancy :
            o Bony metastases that are osteolytic (bone erosion &/or PTHrP release)
            o Multiple myeloma
            o Paraneoplastic syndromes (secrete PTH or PTHrP) : lung SCC, cervix, pancreas
   Vitamin D excess :
            o Sarcoidosis & TB (MΦ‟s in granulomas make vitD)
            o Intoxication (dietary)
   Drugs : lithium, thiazides (↓ Ca2+ excretion)
   Hyperthyroidism causing ↑ bone turnover
   Addison‟s disease (glucocorticoids normally ↓ GIT Ca2+ absorption & ↑ renal Ca2+ excretion)
   Other : familial hypocalciuric hypercalcaemia, adrenocortical insufficiency, immobilisation,
    Paget‟s disease, excess ingestion, iatrogenic IV calcium

 Remember HMV : Hyperparathyroidism/hyperthyroidism, Malignancy (osteolytic), Vitamin
D excess

List ≥ 5 symptoms.

„Bones, stones, abdominal groans & psychic moans‟
 Bone pain, pathological fractures
 Renal (stones) = calculi & nephrocalcinosis; renal failure
           o Polyuria (nephrogenic DI) & polydipsia
   GIT (groans) = abdo pain, constipation, nausea & vomiting, anorexia, peptic ulcers
   Neurologic (psychic moans) = depression, drowsiness, lethargy, weakness, stupor, coma;
    proximal myopathy & hypotonia

What would be the 1st test done to differentiate the cause ?


Other tests
 Other blood tests to do
            o Albumin – dehydration, alters Ca2+ reading
            o Phosphate – low in 10 hyper-PTH & osteomalacia; high in 20/30 hyper-PTH
            o Alk Phos – raised in hyper-PTH & other bone diseases (eg Paget‟s)
            o U&Es – check for CRF
 Differential diagnosis of hypercalcaemia is based on serum PTH levels
            o ↑ [Ca2+], ↑ PTH & ↓ PO42- = hyperparathyroidism
            o ↑ [Ca2+] & ↓ or normal PTH = non-parathyroid aetiology
            o ↓ PO42- levels & ↑ alkaline phosphatase (bone disease)
 Urinalysis : hypercalciuria
 Radiography of hands : subperiosteal bone reabsorption of phalanges (↑ PTH)
 Look for cause – U/S or CT of parathyroids, N/M, etc

How would you manage this ?

   Diuresis with frusemide & IV saline (5-10L/day)  ↑ renal Ca2+ excretion
   Bisphosphonates, eg pamidronate 90mg IV over 4 hours  inhibit osteoclast activity which
    causes a fall in [Ca2+] – maximal at 2-3 days & lasts a few weeks
   Glucocorticoids if severe (eg 40mg prednisolone PO nocte)  ↓ GIT Ca2+ absorption & ↑
    renal Ca2+ excretion
   Mithramycin (plicamycin) IV will ↓ bone reabsorption

Picture showing tongue with leukoplakia & an ulcer (Browse p240/243)

What causes leukoplakia ?

   „White plaque‟ on oral mucous membranes that cannot be removed by scraping & cannot be
    classified clinically or microscopically as another disease entity
            o „Cracked white paint‟ appearance with areas of adherent grey-white plaques
   Caused by epidermal proliferations & ↑ keratinisation
   May be a local physiological response to a chronic irritant – the 6 S‟s – syphilis, smoking,
    sharp tooth, spirits, spices, sepsis (chronic superficial glossitis)
   Premalignant – 25% will become cancers

What causes ulceration ?
    Sharp teeth or ill-fitting dentures
    Aphthous ulcers – non-specific ulceration (eg HSV, HPV, HIV, idiopathic)
    Malignancy – raised, irregular rolled margin & red indurated base
    Syphilitic chancre

Oral cancer is suggested when the 2 are present

    Leukoplakia is premalignant (25% conversion to malignancy)
    Linked to smoking (tobacco/marijuana), tobacco chewing, alcohol & chronic dental sepsis
    Most are SCC‟s

Presentation                         (Browse p243)
 Plaque – raised, firm, pearly plaques – may have superimposed leuko/erythroplakia
 Ulcer – raised, irregular rolled margin & red indurated base
 Fissure – chronic in nature w/ no signs of healing
 Protuberant lesion – varies from small projection to a large „cauliflower-like‟ mass

Lymphatic spread
 Tongue tumours spread earlier than lip tumours – large, firm & fixed node/s
 Lower lip & tip of tongue  submental LNs
 Upper lip & anterior 2/3 of tongue  submandibular LNs
 Post 2/3 of tongue superior deep cervical LNs (bilaterally)


Skin cancer

Fill out this table.

    Lesion             BCC                        SCC                       Malignant Melanoma
    % & epidemiology   75% (most common!!)        15-20%                    5%, but leading mortality
                       (> 750/100,000/yr)         (> 300/100,000/yr)        (50/100 000/yr; 1:15 life)
    Histology          Cells appear BLUE (↑↑      Keratin whirls and        BROWN. Nests of large
                       N:C ratio). Nests invade   hyperkeratosis (PINK)     cells or single cells
                       dermis with peripheral     invading into dermis      invading dermis.
    Types              Superficial multifocal     Solar keratosis           Superficial spreading
                       Nodular                    Bowen disease (in-situ)   Nodular (worst)
                       Morphoeic/sclerosing       SCC                       Lentigo maligna
                                                                            Acral lentiginous
    Clinical           Pearly papule/nodule       Erythematous, scaly       ABCDE‟s.
                       with central               lesion. Ulceration has    Expanding, irregularly
                       umbilication &             raised, everted edges.    brown-black pigmented
                       telangiectasia.                                      macule or plaque.
                       Ulcers have rolled edges
    Local growth       Local invasion of          Local invasion thru the   Radial (epidermis) vs
                       bone/cartilage may form    dermis. Usually found     vertical (dermis) growth
                       „rodent ulcer‟.            when small.               phase.
    Spread             Does not metastasises (≈   < 5% metastasise via       Spreads in vertical phase
                       1 in 20 000 do)            lymphatics. Worser         Lymph first
                                                  prognosis if Marjolin‟s.   Later blood-border to
                                                   check draining LN‟s.     skin, lung, liver, brain,
                                                                             bone or GIT.
    Management         Surgical excision          Surgical excision +/-      Surgical excision with
                       usually curative.          XRT                        appropriate margins.

What are the key adverse prognostic factors in melanoma ?

    Male sex
    Increasing age
    Site (BANS) : Back of Arm, Neck, Scalp
    Cutaneous ulceration
    Increasing Breslow thickness =  prognostic indicator (< 0.76mm, > 3.65mm) – superficial
     spreading & lentigo maligna melanoma have better prognosis (longer radial phase)
    High mitotic rate/mitotic index (> 6/mm2)
    Microscopic satellite deposits
    Lack of infiltrating lymphocytes
    Local recurrence
    Involvement of LNs or distant metastases

What is the Breslow thickness & Clark level ? How do they affect prognosis ?

    Likelihood of tumour progression & metastasis is related to depth of the lesion
    Breslow thickness : measured from the top of the stratum granulosum to the deepest tumour
            o < 0.76mm (thin melanoma) = not likely to metastasise
            o > 3.65 mm = likely to develop metastases
    Clark’s level
            o Level 1 = Intraepidermal (melanoma in-situ)
            o Level 2 = Invades the papillary dermis
            o Level 3 = Invasion to the papillary/reticular dermal interface
            o Level 4 = Invasion into the reticular dermis
            o Level 5 = Invasion into SC fat

hot liquids
chemicals (corrosive/caustic)

How are burns classified?

1. Epidermal (“first degree) : eg sunburn
- red
- moderately painful
- blanch with pressure
- no scar
    topical (Neosporin)
2. Partial thickness (“second degree”)
- into, but not through dermis
- blisters
- moist exposed dermis, which blanches w/ pressure
- v. painful b/c cutaneous nerves are intact
- deep ones heal badly b/c damaged dermis does not regenerate – replaces by rigid, tender and
friable scar
eschar = coating of dead tissue, coagulated serum, debris
- separates 10-14 days after injury, exposing punctate area of new epidermal lining of hair
follicles and sweat glands (“skin buds”)
    excision/skin grafting
3. Full-thickness (“third-degree”)
- all layers of skin destroyed (dermis, epidermis, subcutis/fat)
- white/waxy
- all skin appendages gone
- dry, avascular, leathery skin
- insensate

What is the rule of 9’s ? Illustrate it

1 trunk: 36
2 legs: 36
2 arms: 18
1 head: 9
1 penis: 1

Complications of the burns

1. Inhalation (CO poisoning)
- suspect anyone found unconscious during fire
- “cherry-red” cheeks, neuro dysfunction, h/a
- Po2 is N, but So2 is low
- CO displaces O2 from Hg (carboxyHg)  hypoxia
2. Upper airway obstruction
- up to 24 hrs after
- hot particles damage oro-pharyngeal mucosa sloughing, edema  obstruction
3. Pulmonary injury
- can be days after injury
- caused by toxic chemicals in fumes and gases, damaging lung epithelium
         high-flow O2
         pulmonary hygiene: coughing, suctioning, clearing secretions
- infection
- immunesuppression
- fluid loss
- severe pain
- intense inflammatory response – multi-system failure
- contractures/immobility

≥ 4 signs of inhalation burn

   Nasal/facial hair burns
   Smoke & soot in sputum/mouth/nose
   Erythema/oedema/burns/blistering of the nose, mouth, tongue & throat
   SOB
   Stridor or hoarseness
   Confusion, headache, Hx of loss of consciousness, coma

 Signs of inhalation/obstruction – ventilate with bag & mask while preparing for ETT
   intubation (intubate early to avoid later oropharyngeal oedema)

Nutritional requirements after burn

-BMR rises dramatically (stress hormones influence on metabolism)
-Negative Nitrogen balance  CATABOLIC state
- aggressive nutritional support

What is the equation for fluid resuscitation ?

   Resuscitation usually involves the use of crystalloid fluids (Hartmann’s = Ringer‟s lactate)
    thru 2 large-bore peripheral venous catheters introduced thru unburned skin
   Various formulas have been developed to guide fluid volumes in early post-burn phase (<
    24hrs) – half volume given in first 8 hours, other half given in next 16 hours

       o Adults (‘Parkland formula’)***
       V (mL) = TBSA (%) x Weight (kg) x 4
       first 8 hrs: ½ of total
       next 8 hrs: ¼ total
       next 8 hrs: ¼ total
                                                        [70kg male, 10% = 2800mL]
                                             3-4mL Hartmans / kg bodyweight / % TBSA
       o Children – as above plus maintenance fluids according to bodyweight using 4%
           glucose in ¼ or 1/5 normal saline
   > 24hrs post-burn, use colloids
       o 5% dextrose and 5% albumin at 0.5mL / kg bodyweight / % TBSA
       o Delivered over 4-8 hours

Monitoring adequacy of fluid resuscitation
 Monitor urine output – aim for 0.5mL/kg/hr (adults) or 1.0mL/kg/hr (kids)
      o Red or brown urine indicates myoglobinuria, suggesting muscle injury  beware of
          ARF due to deposition in proximal renal tubules, maintain ↑ urine output
 Cardiovascular monitoring – BP, HR, peripheral perfusion, mental status
 If severe – CVP &/or PCWP



What are the causes of ↓ UO ?

   Pre-renal = inadequate blood perfusing kidney
       o Inadequate fluids
       o Dehydration (burns, vomiting, diarrhoea, pancreatitis)
       o Hypotension/haemorrhage
       o Pump failure : CCF, cardiogenic shock
       o 3rd spacing
   Renal = kidney parenchyma dysfunction
       o Acute tubular necrosis
       o Nephrotoxic drugs (eg gentamicin, contrast agents)
       o Myoglobinuria (rhabdomyolysis)
   Post-renal = obstruction to outflow of urine from kidney
       o Foley catheter obstruction/blockage
       o Stone
       o Ureteral/urethral injury
       o BPH
       o Bladder dysfunction – medications, spinal anaesthesia

What would be your actions ?

   Check ABCs & vital signs
   Check or place Foley catheter & irrigate it
   IV fluids to restore circulating blood volume (may need initial boluses)

What are the causes ? Give a rough time-line.

Classic W‟s of post-op fever
 Wind = atelectasis = first 24-48 hours (also pneumonia, > 3 days)
 Water = UTI = after day 3
 Wound = wound infection = after day 5
 Walking = DVT/thrombophlebitis = days 7-10
 Wonder drugs = drug fever = anytime

Time post-op                      Causes of fever
Few hours                         Trauma of surgery, GA, blood transfusion
< 24hrs                           Atelectasis, β-haemolytic strep or clostridial wound infections,
                                  anastomotic leak
Days 3-5                          UTI, pneumonia, IV site infection, wound infection
Days 5-10                         Wound infection, pneumonia, abscess, C. difficile colitis,
                                  anastomotic leak, septicaemia
                                  DVT/PE, peritoneal abscess, drug fever, parotitis

What work-up is indicated ?

   Physical exam – wound, lungs, abdomen
   CXR
   Urinalysis
   FBC, U&Es
   M/C/S : blood, sputum, urine, stool, CSF


   Hypoxia – until proven otherwise – causes include pneumonia, PE & LVF
   Infection – septicaemia, UTI, RTI, wound infection, meningitis, encephalitis
   Metabolic : hyponatraemia, hypo- or hypercalcaemia, thyrotoxicosis, , hypo- or
   Neurologic : CVA, intracranial bleeding, seizure, tumour, hydrocephalus, head injury
   Hypotension : dehydration, cardiogenic shock (MI, CCF), hypovolaemic shock
   Organ failure : CCF, liver, kidneys, lungs
   Output failure : urinary retention, constipation
   Drugs
       o Drug reaction, narcotics, BZDs, anticholinergics (eg cimetidine), antibiotics
       o Withdrawal : alcohol, opiates

Use of an IDC
Give 3 indications for insertion of an IDC

   Urologic or pelvic surgery
   Acute urinary retention
   Monitoring urinary output (eg IV fluid therapy, critically ill)
   Collection of sterile urine specimen
   Radiology – MCU

What are potential complications ?

   Paraphimosis
   Infection
   Balloon breakage
   Blockage (anuria)
   Urethral trauma or bleeding  stricture
   Failure of balloon to deflate

What does this CXR demonstrate ?

Shows inferior displacement of the horizontal fissure, diffuse opacification of the RLZ & partial
silhouetting of the right heart border.

What are the radiological signs of atelectasis ?

   Rapidly appearing (& disappearing) opacification of part of the lung, classically basally
   Evidence of volume loss
       o Crowding of the pulmonary vessels &/or ribs
       o Displacement of the fissures
       o Elevation of the hemidiaphragm
        o Displacement of the hilus/mediastinum (severe)
   Compensatory hyperinflation of normal lung
   Linear or plate-like atelectasis appears as horizontal or oblique opacified bands of volume
    loss in the lungs, often visible in two projections & often transient


Fluid balance

What are the principles of fluid replacement ?

    1. Replace deficits
    2. Fulfil daily maintenance requirements
    3. Replace ongoing losses

“Losses” may include
       o Pre-op & pre-admission
       o Ongoing losses – usually rich in Na+ ( give 0.9% saline)
       o NG aspirate – Na+ 110mmol/L, Cl- 100mmol/L, K+ 5mmol/L
       o Intestinal aspirate – Na+ 120mmol/L, Cl- 100mmol/L, K+ 10mmol/L
       o Vomit, diarrhoea
       o Stoma, drains, fistula, etc
       o 3rd space losses

What are the normal daily requirements for water, Na+ & K+ ?

   Daily maintenance fluid requirements vary b/w individuals
       o Rough guide : 35-40ml/kg/day, 1.5-2mmol/kg Na+ & 0.5-1mmol/kg K+
       o 70kg ♂ = 2.5–3.0L water, 120-140mmol Na+, 170-190mmol Cl- & 70mmol K+
       o 40kg ♀ = 2.0L water, 70-90mmol Na+ & 40mmol K+
   100/50/20 rule for daily fluids (esp for paediatrics)
       o 100mL/kg for first 10kg
       o 50mL/kg for next 10kg
       o 20mL/kg for every kg over 20kg

How many mmol of sodium is there in 1L N/S ?

154mmol Na+ (0.9% NaCl)

What is a normal maintenance regime ?

   Maintenance requirements for 24h is 1L N/S and 2L of 5% dextrose (= 3L of water &
    154mmol Na+)
   Potassium supplements are not necessary for 48hrs (ADH retains Na+ & K+) – after this add
    20mmol/L of K+ (20mmol per bag)
Standard maintenance orders :
 Alternating q8h 1L bags of N/S & 4% dextrose 1/5 N/S (4% 1/5) – add 20mmol/L K+ to
   each bag
 Q8h 3% 1/3 1L bag every 8 hrs + KCl 20mmol per bag

What fluids should be used to replace losses ?

   N/S
   Hartmann‟s/LR – don‟t use LR for maintenance – the lactate is converted to bicarbonate –
    prolonged use will cause alkalosis

How much fluid is usually lost daily in the faeces (ie maintenance for faecal losses)

   100mL/day – anything above this (eg from stoma) should be added to maintenance fluids (eg
    stoma output 500mL/day  ↑ fluids by 400mL/day to account for this ↑ loss)

Trauma – gun shot wound – what is your management ?

Primary survey
 Airway & C-spine
 Breathing & ventilation, give O2
 Circulation & haemorrhage control – assess haemodynamic status, IV access, NGT, IDC
 Disability – AVPU or GCS
 Exposure & environment

AMPLE brief history
 A – allergies
 M – medications
 P – past Hx
 L – last ate
 E – events, environmental exposures (eg trauma, drugs)

Secondary survey
 Head to toe physical examination including all orifices
 Head & face, eyes & pupils
 C spine & neck, x-ray C spine
 Chest – wall, lungs, heart, CXR
 Abdomen – check for tenderness, guarding, rebound tenderness, progressive distension,
   shoulder tip pain – may need DPL or FAST
 Perineum, PR & PV exam
 Back – log-roll patient
 Extremities & pelvis
 Neuro exam – motor, sensory, pupils

Management of gun-shot wound
   Mandatory exploratory laparotomy (high-velocity injury – tears & disrupts)
   Wounds of entry (& exit) must be excised & left open initially


What are the legal requirements for valid consent ?

    1. Competent – the doctor must determine if the patient is mentally competent to consent
       (see below)
    2. Free & voluntary – influencing vs coercion
    3. Disclosure : Informed as to broad nature of Tx (to prevent negligence must be accurate &
       cover material risks – subjective & objective person standard according to R v W)
    4. Understanding & acceptance of info – simple language, check understanding
    5. Covers the actual procedure to be performed
    6. Procedure must be legal (eg excludes euthanasia)
    7. Consent given to specific doctor, but exceptions (eg in public hospital – registrars)

Capacities that define a competent patient
1. Comprehend & retain relevant information
2. Understand nature & effects of decisions
3. Evaluate information & predicted consequences in relation to one‟s situation, goals & values
4. Offer reasons for one‟s decision
5. Communicate one‟s decision
6. Able to persevere with decision

What information must be given to the patient for them to consent ?

   Diagnosis
   Natural history of disease & likely prognosis (with & without Tx)
   Treatment options (incl non-surgical options)
   Advantages & disadvantages of treatment options
   Recommended treatment & details of that operation
   Outcomes of treatment
   Risks, side effects & complications – list common risks & significant risks – include worst-
    case scenario (eg amputation, stoma)
   Post-op details – recovery, hospital stay


What are the indications for splenectomy ?

   Traumatic spleen injury (blunt abdominal trauma) – causing bleeding
   Haemolytic anaemias – spleen is involved in trapping & destruction of abnormal RBCs
       o Hereditary spherocytosis (defective, fragile RBC membrane trapped in spleen)
       o Thalassaemia
       o Sickle cell disease (in ↓ pO2, RBCs elongate & distort, causing thrombosis)
   Thrombocytopenias
        o Idiopathic thrombocytopenic purpura (ITP) – spleen produces IgG against platelets
        o Thrombotic thrombocytopenic purpura (TTP)
   Hypersplenism - secondary (eg in portal HT) or primary
   Myeloid metaplasia & myelofibrosis (proliferation of liver, spleen & long bones)
   Neoplasia – splenectomy indicated if symptomatic splenomegaly or cytopenias
        o Lymphomas – Hodgkin‟s disease or NHL
        o Leukaemias (esp hairy cell leukaemia)
        o Primary tumour
   Vascular
        o Splenic artery aneurysm
        o Splenic AV fistula
        o Splenic vein thrombosis
   Felty’s syndrome (RA, splenomegaly & neutropenia)
   Sarcoidosis – if splenomegaly with hypersplenism present
   Gaucher’s disease

What are you at risk of after splenectomy ?

   Immunologic defects
       o ↑ risk of infection w/ encapsulated bacteria, esp Strep. Pneumoniae, H. influenzae &
           N. meningitidis
       o Poor response to immunisations
       o Overwhelming post-splenectomy infection (OPSI) – more susceptible to fulminant
           septicaemia by encapsulated bacteria – 50% mortality rate
   Haematologic effects
       o Howell-Jolly bodies, Heinz bodies & siderocytes
       o Leukocytosis
       o Thrombocytosis
       o Red marrow increases
       o Iron excretion increases
   Damage to adjacent structures
       o Stomach – greater curve
       o Colon – splenic flexure
       o Pancreas – tail
   LLL atelectasis
   Subphrenic haematoma &/or abscess
   Pancreatic fistula
   Pancreatitis

How do you prevent OPSI ?

   Vaccination against Hib, meningococcus & pneumococcus
   Give vaccinations 10 days pre-op, then regular vaccination
   Oral penicillin for 2 years in children
Palpable lumps

Give a specific feature suggesting cancer in :

       Parotid swelling
                  Painful, hard, irregular, craggy lump
                  Facial nerve palsy

       Thyroid swelling :
              Hard, irregular gland with evidence of local spread (oesophagus, trachea,
                recurrent laryngeal nerve)
              Solitary thyroid nodule
              Neck lymphadenopathy

       Testicular swelling :
               Hard, irregular, non-tender testicular mass – contained within the testis

What are the causes of a groin lump ?

Above inguinal ligament
 Inguinal hernia (direct or indirect)
 Encysted hydrocele of cord (♂) or canal of Nuck (♀)
 Testicular maldescent
 Iliac lymph node
 Spigelian hernia

Below inguinal ligament
 Inguinal lymph node/s
 Femoral hernia
 Saphena varix
 Femoral aneurysm
 Psoas abscess
 Ectopic testis

 Sebaceous cyst
 Lipoma

What are the causes of forearm lump ?

   Lipoma
   Sebaceous cyst
   Dermoid cyst
   Abscess/furuncle
   Ganglion
   Benign tumour – fibroma, exostosis
   Malignancy – fibro/lipo/leiomyo/rhabdosarcoma
   Rheumatoid nodules
   Lymph nodes
   # callus or malunion
   Radial A aneurysm

Surgical fistula

What is a fistula ?

   An abnormal communication b/w two hollow organs or a hollow organ & the exterior
   Form when a chronic abscess bursts in 2 directions, and so connects 2 epithelial surfaces
   Clinically appears inflamed with a discharge

What conditions maintain the patency of a surgical fistula ?

 High output fistula (> 500cc/day)
 Intestinal destruction (> 50% of circumference)
 Short segment fistula < 2.5cm
 Foreign body (eg G-tube)
 Radiation
 Infection
 Epithelialisation (eg colostomy)
 Neoplasm
 Distal obstruction

Wound healing

What factors can impair wound healing ?

   Systemic factors
           o Age
           o Nutrition – protein, vitamins A & C, zinc, manganese
           o Circulatory status – eg. atherosclerosis, venous drainage
           o Metabolic status – diabetes mellitus
           o Steroid therapy (anti-inflammatory & inhibit collagen synthesis) – give vit A
           o Chemotherapy
           o Ionising radiation
           o Organ failure – uraemia, jaundice
   Local Factors
           o Infection – prolongs the inflammatory phase of wound healing, retards collagen
               synthesis & encourages collagen breakdown
            o Ischaemia – tension (sutures/haematoma/oedema), compartment syndrome, shock,
              anaemia, vascular disease – wounds of face & hands heal faster
            o Poor surgical technique
            o Mechanical factors – eg. early motion, non-union
            o Foreign bodies – sutures, bone, glass – prolongs healing & acts as nidus for
            o Local malignancy (eg Marjolin‟s ulcer)

What are the causes of wound dehiscence ?

   Infection
   Inadequate closure (or too tight causing ischaemia)
   Pulled apart by distractive forces (eg coughing or straining)
   Patient factors – malnutrition, steroids, diabetes, renal/liver failure

What are the usual microbiological causes of wound infection ? What causes predominate
following GI surgery?

   Staphylococci : often coagulase-positive, penicillin-resistant staph carried by the nose, face &
    hands of patients/staff – eg S. aureus, S. epidermis
   Streptococci : β-haemolytic strep (via nasopharynx) can result in wound infection by airborne
    or contact routes – example is Strep. pyogenes
   Coliforms : E. coli, Proteus & Pseudomonas normally inhabit the bowel & are usually
    predominant in wound infections after GIT operations
   Anaerobes : such as Clostridium perfringens (gas gangrene), tetanus & Bacteroides

What systemic ABs would be implied if wound infection is present ?

   Mild-moderate : flucloxacillin (500mg PO q6h) or cephalexin (500mg PO q6h) – gets staph
    & strep
   Gram-negative : amoxicillin+clavulanate (875+125mg PO bd)
   Severe, sepsis : flucloxacillin (2g IV q6h) or cephalothin (2g IV q6h)
   MRSA : vancomycin (1g IV bd)
   Contaminated : flucloxacillin + gentamicin + metronidazole
   Anaerobes : cefoxitin, clindamycin or metronidazole

 Remember to open & pack the wound until infection subsides.

Surgical wound drains

What are the types of wound drains ?

   Open drains : drain fluid collects in gauze pad or stoma bag
   Closed drains : tubes draining into a bag or bottle, eg chest or abdominal drains
       o Jackson-Pratt drain : closed drainage system attached to a suction bulb (“grenade”)
   Active drains : maintained under suction
   Passive drains : no suction – function by differential pressure b/w body cavity & exterior

When would you use a drain ?

   Evacuate established collections of pus, blood or other fluids
   Drain potential collections – remove a potential space for infection
   Indicate possibility of leaking anastomosis or haemorrhage
   Monitor fluid/blood loss – indicate need for IV replacement

How long does the drain remain in-situ ?

   Removed when the volume of effluent diminishes towards zero (< 25mL/day), ie when the
    drain no longer has a purpose

What are the prophylactic ABs used in surgery ?

What is the class, MOA, spectrum & SE’s of gentamicin ?

   MOA : Aminoglycoside antibiotic – bactericidal – inhibits protein synthesis
   Spectrum : Synergy with penicillins – used for gram negatives, esp Pseudomonas, Proteus,
    E. coli, Klebsiella, Enterobacter & Serratia
   SE’s : nephrotoxic, ototoxic & neurotoxic

What is the class, MOA, spectrum & SE’s of ampicillin ?

   MOA : Broad spectrum β-lactam antibiotic – bactericidal – inhibits cell wall synthesis
   Spectrum :
       o Gram positives – strep, staph, listeria
       o Gram negatives – Klebsiella, E.coli, H. influenzae, Proteus, Shigella, Salmonella
   SE’s : diarrhoea, skin rash, allergic reaction

What is the spectrum, MOA & SE’s of metronidazole ?

   MOA : interferes with DNA synthesis
   Spectrum : anaerobes, including parasites, C. difficile & H. pylori
   SE’s : alcohol reaction, dizziness, headache, GI upset, anorexia, urine discolouration

Discuss the lymphatic drainage of…

   Lip (see Scott p168)
       o Upper lip  submandibular LNs
       o Lower lip  submental LNs
   Tongue (SCC spreads earlier than lip SCC – large, firm nodes that become fixed)
       o Tip  submental LNs (bilaterally)
       o Anterior 2/3  submandibular LNs (unilaterally)  deep cervical chain
       o Post 2/3  superior deep cervical LNs (bilaterally)
   Pharynx  Deep cervical LNs
   Neck
        o Upper neck & scalp  occipital LNs
        o Lower neck  supraclavicular LNs & deep cervical LNs
   Arms  axillary LNs
   Thorax skin to level of umbilicus  axillary LNs
   Upper outer breast  axillary LNs (pectoral  central  apical)
   Lungs  bronchopulmonary (hilar LNs)  tracheobronchial LNs  bronchomediastinal
   Oesophagus – tumours disseminate widely
        o Upper  Cervical LNs
        o Lower  Coeliac LNs
   Stomach & duodenum  para-aortic (coeliac) LNs  thoracic duct (mets to L
    supraclavicular (Virchow‟s) nodes known as Troisier‟s sign)
   Liver
        o Peripheral  internal thoracic (parasternal) LNs
        o Deep  coeliac (pre-aortic) LNs  thoracic duct
   Pancreas  coeliac & para-aortic LNs (+/- supraclavicular LNs)
   Spleen  pancreaticosplenic LNs  coeliac (pre-aortic) LNs
   Small intestine follows vessels via lacteals  superior mesenteric LNs
   Large intestine follows vessels  superior & inferior mesenteric LNs
        o Caecum & appendix  ileocolic LNs & mesoappendix LNs  superior mesenteric
   Rectum
        o Upper part  inferior mesenteric LNs
        o Lower part  internal iliac LNs
   Anus  inguinal LNs
   Gonads  lumbar (para-aortic) LNs
   Scrotum  superficial inguinal LNs
   Kidneys & adrenals  lumbar (para-aortic) LNs
   Bladder
        o Superior part  external iliac LNs
        o Inferior part  internal iliac LNs
        o Also to sacral &/or common iliac lymph nodes
   Prostate  obturator, internal iliac & pre-sacral LNs
   Abdominal wall below umbilicus  inguinal LNs
   Legs  inguinal LNs

 Troisier’s sign is an enlarged left supraclavicular (Virchow’s) node
       Look for intra-abdominal pathology (esp. gastric Ca)
       Due to drainage of thoracic duct into L subclavian vein
Discuss SNS innervation levels…

Organ                 PNS innervation                   SNS innervation
Eye                   CNIII – ciliary ganglion          T1-T2 – sup. cervical ganglion
                       pupil constriction               pupil dilation
Lacrimal & salivary   VII/IX cranial nerves             T1-T2
glands                 stimulates secretion             inhibits secretion
Heart                 CNX (vagus)                       T1-T5
                       ↓ HR                             ↑ HR & inotropic state (force)
Bronchi & lungs       CNX (vagus)                       T2-T4 (T6)
                       Bronchoconstriction & ↑          Bronchodilation & ↓ secretions
Lower oesophagus      CNX (vagus)                       T5-T6
Stomach/spleen/       CNX (vagus)                       T6-T10 (coeliac ganglion)
pancreas/liver/GB      ↑ motility & secretions          ↓ motility & secretions
Small bowel           CNX (vagus)                       T9-T11 (coeliac ganglion)
Proximal colon        CNX (vagus)                       T10-T12 (various ganglia)
                                                        Appendix is T10
Distal colon,         Pelvic splanchnic nerve (S2-S4)   Distal colon = L1-L3
bladder, pelvic ♂/♀    Contract SM, urination,         Pelvic ♂/♀ = T11-L2
                      erection                           Inhibit peristalsis, ejaculation
Gonads                Pelvic splanchnic nerve (S2-S4)   T10-L1
Urinary tract (KUB)   CNX (renal plexus)                T10-L1

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