Key FIMs and Paeds Surgical information

Question 1

What are the general complications of fractures?

Answer 1

• Shock: neurogenic, hypovolaemic
• Crush syndrome: Myonecrosis → acute renal failure
• Acute respiratory distress syndrome (ARDS)
• Disseminated intravascular coagulation (DIC)
• Fat embolus
• DVT
• Infection: tetanus, gangrene, septicaemia

Question 2

What are the local bony complications of fracture?

Answer 2

• Sepsis: acute osteitis, acute osteomyelitis, chronic osteomyelitis
• Epiphyseal injury: Types “Salter Harris”
• Joint stiffness/ early OA
• Avascular necrosis
• Malnutrition: e.g. rotational deformity, angulation/ shortening of the bone
• Non- or delayed union. Causes:
  
  • Infection
  • Ischaemia
  • Distraction
  • Interposition of soft tissue
  • Movement of bone ends

Question 3

What are other tissue compications of fracture?

Answer 3

Question 4

How do you examine a fractured limb?

Answer 4

• Always compare w/ normal side
• Closed vs open # : look for skin openings (need invasive therapy urgently)
• Assess distal neurovascular function
  
  • Circulatory function: cap refill, pulses, skin colour (urgent if blood flow compromised)
  • Neurology : test motor & sensory function of major peripheral nerves
• Local inspection and palpation
• Active & passive & stress testing of bone/s & ligaments → ROM, continuity, pain…
• Examine joints above & below (eg # involvement, synovial swelling, fat pad)
• Consider child abuse in infants with #’s

Question 5

Describe how the eye dilates and constrict.

Neural pathway.

Answer 5

• Pupil size depends on the effects of the autonomic nervous system and the iris muscle.
• From the autonomic nerve standpoint, the parasympathetic system constricts the iris, while the sympathetic channels dilate the iris.
• The sympathetic system begins in the hypothalamus, descends through the brain stem (including the lateral medulla) and into the cervical cord to synapse in the ciliospinal center of Budge-Waller at the C8-T1 level.
• The second-order neuron then exits the C8-T1 nerve root, travels over the lung apex, and ascends to the superior cervical ganglia with the carotid artery. The third-order neuron leaves the superior cervical ganglia to ascend as a plexus around the internal carotid artery through the cavernous sinus, where fibers destined for the pupil dilator and the Mueller muscle of the eyelid travel with the trigeminal nerve through the superior orbital fissure to their orbital targets. Fibers destined to modulate sweating of the face travel with the external carotid artery.
• The parasympathetic fibers begin in the Edinger-Westphal subnucleus of cranial nerve III in the midbrain. Parasympathetic fibers travel with the oculomotor (cranial III) nerve, traverse the cavernous sinus, and enter the orbit via the superior orbital fissure to synapse in the ciliary ganglia. The short ciliary nerves then innervate the iris sphincter and muscles of accommodation.

Question 6

How do you report fractures to an orthopaedic registrar?

Answer 6

• Name and details of patient and technique (types of views performed and position)
• Anatomical site: which side, which bone, where it is (proximal 1/3, mid-shaftor distal 1/3)
• Open or closed (gas in soft tissue may indicate open # or infection)
• Fracture line: transverse/oblique/spiral/comminuted/greenstick; complete/incomplete
• Degree of displacement or angulation of the distal segment
  
  • Undisplaced = fragments in rough anatomical position, reduction not required
  • Displacement is due to traumatic force, gravity &/or muscle pull
    
    • Displacement/apposition: What % of bone ends remain in contact & in what direction (eg dorsal vs volar, valgus vs varus)
    • Angulation/tilt: anterior or posterior, medial or lateral
    • Rotation : About longitudinal axis, distal fragment cf proximal fragment
    • Length of bone : distraction (↑ length) or overlap/impaction (↓ length)
• Involvement of articulations
  
  • Does # line involve a joint or the epiphysis?
  • In kids, involvement of epiphyseal plate (Salter-Harris classification)
• Bone texture: Does the bone look normal or is there evidence that it is a pathological #?
• Soft tissue : calcification, gas, FBs, etc
• Neurovasculature – presence of pulses; motor & sensory function; compartment syndrome.

Question 7

Describe what compartment syndrome is, its clinical features and management?

Answer 7

• Soft tissue swelling (oedema) & bleeding into a tight osterofascial compartment causing increased compartment pressure (non-expansile) therefore impairing venous drainage. If pressure >40mmHg occlusion of arterial input causing ischaemia and necrosis of contained muscles and nerves (within 12 hrs) and later muscle fibrosis.
• Major causes:
  
  • # of forearm, elbow, or upper tibia; vascular compromise, reperfusion injury, compressive dressings, any MSK injury.
  • Most commonly involves anterior compartment of calf following closed titbial #.
• Complications: fibrotic contractions of muscle (e.g. Volkmann’s ischaemic contracture of forearm flexor); nerve damage; myoglobinuria.
• Early signs and symptoms: Diagnosis is made almost solely on the clinical findings.
  
  • Swollen and tense limb - palpation of firm, tender compartment
  • Unrelenting pain out of proportion to hte injury which is not relieved by opiates.
  • Passive hyperextension of toes or fingers will increase ↑↑ pain in calf or forearm
  • Loss of sharp sensation
• 6 P’s: pain, pallor, pulselessness, paralysis, paraesthesia and perishingly cold.
• Ix: measure intracompartmental pressure (urgent Tx if >40mmHg) - normal is 0-10mmHg.
• Mx if >30mmHg: elevate & ice limb; hyperbaric therapy → some advocate fasciotomy.
• Mx if >40mmHg: decompression of skin and fascial compartment (open fasciotomy) within 4 hrs → wound left open until swelling had subsided
  
  • Monitor UO for signs of myoglobinuria and ARF

Question 8

Describe the parts of a normal bone.

Answer 8

• 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)
  
  • Outer fibrous layer – dense fibrous CT (with BV’s, lymph V’s, nerves)
  • Inner osteogenic layer – mesenchymal osteoprogenitor cells (can become osteoblasts or osteoclasts) → bone growth in diameter, repair
• Endosteum: Internal covering – CT monolayer of osteoprogenitor cells

Question 9

Describe the 2 types of bone growth.

Answer 9

Intramembranous ossification

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

Endochondral ossification

• Occurs in most bones, eg long bones
  
  • Hyaline cartilage model from mesenchymal tissue
  • Outer layer of mesenchymal cells, chondroblasts & osteoprogenitor cells form perichondrium
  • BVs enter diaphysis, with chondrocyte proliferation (↑ length/width) & osteoblasts beginning osteoid formation → primary ossification centre
  • Continued osteoid formation & remodelling forms central network of trabecular bone
  • After birth, BV’s invade the epiphysis & bring osteoprogenitor cells, which convert the cartilage model into trabecular bone, forming the secondary ossification centre
  • Remaining hyaline cartilage forms epiphyseal plate in the metaphysis & articular cartilage
  • 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
  • Puberty → ↑↑ hormones therefore ↑↑ bone growth > cartilage proliferation therefore 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 therefore enlarges marrow cavity while retaining cortical thickness

Question 10

Epiphyseal injury is classified by the Salter-Harris classification.
Describe this classification system.

Question 11

How do you describe a lump?

Answer 11

1. Size
2. Site
3. Shape
4. Surface
5. Margns/edges
6. Tenderness
7. Composition:
   
   1. Consistency:
   2. Fluctuation (fluid-filled)
   3. Fluid thrill
   4. Transillumination (fluid filled)
   5. Resonance
   6. Pulsatility
8. Reducibility
9. Mobility/fixation of lump and its tissue layer
10. Overlying skin
11. Regional lymph nodes
12. Other: general physical examination

Question 12

What are the ortopaedic emergencies?

Answer 12

• Open fracture/dislocation (OT in 6 hours)
• Vascular injuries
• Compartment syndrome
• Neural compromise, esp. spinal injury
• Acute septic arthritis or osteomyelitis
• Exsanguinationg pelvic #
• Hip dislocation

Question 13

What are the indications for open reduction of fractures?

Answer 13

NOCAST

• N - Non-union, failure of closed reduction or unstable fractures prone to redisplacement
• O - Open # (needs ex fix)
• C - Compromise of neurovascularture; compartment syndrome; co-morbidities
• A - Articular surface malalignment (intra-articular#, requires anatomic reduction)
• S - Salter-Harris III or IV
• T - Trauma patient’s - earlier mobilisation & decrease risk of ARDS
• Pathological fractures

Question 14

What is external fixation?

Why is it used?

What are the complications?

Answer 14

• A scaffold or ganry attached to threated pins set in the bone fragments (e.g. ring rixator)
• Reasons for using external fixation - see NOCAST above
  
  • Open fractures
  • Fractures with skin loss or infection
  • Able to easily adjust fragments
  • Non-union or malunion
• Complications:
  
  • Non-union (if hold fracture fragments too tight)
  • Pin-track infection
  • neurovascular damage
  • Refracture when Ex Fix is removed

Question 15

What is a Colles #?

What are the complications?

Why use external fixation?

Answer 15

• FOOSH in older women
• # distal radius with dorsal angulation, often assoc # 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 and ulnar deviation); cast worn for 4 weeks, check at 1 week
• Complications:
  
  • Median N damage/compression - runs right across site of Colles’ fracture
  • Rupture of extensor pollicus longus (EPL) tendon - EPL runs across # site on dorsum of wrist
  • Sudeck’s atrophy (reflex sympathetic dystrophy) - hand becomes stiff, blotchy and cold
  • Malunion - fracture is unstable & bone is crushed, amy require operative intervention
• External fixation (including precutaneous pin fixation) for intra-articular and displace fractures.

Question 16

How do you manage an open fracture?

Answer 16

• An open fracture is suspected if: wound at # site, leaking haematoma, or protruding bone.
• Emergency management & assessment
  
  • ABCs
  • Assess entire limb, esp neurovasculature
  • Asses wound: state of skin around wound, does wound communicate with #?
  • Assess contaiminated - remove gross debris, clean wound w/ sterile saline, chlorhexidine & cetrimide; cover wound w/ sterile dressing
  • Reduce # & place in backslab, keep NBM
• Give antibacterial prophylaxis: (IV fluclox + benzylpen +/- gent/flagyl) & tetanus toxoid/Ig
• OT in 6 hrs for debridement -extend wound, thoroughly irrigate, remove dead tissue, pack wound & leave open for dynamic compression plate in 3-5 days
• OT to treat the fracture - grade III requires external fixation.

Question 17

What is neuropraxia? Axonotmesis? Neurotmesis?

What are the clinical features?

Answer 17

• Neuropraxia: minimal nerve damage (localised demyelination or compression) - axon intact, but conduction ceases transiently.
  
  • Spontaneous recovery in days or weeks
• Axonotmesis (axonal separation): severe axon damage by compression or traction.
  
  • Distal degenerate, but investing sheath remains intact therefore delayed recovery (1-2mm/day)
• Neurotmesis: complete severance of a peripheral nerve
  
  • Spontaneous recovery does NOT occur → needs surgical repair
  • Assoc w/ degeneration of nerve fibre distal to point of severance.
• Clincal features:
  
  • Symptoms: numbness, sensory alterations (e.g. paraesthesia), weakness.
  • Inspection: skin smooth and skiny, muscle wasting
  • Palpation: decreased power and sensation, Tinel’s sign
  • Tinel’s sign: tingling at lesion site or more distal when the latter is percussed.

Question 18

What nerve would you use for a graft? Why?

Answer 18

• Open injuries: explore at primary operation - if cleanly divided and repair immediately, otherwise leave alone and 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 (e.g. Sural nerve) can be used, followed by splintage
• Only thin nerves are useful, as thick nerves underfo central necrosis after grafting.

Question 19

What are the signs of facial nerve palsy?

How do you tell if its UMN or LMN?

Answer 19

Facial nerve lesion

• LMN lesion of facial nerve causes ipsilateral complete paralysis of that side of the face.
  
  • may be pontine, posterior fossa, petrous termporral bone, #, viral infection
  • If before chorda tympani braches off, will also have taste loss
• UMN lesion will cause contralateral paralysis of the facial muscles below the level of the forehead, with the frontalis and 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)
• Lookm up and wrinkle forehead → look for loss of wrinkline (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’f 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 separaetly each side

Question 20

Describe the anatomy of the facial nerve

Answer 20

• Facial nerve provides motor to muscles of facial expression, and taste via chorda tympani.
• Motor course - lateral surface of pons → thru internal acoustic canals → internal auditory meatus → exits skull at stylomastoid foramen → thru parotid gland → 5 branches.
• The UMN from the motor homunculus innervates the facial nerve nucleus in the brainstem
• facial nucleus receives crossed and uncrossed fibres by way of the corticobulbar tract
• UMN from RHS innervates whole right nucleus as well as forehead area of RHS nucleus. Conversely, left UMN innervates whole LHS nucleus and forehead area of RHS nucleus.
• Therefore facial muscles below the forehead receive contralateral cortical innervation, while those muscles of the forehead receive bilateral innervation (NB skin of forehead via CNV₁)

Question 21

Describe the anatomy of the ulnar nerve.

Answer 21

• Medial arm (medial to brachial artery) → superficial course thru ulnar groove (cubital tunnel) next to medial epicondyle of ulna (vulnerable to injury = funny bone) → medial to ulna in forearm
• Motor: FCU and medial 1/2 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: medial 1/3 of hand, little finger (V) & medial 1/2 of ring (IV) finger (palmar & dorsal).

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
  
  • Hyperextension of MCPJ 4&5 (lumbricals gone)
  • Unable to flex 4th and 5th fingers at DIPJ’s, PIPJ’s bent
  • Abducted thumb (adductor pollicis

Question 22

What are the causes of low back pain?

Answer 22

• Classified into mechanical, non-mechanical & non-spinal back pain by Hx and O/E
• >90% of pts no anatomical cause is found; _~70% are presumed to be intervertebral dysfunction. <10% have structural lesions.

Question 23

What are the pathological causes of low back pain?

Answer 23

Question 24

List >8 red flag signs for low back pain indicating radiologic investigation.

Answer 24

• 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
• Increased ESR

Question 25

List >5 conditions in which bone scan investigation of lower back pain would help?

Answer 25

• Mets or primary malignancy - 90% positive
• Infections
• Fractures
• Osteomalacia/osteodystrophy
• Spondylarthropathies (ankylosing spondylitis, psoriasis, IBD, reactive arthritis) - SI joints positive
• Hyperparathyroidism - 50% positive
• Paget’s disease

Plain x-rays are only 70% sensitive and give the diagnosis only 33% of the time.

Question 26

What are the causes and classification of scoliosis?

Answer 26

• Postural (non-structural) scoliosis - compensatory to some condition outside the skin e.g. short leg, pelvic tilt or prolapsed IV disc
  
  • Disappears on sitting)
• Structural scoliosis - caused by bony abnormality or vertebral rotation -secondary curves nearly always develop to counterbalance the primary deformity
  
  • Deformity is fixed & does not disappear with changing posture
  • Major typoes:
    
    • Adolescent idiopathic scoliosis - usually thoracic curve convex to the right - presents before puberty and progresses until skeletal growth ceases
    • Infantile (congenital) scoliosis - may regress
    • Neuromuscular scoliosis, e.g. polio, cerebral palsy
    • Osteopathic scoliosis (congenital vertebral abnormality)

Question 27

What are the clinical signs of scoliosis?

Answer 27

• Curved spine accentuated by bending forwards (postural curves disappear)
• Shoulder & waist are asymmetrical
• Thoracic scoliosis - rib angle protrude (posterior hump), breasts asymmetrical

Question 28

What are the causes of a painful hip?

Answer 28

Question 29

What is the Trendelenburg test?

Answer 29

• Patient asked to stan, unassisted, on each leg; Lift other leg by bending knee (not hip)
• Weight-bearing hip held stable by abductors and pelvis rises on unsupported side (-ve sign)
• If the hip is unstable, or very painful, the pelvis drops on the unsupported side (+ve sign)

Question 30

What may cause a positive Trendelenburg sign? Give 4 causes.

Answer 30

• Dislocation or subluxation of hip
• Weakness of the ABductors: gluteus medius & minimus via superior gluteal nerve
• Shortening of the femoral neck
• Any painful disorder of the hip (causes gluteal inhibition)

Question 31

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

Answer 31

• 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 and decrease ROM in 3-8 year olds (male>female)
• DDx = transient synovitis (irritable hip)

Radiological signs - Frogleg view

• Initally normal (cold on bone scan) - bone necrosis
• Increased density of epiphysis and widening of the joint space - revascularisation and repair
• Fragmentation of the epiphysis (collapse and remodelling)
• Epiphysis flattened and enlarged (coxa plana and coxa magna)

Management:

• Containment of femoral head within acetabulum (therefore more likely to retain normal shape) by abduction & internal rotation using ‘broomstick’ plaster or a removable splint
• Alternative is osteotomy (late Dx)