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3rd year - Surgery > Orthopedic Surgery > Flashcards

Orthopedic Surgery Flashcards

1
Q

What is an intra-articular fracture

A

fracture line crossing articular cartilage and enters joint

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2
Q

What is a physeal fracture

A

Growth plate fracture

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3
Q

How do you describe a displaced fracture

A

for displaced fracture, displacement described as distal component relative to more proximal fracture fragment

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4
Q

What is a distracted fracture

A

fracture fragments separated by gap

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5
Q

How is an angulated fracture described

A

angulated fracture is described in terms of direction of fracture apex

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6
Q

How is a translated fracture described

A

translation described in terms of distal relative to proximal segment and percentage of overlapping bone at fracture site

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7
Q

In regards to fracture management, what is the xray rule of 2’s

A

2 sides - always get bilateral (e.g. left and right leg) for comparison

2 views - AP + lateral

2 joints - joint above and joint below

2 times - before and after reduction

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8
Q

Indication for reduction

A

Displaced fracture

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9
Q

How to perform closed reduction

A

apply traction in long axis of limb and reverse mechanism that produced fracture with IV sedation and muscle relaxation

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10
Q

Indication for open reduction

A 
N = Non-union
O = Open fracture
C = neurovascular Compromise
A = intra-Articular fracture
S = epiphyseal fracture Salter-Harris >3
T = poly-Trauma

failure of closed reduction

cannot cast or apply traction due to site

pathologic fracture

potential for improved function with ORIF

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11
Q

What are potential complications of open reduction

A 
infection
mal-union
non-union
implant failure
new fracture
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12
Q

What are steps that should be completed post reduction

A
  1. re-check neuromuscular status

2. obtain post-reduction X-ray

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13
Q

How to maintain reduction post reduction

A

external stabilization = splints, casts, traction, external fixator

internal stabilization = percutaneous pinning, extra-medullary fixation (screws, plates, wires), intra-medullary fixation (rods)

follow up to evaluate bone healing and reduction

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14
Q

Fracture healing stages through time

A

fracture usually heal by 1-2 years

<1 months: hematoma, macrophage around fracture site

1 month: osteoclast remove sharp edges, callus formation within hematoma

1-3 months: bone formation within callus, bridging fragments

6-12 months: cortical gap bridged by bone

1-2 years: normal architecture achieved through remodelling

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15
Q

Local, early general fracture complications

A

Compartment syndrome

Neurological injury

Vascular injury

Infection

Implant failure

Fracture blisters

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16
Q

Systemic early general fracture complications

A

Sepsis

DVT

PE

ARDS secondary to fat embolism

Hemorrhagic shock

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17
Q

Local late general fracture complications

A

Mal/non-union

AVN

Osteomyelitis

HO (heterotopic ossification)

Post-traumatic osteoarthritis

Joint stiffness/adhesive capsulitis

CRPS (complex regional pain syndrome) type I/RSD (reflex sympathetic dystrophy)

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18
Q

Compartment syndrome etiology

A

intra-compartmental causes

  1. fracture: tibial shaft fracture, pediatric supracondylar fracture, forearm fracture
  2. crush injury
  3. ischemia-reperfusion injury

extra-compartmental causes

  1. constrictive dressing: circumferential cast, poor positioning during surgery
  2. circumferential burn
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19
Q

Compartment syndrome pathophysiology

A

compartment syndrome is defined by increased interstitial pressure in anatomical compartment (forearm, calf) where muscle and tissue are bounded by fascia and bone with little room for expansion

1) increased pressure lead to decreased venous and lymphatic drainage, propagating increase in intra-compartmental pressure
2) high intra-compartmental pressure exceed capillary perfusion pressure, stopping blood supply
3) lack of blood supply result in muscle and nerve anoxia -> ischemia -> necrosis

muscle and nerve anoxia result in anaerobic metabolism, resulting in metabolic lactic acidosis

necrosis of nerve and muscle result in edema and swelling into compartment, further increasing intra-compartment pressure

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20
Q

Compartment syndrome clinical presentation

A

history suggestive of cause

early signs: pain with active contraction and passive stretch of muscle in compartment; swollen and tense compartment

large signs: 5 Ps

  1. Pain out of proportion for injury and not relieved with analgesia
  2. Paresthesia -> 3. Pallor
  3. Paralysis
  4. Pulselessness
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21
Q

Compartment syndrome most important symptoms

A

pain out of proportion and with passive stretch of muscle are most important and early signs of compartment syndrome

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22
Q

Compartment syndrome complications

A
  1. Muscle / nerve necrosis
  2. Lactic acidosis
  3. Rhabdomyolysis
  4. Myoglobinuria -> renal failure
  5. Volkmann’s ischemic contracture (ischemic necrosis of muscle resulting in fibrosis and calcification resulting in muscle and joint contracture)
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23
Q

Compartment syndrome diagnosis

A

compartment syndrome is a clinical diagnosis based on history and physical exam

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24
Q

Compartment syndrome management

A

1) Non-operative measures
remove constrictive dressings (cast, splints)
elevate limb at level of heart

2) Operative measures
procedure = urgent fasciotomy leaving open for 2-3 days -> wound closure +/- necrotic tissue debridement

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25
Q

Open fracture management

A 
1) Source control
removal of foreign material from wound
irrigate wound with normal saline if wound is grossly contaminated
cover wound with sterile dressing
reduce and splint fracture

2) Prevention of infection
determine tetanus vaccination status and give tetanus vaccination if required
immediate IV antibiotics based on Gustilo Classification of Open Fracture
Gustilo Classification of Open Fracture predicts risk of infection:
grade 1 = 0-2%
grade 2 = 2-10%
grade 3 = 10-50%

3) Surgery
Prepare for OR:
NPO, blood work (CBC, electrolytes, renal function, aPTT, INR), ECG, chest X-ray

Procedure:

  1. operative irrigation and debridement within 6-8 hours
  2. open reduction and internal fixation (ORIF)
  3. traumatic wound left open to drain (delayed closure) or vacuum assisted closure dressing
  4. re-examination with repeat incision and drainage within 2 days, then repeat 2-3 days as necessary
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26
Q

What is the Gustilo Classification of Open Fractures

A

Grade 1
Length of open wound: <1 cm
Description: Minimal contamination and soft tissue injury. Simple or minimally comminuted fracture
Prophylactic antibiotic regimen: First gen cephalosporin (cefazolin) x3d
If allergy use fluroquinolone
If MRSA +ve use vancomycin

Grade II
Length of open wound: 1-10 cm
Description: Moderate contamination. Soft tissue injury.
Prophylactic antibiotic regimen: First gen cephalosporin (Cefazolin) x3d +
Gram-negative coverage (gentamycin) x3d minimum

Grade III+
Length of open wound: >10 cm
Description:
IIIA - extensive soft tissue injury with adequate ability of soft tissue to cover wound
IIIB - Extensive soft tissue injury with periosteal stripping and bone exposure, inadequate soft tissue to cover wound
IIIC - vascular injury/compromise
Prophylactic antibiotic regimen: as per grade II
For soil contamination, penicillin is added for clostridial coverage

Note that any high energy, comminuted fracture, shot gun, farmyard/soil/water contamination, exposure to oral flora, or fracture more than 8h old is immediately classified as grade III

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27
Q

What are the motor tests that can test each of the following levels: C5, 6, 7, 8, T1

A 
C5 = shoulder abduction, elbow flexion
C6 = elbow flexion and wrist extension
C7 = elbow extension and wrist flexion
C8 = finger flexion
T1 = finger abduction
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28
Q

What are the nerve roots, plexus and terminal branches that peripherally innervate the arm

A

C5-T1 -> brachial plexus -> 5 terminal branches MARMU = musculocutaneous, axillary, radial, median, ulnar nerve

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29
Q

Musculocutaneous nerve motor and sensory distribution

A

motor = biceps & brachialis (elbow flexion)

sensory = lateral forearm

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30
Q

Axillary nerve motor and sensory distribution

A

motor = deltoid (shoulder abduction) & teres minor

sensory = seargeant patch on lateral shoulder

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31
Q

What is a potential complication that can occur in a proximal humerus fracture

A

Axillary nerve have risk of being damaged in proximal humerus fracture

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32
Q

Radial nerve motor and sensory distribution

A

motor = triceps (elbow extension), all muscles in posterior compartment (extensors) of forearm (wrist extension, finger extension)

sensory = first web space of dorsal hand

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33
Q

What is a potential complication that can occur in a mid shaft humerus fracture

A

radial nerve have risk of being damaged in mid-shaft humerus fracture

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34
Q

Median nerve motor and sensory distribution

A

motor = most of anterior compartment (flexors) of forearm (wrist flexion, finger flexion)

sensory = 1st, 2nd, 3rd and radial half of 4th finger; radial portion of palm

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35
Q

What is a potential complication that can occur in a supracondylar fracture

A

median nerve have risk of being damaged in supra-condylar fracture

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36
Q

Ulnar nerve motor and sensory distribution

A

motor: flexor carpi ulnas (wrist flexion), medial half of flexor digitorum profondus (finger flexion), interosseus muscle (finger abduction & adduction)

sensory = ulnar half of 4th and 5th finger; ulnar portion of palm

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37
Q

What is a potential complication that can occur in a fracture involving the medial epicondyle

A

ulnar nerve have risk of being damaged in fracture involving medial epicondyle

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38
Q

Supracondylar fracture epidemiology

A

most common in children (peak age ~7 years)

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39
Q

Supracondylar fracture mechanism

A

95% cases due to extension injuries with falling onto outstretched hands
5% cases due to flexion injuries

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40
Q

Supracondylar fracture potential complications

A

neuromuscular compromise of median nerve, radial nerve, radial artery

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41
Q

Supracondylar fracture investigations

A

X-ray elbow: fracture line in distal humerus above condyles, commonly displaced posteriorly, may have fat pad sign at elbow

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42
Q

Supracondylar fracture treatment

A

non-displaced and uncomplicated fracture: long arm plaster slab with elbow in 90 degrees flexion x 3 weeks

indication for surgical reduction: neurovascular compromise, displacement, open fracture

surgery: open reduction with percutaneous pinning followed by limb cast with elbow in 90 degrees flexion; open reduction and internal fixation for adults

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43
Q

Galeazzi fracture mechanism

A

falling onto outstretched hand with axial loading of pronated forearm

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44
Q

Galeazzi fracture clinical presentation

A

fracture at distal 1/3 of radius near junction of metaphysis and diaphysis

unstable or widening of distal radial ulnar joint (DRUJ)

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45
Q

Galeazzi fracture investigation

A

X-ray of wrist:
fracture at distal 1/3 radius

shortening of distal radius >5mm relative to distal ulna

widening or dislocation of DRUJ

intact ulna

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46
Q

Galeazzi fracture treatment

A

1) ORIF of radius and then assess DRUJ stability by balloting distal ulna relative to distal radius

2)
stabilization of DRUJ: splint for 48 hours if DRUJ stable and reducible
ORIF or percutaneous pinning with long term cast in supination for 6 weeks if DRUJ is unstable

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47
Q

Colles’ fracture epidemiology

A

most common wrist fracture
common in older adults age >40
risk factor: osteoporosis

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48
Q

Colles’ fracture mechanism

A

falling onto outstretched hand with wrist in extension

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49
Q

Colles’ fracture clinical presentation

A

swelling, tenderness and bruising at wrist

dinner fork deformity (dorsal angulation and displacement of distal radius)

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50
Q

Colles’ fracture investigation

A

X-ray wrist: distal radius fracture with dorsal displacement and angulation, may involve distal ulna

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51
Q

Colles’ fracture treatment

A

goal of treatment = restore radial height, radial inclination (22 degrees), volar tilt (11 degrees), DRUJ stability, forearm rotation

1st line = closed reduction, which is traction with wrist extension to exaggerate injury -> traction with ulnar deviation, forearm pronation and flexion of distal fragment

closed reduction done under hematoma block (local anesthetic injection into fracture side) or conscious sedation

stabilization post closed reduction = dorsal slab or short arm (below elbow) cast for 5-6 weeks with follow up X-ray weekly for first 3 weeks and at cessation of immobilization to ensure reduction is maintained

2nd line = ORIF if closed reduction fails (post reduction X-ray shows radial shortening >3mm or dorsal tilt >10 degrees or intra-articular displacement / step off >2mm)

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52
Q

Smith fracture mechanism

A

falling onto the back of a flexed hand

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53
Q

Smith fracture clinical presentation

A

swelling, tenderness and bruising at wrist

volar angulation and displacement of distal radius

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54
Q

Smith fracture investigation

A

X-ray wrist: distal radius fracture with volar displacement and angulation, may involve distal ulna

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55
Q

Smith fracture treatment

A

usually unstable, therefore requiring ORIF

closed reduction with hematoma block = reduction opposite of Colle’s fracture

stabilization by long arm cast in supination for 6 weeks

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56
Q

What are the most common complications following wrist fracture

A
  1. poor grip strength
  2. wrist stiffness
  3. radial shortening
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57
Q

Wrist fracture prognosis

A

80% cases have restored to complete normal function in 6-12 months

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58
Q

Wrist fracture early complications

A 
difficult reduction, loss of reduction
compartment syndrome
extensor pollicis longus tendon rupture
acute carpal tunnel syndrome
finger swelling due to venous or lymphatic block
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59
Q

Wrist fracture late complications

A 
mal-union, radial shortening
painful wrist secondary to ulnar prominence
frozen shoulder
post-traumatic arthritis
carpal tunnel syndrome
complex regional pain syndrome
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60
Q

Scaphoid fracture epidemiology

A

common in young men

most common carpal bone fracture

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61
Q

Scaphoid fracture mechanism

A

falling onto outstretched hand with impaction of scaphoid on distal radius

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62
Q

Scaphoid fracture location

A

fracture at waist of scaphoid in 70% cases

fracture at proximal scaphoid in 20% cases

fracture at distal pole of scaphoid in 10% cases

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63
Q

Scaphoid fracture clinical presentation

A

anatomical snuff box tenderness

pain with wrist movement

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64
Q

Scaphoid fracture complication

A

avascular necrosis of bone proximal to fracture especially if proximal pole injury, delayed union, or non-union

blood supply of scaphoid runs distal to proximal, so more proximal fracture of scaphoid have higher risk of avascular necrosis and also non-union

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65
Q

Scaphoid fracture investigation

A

X-ray of wrist and scaphoid views: fracture line of scaphoid

scaphoid fracture may not be evident on X-ray for up to 2 weeks post injury, so patient complaining of wrist pain and anatomical snuff box tenderness with negative X-ray should be treated with cast with repeat X-ray in 2 weeks to rule out fracture followed by CT or MRI if repeat X-ray still negative

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66
Q

Scaphoid fracture treatment

A

Suspected scaphoid fracture with negative X-ray: long arm thumb spica cast with repeat X-ray in 2 weeks

Non-displaced scaphoid fracture (<1mm displacement and <15 degrees angulation): long arm thumb spica cast for 4 weeks then short arm cast until radiographic evidence of
healing, usually for 2-3 months

Displaced scaphoid fracture (>1mm displacement or >15 degrees angulation): ORIF with headless / countersink compression screw or percutaneous K-wire fixation

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67
Q

Pelvic fracture mechanism

A

young: high energy trauma (direct or force transmitted longitudinally through femur)
elderly: fall from standing height, low energy trauma

most commonly lateral compression of pelvis, but may be due to vertical shear or anteroposterior compression

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68
Q

Pelvic fracture clinical presentation

A

local pelvic swelling or tenderness
deformity of lower extremity
pelvic instability

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69
Q

Pelvic fracture complication

A

hemorrhage (life threatening)

injury to rectum or urogenital structure

obstetrical difficulty

sexual & voiding dysfunction

persistent SI pain

post-traumatic arthritis of hip

high risk of DVP and PE

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70
Q

Pelvic fracture classification

A

Tile classification for stability in pelvic fracture

Type A
Stability - rotationally and vertically stable
Description -
A1: fracture not involving pelvic ring
A2: minimally displaced fracture of pelvic ring (ex. ramus fracture)

Type B 
Stability - rotationally unstable, vertically stable 
Description - 
B1: open book 
B2: lateral compression - ipsilateral 
B3: lateral compression - contralateral 
Type C 
Stability - rotationally and vertically unstable 
Description - 
C1: unilateral 
C2: bilateral 
C3: associated acetabular fracture
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71
Q

Pelvic fracture investigations

A

X-ray pelvis:
AP
Inlet & outlet view
Judet view (oblique)

CT pelvis: evaluation of posterior pelvic injury and acetabular fracture

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72
Q

Pelvic fracture treatment

A

1) Trauma management
ABCDE

2) Treatment of complication
assess for genitourinary injury: rectal exam, vaginal exam, hematuria, blood at urethral meatus
if genitourinary injury, then considered open fracture and treat accordingly

treatment for hemorrhage: aggressive IV fluid and blood resuscitation, stabilization of pelvis with pelvic binder or sheeting, external fixation or emergent angiography embolization,
laparotomy if intra-abdominal bleed

2) Treatment of fracture
stable and non-displaced fracture: non-operative treatment, protected weight bearing

unstable and / or displaced fracture: surgical external or internal fixation

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73
Q

Pelvic fracture indication for surgery

A

Indication for surgery includes any of the following:

  1. unstable pelvic ring injury
  2. disruption of anterior and posterior SI ligament
  3. symphysis diastasis >2.5cm
  4. vertical instability of posterior pelvis
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74
Q

Hip fracture epidemiology

A

common elderly

risk factors: osteoporosis

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75
Q

Hip fracture mechanism

A

young: fall from height, motor vehicle collision
elderly: fall from standing height, pathologic fracture

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76
Q

Hip fracture classification

A

intra-capsular: femoral head (capital) fracture and femoral neck (sub-capital, transcervical, basicervical)

extra capsular: inter-trochanteric and subtrochanteric

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77
Q

Hip fracture clinical presentation

A 
acute onset hip pain
unable to weight bear
shortened and externally rotated leg
painful hip range of motion
bruising at back of upper thigh
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78
Q

Hip fracture complications

A

deep vein thrombosis

non-union

displacement (mal-rotation, mal-alignment)

avascular necrosis (in capital and sub-capital fracture)
femoral head supplied by distal to proximal blood supply along femoral neck to head (medial and lateral femoral circumflex arteries), thus fracture of femoral neck may disrupt blood supply causing avascular necrosis of femoral head
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79
Q

Hip fracture investigations

A

X-ray hip AP and lateral: fracture line, may have displacement or angulation of distal femur

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80
Q

Hip fracture treatment

A

a) femoral neck fracture management based on Garden classification
type 1 & 2: internal fixation to prevent displacement
type 3 & 4: ORIF in young; hemiarthroplasty (replacing broken bone with metal implant) or total hip replacement in elderly

b) intertrochanteric fracture: closed reduction under fluoroscopy, followed by dynamic hip screw or intramedullary nail
c) sub-trochanteric: closed or open reduction under fluoroscopy, followed by plate fixation or intramedullary nail

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81
Q

What is the Garden Classification of femoral neck fractures

A 
Type I 
Displacement: None
Extent: Incomplete
Alignment: Valgus 
Trabeculae: Malaligned
Treatment: Internal fixation to prevent displacement 
Type II 
Displacement: None
Extent: Complete 
Alignment: Neutral 
Trabeculae: Aligned 
Treatment: Internal fixation to prevent displacement 
Type III 
Displacement: Some 
Extent: Complete 
Alignment: Varus 
Trabeculae: malaligned 
Treatment: 
Elderly: hemi/total hip arthroplasty 
Young: ORIF 
Type IV
Displacement: Complete 
Extent: Complete 
Alignment: Varus 
Trabeculae: Aligned 
Treatment: 
Elderly: hemi/total hip arthroplasty 
Young: ORIF
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82
Q

Patellar fracture mechanism

A

direct blow to patella: fall, motor vehicle collision

indirect trauma by sudden flexion of knee against contracted quadriceps

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83
Q

Patellar fracture types

A

Vertical

Comminuted

Displaced

Undisplaced

Lower/upper pole

Osteochondral

Transverse

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84
Q

Patellar fracture clinical presentation

A 
patellar tenderness
inability to extend knee or straight leg raise
proximal displacement of patella
palpable patellar deformity
knee joint effusion, hemarthrosis
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85
Q

Patellar fracture complication

A

knee stiffness
non-union
infection

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86
Q

Patellar fracture investigations

A

X-ray knee AP, lateral, skyline

fracture line on patella

lipohemarthrosis (fat and / or blood) in pre-patellar pouch

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87
Q

Patellar fracture treatment

A

goal: restore extensor mechanism with maximal articular congruency

non-displaced (step off <2-3mm and fracture gap <1-4mm): straight leg immobilization 1-4 weeks with hinged knee brace, physiotherapy with quadriceps strengthening

indication for ORIF: displaced (step off >3mm or fracture gap >4mm), comminuted patellar fracture, disrupted extensor mechanism

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88
Q

What normal variant can be confused with a patellar fracture

A

normal variant have bi-partite patella, but it has well corticated border where extra piece does not fit exactly into adjacent patellar defect

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89
Q

Tibial plateau fracture mechanism

A

axial loading: fall from height

femoral condyles driven into proximal tibia

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90
Q

Tibial plateau fracture clinical presentation

A

lateral fractures more common than medial fractures
medial fractures associated with concomitant vascular injuries
knee effusion and swelling
inability to bear weight

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91
Q

Tibial plateau fracture complications

A

ligament injuries, meniscal injuries, avascular necrosis, infection, osteoarthritis

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92
Q

Tibial plateau fracture investigation

A

X-ray knee AP lateral:
depression of tibial fracture
oblique fracture line from tibial plateau
lipohemarthrosis (fat and / or blood) in pre-patellar pouch

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93
Q

Tibial plateau fracture treatment

A

tibial plateau depression <3mm: straight leg immobilization for 4-6 weeks with progressive ROM and weight bearing

tibial pleaeau depression >3mm: ORIF with bone grafting to elevate depressed fragment

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94
Q

Ankle fracture mechanism

A

commonly rolled ankle (inversion or eversion), resulting in ipsilateral ligament tears & bony avulsion and contralateral shear fractures

inversion -> lateral malleolus fracture + tear of anterior distal tibiofibular ligament + distal fibular fracture + transverse medial malleolus fracture

eversion -> avulsion of medial malleolus + anterior distal tibiofibular ligament tear + fibular fracture

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95
Q

Ankle fracture classification

A

Weber’s ankle fracture classification for lateral malleolus fracture

type A (infra-syndesmotic) = inversion injury with avulsion of lateral malleolus +/- shear fracture of medial malleolus
below level of ankle joint (talar dome)
stable if medical intact 
type B (trans-syndesmotic) = external rotation and eversion with spiral fracture level of ankle joint +/- avulsion of medial malleolus and rupture of deltoid ligament
extending superiorly and laterally up fibula (usually spiral fracture)
distal extent at level of talar dome
variable stability
Tibiofibular syndesmosis usually intact 
type C (supra-syndesmotic) = external rotation with avulsion of medial malleolus or torn deltoid ligament +/- posterior malleolus avulsion (trimalleolar) with posterior tibia-fibular ligament and syndesmosis disruption
above level of ankle joint (talus dome) always unstable requiring open reduction and internal fixation

type C fracture may have associated proximal fibular fracture (Maisonneuve fracture) that would require knee/full length tibia/fibula films

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96
Q

Ankle fracture clinical presentation

A

tenderness at medial or lateral malleolus
inability to bear weight
ankle joint effusion / swelling
complication: post-traumatic arthritis

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97
Q

Ankle fracture investigation

A

Ottawa ankle rule:

ankle X-ray if bone tenderness at posterior aspect of medial or lateral malleolus up to 6cm from malleolar tip or inability to bear weight both immediately post injury
and in emergency department

X-ray ankle AP, lateral, mortise: fracture line, ankle joint space widening

98
Q

Maissoneuve fracture findings on imaging

A

fracture in proximal fibula (left) resulting in joint space widening especially in medial ankle joint and small bone avulsion

99
Q

Ankle fracture treatment

A

non-displaced: non-weight bearing below knee cast

indication for ORIF:
displaced fracture
type B and C Weber fracture
trimalleolar (medial, posterior, lateral) fracture
talar tilt >10 degrees
widened ankle joint (medial clear space > superior clear space between talar dome and fibula)
open joint injury

100
Q

Anterior shoulder dislocation epidemiology

A

shoulder is most commonly dislocated joint

95% shoulder dislocation cases are anterior dislocation

101
Q

Anterior shoulder dislocation mechanism

A

blow to posterior shoulder

abducted arm that is external rotated or hyper extended

102
Q

Anterior shoulder dislocation clinical presentation

A

shoulder pain, arm slightly abducted and externally rotated with inability to internally rotate

inspection: squared off shoulder (sharp shoulder corner)

positive apprehension test: patient looks apprehensive with gentle shoulder abduction and external rotation to 90 degrees, recreating feeling of anterior dislocation

positive relocation test: posterior force applied during apprehension test relieves apprehension by preventing anterior subluxation

positive sulcus sign: presence of subacromial indentation with distal traction on humerus

requires neuromuscular exam including axillary nerve (shoulder patch sensation, deltoid abduction / contraction) and musculocutaneous nerve (lateral forearm
sensation, biceps flexion)

103
Q

Anterior shoulder dislocation complications

A

rotator cuff / capsular tear

shoulder stiffness

injury to axillary nerve / axillary artery / brachial plexus

unreduced dislocation

recurrence
high recurrence rate (1st dislocation at age <20 years = 65-95% recurrence; at 20-40 years = 60-70% recurrence; at >40 years = 2-4% recurrence)

104
Q

Anterior shoulder dislocation investigation

A

X-ray shoulder AP, trans-scapular “Y”, axillary views

anterior dislocation of humeral head from glenoid fossa, best seen on “Y” view

Bankart and Hill Sachs

105
Q

Anterior shoulder dislocation treatment

A

closed reduction under IV sedation and muscle relaxation

external rotation method = patient supine with elbow flexed 90 degrees where examiner grasp elbow and slowly externally rotate the shoulder

traction-counter traction method = assistant stabilize torso while physician apply gentle steady traction on arm

Milch = patient supine with arm abducted 90 degrees and externally rotated 90 degrees where examiner applies traction in line with humerus and push humeral head

Stimson = patient prone dropping arm toward ground with 10-15lbs weight suspended from wrist to pull arm downward

Hippocratic method = physician place heel into patient’s axilla and apply traction to arm

post reduction, X-ray to confirm reduction and neuromuscular exam to ensure intact neurovasculature

sling for 3 weeks (avoid abduction and external rotation), followed by shoulder rehabilitation (dynamic stabilizer strengthening)

106
Q

What is a Bankart lesion

A

impaction fracture at inferior anterior glenoid rim

107
Q

What is a Hill-Sach’s lesion

A

impaction fracture at superolateral aspect of humeral head

108
Q

Posterior shoulder dislocation epidemiology

A

5% shoulder dislocation are posterior dislocation

109
Q

Posterior shoulder dislocation mechanism

A

aetiology 3 E’s = electrocution, epileptic seizure, ethanol

adducted, internally rotated, flexed arm in setting of blow to anterior shoulder or falling onto outstretched hand

110
Q

Posterior shoulder dislocation clinical presentation

A

arm held in adduction and internal rotation, inability to externally rotate

inspection: anterior shoulder flattening, prominent coracoid process

palpable posterior mass to shoulder

posterior apprehension test: patient supine with elbow flexed at 90 degrees and adduct while internally rotate the arm and applying posterior force to shoulder, where patient will jerk back with sensation of subluxation

111
Q

Posterior shoulder dislocation investigation

A

X-ray shoulder AP, trans-scapular “Y”, axillary views: posterior dislocation of humeral head from glenoid fossa, best seen on “Y” view

reverse Bankart lesion and reverse Hill-Sach’s lesion

112
Q

Posterior shoulder dislocation treatment

A

closed reduction: inferior traction on flexed elbow with pressure on back of humeral head
post reduction, X-ray to confirm reduction and neuromuscular exam to ensure intact neurovasculature
sling for 3 weeks, followed by shoulder rehabilitation

113
Q

What is a reverse Bankart lesion

A

impaction fracture at posterior glenoid rim

114
Q

What is a reverse Hill-Sach’s lesion

A

impaction fracture at anterior aspect of humeral head

115
Q

Hip dislocation epidemiology

A

risk factors: post total hip replacement with risk factors (neurological impairment, post-traumatic arthritis, revision hip surgery, substance abuse)

116
Q

Hip dislocation mechanism

A

posterior dislocation: fall, trauma with great force posteriorly onto a flexed and adducted hip (knee into dashboard in motor vehicle collision)

anterior dislocation: posterior directed blow to knee with hip widely abducted

117
Q

Hip dislocation clinical presentation

A

hip pain

inability to move leg about hip joint

posterior dislocation: shortened leg, internally rotated and adducted hip

anterior dislocation: shortened leg, externally rotated and abducted hip

traumatic hip dislocation associated with acetabular fracture and other injuries including head, back, abdomen, pelvis, legs

118
Q

Hip dislocation complication

A

neurovascular compromise especially sciatic nerve (sensation of lateral lower leg and foot; motor of posterior thigh, lower leg and foot)

avascular necrosis of femoral head

femoral head / neck / shaft fracture

heterotopic ossification

DVT/PE

119
Q

Hip dislocation investigations

A

X-ray hip AP and lateral: dislocation of femoral head from acetabulum

120
Q

Hip dislocation treatment

A

1) Trauma Survey
assess for other injuries

2) Reduction
immediate reduction ideally within 6 hours to reduce risk of avascular necrosis
closed reduction under conscious sedation or general anesthesia
closed reduction by Rochester method
post reduction, hip CT to assess joint congruity and fractures

3) Post Reduction Management
indication for ORIF: unstable hip, intra-articular fragments in hip, posterior acetabular wall fracture
if reduction is unstable, then traction for 4-6 weeks

121
Q

What is the Rochester method

A

Method to reduce hip dislocations

Patient lying supine with hip and knee flexed on injured side

Surgeon stands on patient’s injured side

Surgeon passes one arm under patient’s flexed knee, reaching to place that hand on patient’s other knee (supporting injured leg)

With other hand, surgeon grasps patient’s ankle on injured side, applying traction, while assistant stabilizes pelvis

Reduction via traction, internal rotation then external rotation once femoral head clears acetabular rim

122
Q

Knee dislocation mechanism

A

high energy trauma causing tears of multiple ligaments in the knee

knee dislocation described as tibia relative to femur as anterior, posterior, lateral, medial or rotary

anterior knee dislocation: hyperextension injury to knee

posterior knee dislocation: direct blow to proximal tibia to displace it posteriorly

medial dislocation: valgus force to proximal tibia

lateral dislocation: varus force to proximal tibia

rotatory: indirect rotational forces usually caused by body rotating in opposite direction of planted foot

123
Q

Knee dislocation clinical presentation

A

knee pain, knee effusion

unstable knee

associated with popliteal artery tear, peroneal nerve injury and capsular tear

popliteal artery tear present with acute limb ischemia, ankle brachial index <0.9, abnormal pedal pulses

knee dislocation require thorough assessment of peroneal nerve (deep fibular nerve = extensor compartment, sensation of web between 1st & 2nd toe; superficial
fibular nerve = sensation of anterior lateral leg and dorsal foot), popliteal & tibial artery (dorsalis pedis pulses), and knee ligaments (medial & collateral ligament,
meniscus, ACL and PCL)

124
Q

Knee dislocation complications

A

unstable knee
knee stiffness
post-traumatic arthritis

125
Q

Knee dislocation investigations

A

X-ray knee AP, lateral, skyline: dislocation of femoral condyle with tibial plateau

if suspected vascular compromise, then arteriogram

126
Q

Knee dislocation treatment

A

1) Reduction
urgent closed reduction
closed reduction = one clinician stabilize distal femur, other clinical grasp tibia to apply longitudinal traction then reverse direction of dislocation (e.g. for anterior dislocation, lift
distal femur anteriorly and push tibia posteriorly)
knee X-ray post reduction to confirm reduction

2) Assess for Neuromuscular Injuries
post reduction, re-assess neuromuscular status, especially dorsalis pedis, ankle brachial index and bedside duplex ultrasound if available
if vascular injury, then consult vascular surgeon for vascular repair
repair of associated neurovascular injuries
if acute limb ischemia or vascular repair, then decompressive fasciotomy

3) Post-Reduction Management
knee immobilization for 6-8 weeks

127
Q

Cervical spondylosis epidemiology

A

elderly patients

128
Q

Cervical spondylosis pathophysiology

A

degenerative changes (osteoarthritis) of spine result in osteophytes, which can compress on spinal cord or spinal nerve root (i.e. compressive myelopathy)

other degenerative changes including decreased vertebral disc space, disc herniation and stiff spinal ligament can also contribute to compressive myelopathy

129
Q

Cervical spondylosis clinical presentation

A

cervical radiculopathy: sharp pain radiating from neck down arm

nerve root neurologic findings: paresthesia, anesthesia, motor weakness in cervical nerve root distribution

spinal cord neurologic findings: impaired gait, lower extremity weakness with upper motor neuron characteristics (hyperreflexia, increased tone, bladder dysfunction (urgency, frequency, retention)

physical exam: positive Spurling maneuver (extending and rotating neck to side of pain followed by downward pressure on head, which then reproduce pain or paresthesia)

130
Q

Cervical spondylosis investigations

A

cervical X-ray: osteoarthritis with spinal canal narrowing and osteophytes, which is not specific and can be found in asymptomatic cases

electromyogram (EMG) and nerve conduction studies (NCS): decreased reduced evoked compound action potential, preserved nerve conduction velocity, suggestive of axonal injury

MRI: impingement of spinal cord or spinal nerve root with abnormal signal in spinal cord, which confirms diagnosis

131
Q

Cervical spondylosis management

A

1) Conservative management
physiotherapy
restriction of high risk activities and environments
cervical immobilization
pain management: NSAID, anti-convulsant, anti-depressant, corticosteroid

2) Surgical decompression
indication: acute neurologic deterioration, severe neurologic deficits, progressive neurological deficit

procedure: cervical discectomy or corpectomy or laminectomy with laminoplasty at single or multiple levels combined with spinal fusion with bone or synthetic material with plate fixation

132
Q

Pancoast tumour pathophysiology

A

usually lung cancer located at lung apex that compresses on cervical nerves, which may include brachial plexus, sympathetic trunk, vagus nerve and phrenic nerve

133
Q

Pancoast tumour clinical presentation

A

compression of brachial plexus (mainly C8 and T1): cervical radiculopathy (neck / shoulder pain radiating down arm), neurological deficit (paresthesia, anesthesia, weakness)

compression of sympathetic trunk: Horner’s syndrome = ipsilateral ptosis (droopy eye lid), miosis (constricted pupil), enopthalmos (inset eyeball), anhidrosis (lack of sweating)

other symptoms:
phrenic nerve neuropathy -> elevated diaphragm
recurrent laryngeal neuropathy -> vocal cord paralysis
superior vena cava obstruction syndrome

134
Q

Pancoast tumour investigation

A

CT chest: tumor at lung apex

additional imaging as necessary for staging of cancer

135
Q

Pancoast tumour management

A

management depend on disease stage

induction chemotherapy and radiotherapy followed by surgical resection if no metastases and no local progression

136
Q

Thoracic outlet syndrome pathophysiology

A

aetiology: congenital cervical rib, trauma, scalene muscle anomalies, hyperabduction

thoracic outlet syndrome = compression of neuromuscular bundle (brachial plexus, subclavian artery, subclavian vein) within thoracic outlet (between clavicle and first rib)

137
Q

Thoracic outlet syndrome clinical presentation

A

nerve thoracic outlet syndrome (from compression of brachial plexus): arm pain, dysesthesia, paresthesia, weakness, classically aggravated by elevation of arm & hands

venous thoracic outlet syndrome (from compression of subclavian vein): arm swelling with pain and cyanosis of affected extremity after repetitive exertion of upper extremity, collateral vein formation

arterial thoracic outlet syndrome (from compression of subclavian artery and thromboembolization): hand ischemia (pain, pallor, paresthesia, polar) and claudication

138
Q

Thoracic outlet syndrome investigations

A

for neurogenic TOS, EMG and NCS: decreased reduced evoked compound action potential, preserved nerve conduction velocity, suggestive of axonal injury

chest X-ray: bony abnormality such as cervical ribs, long transverse cervical processes, rib / clavicular fracture calluses

CT angiography and venography: identify pathology and point of vascular compression

139
Q

Thoracic outlet syndrome management

A

1) Conservative management
neurogenic TOS: physiotherapy, posturing, behaviour modification
venous TOS: anticoagulation
arterial TOS: urgent catheter thrombolysis or surgical embolectomy

2) Surgery
indication: arterial TOS, venous TOS, neurogenic TOS with acute or subacute neurologic deficit or disabling pain or failure of conservative management

procedure: thoracic outlet decompression (removal of vertical rib, anterior scalenotomy, 1st rib resection) via transaxillary, supra-clavicular or infra-clavicular approach

140
Q

Shoulder impingement syndrome pathophysiology

A

shoulder impingement syndrome = constellation of clinical findings due to compression of structures around shoulder joint that occur with shoulder elevation

shoulder impingement syndrome does not suggest specific injury to a specific structure, where it may be due to injury involving rotator cuff, subacromial bursa, biceps tendon and labrum

shoulder impingement syndrome can be caused by any of the following
subacromial bursitis
rotator cuff tendinitis
(rotator cuff tear, labrum tear, and adhesive capsulitis, which is a differential that may mimic impingement syndrome)

141
Q

Shoulder impingement syndrome clinical presentation

A

shoulder impingement syndrome = pain with overhead activity, pain classically localized to deltoid area and lateral arm, often occurring at night when lying on affected shoulder, shoulder stiffness

physical exam: positive painful arc at 80-120 degrees, positive Neer’s test, positive Hawkin’s test, positive empty can test

specific findings on physical exam may point to specific injuries
rotator cuff tendinitis: pain with strength testing of rotator cuff muscle

(rotator cuff tear): weakness on strength testing of rotator cuff muscle, positive drop arm test (dropped arm with slow shoulder adduction)

subacromial bursitis: loss of active / passive range of motion

142
Q

Shoulder impingement syndrome complication

A

adhesive capsulitis

143
Q

Shoulder impingement syndrome investigation

A

shoulder X-ray: usually normal and used to rule out other pathology causing shoulder pain

MSK ultrasound: can visualize site of impingement and muscle tendons involved

shoulder MRI: can diagnose cause of impingement

144
Q

Shoulder impingement syndrome management

A

1) Conservative management
acute management = rest, ice, NSAID
steroid injection of bursa if persistent disabling pain lasting >3 days
alternative treatments: electrical stimulation, phonophoresis, iontophoresis, therapeutic ultrasound, laser therapy, acupuncture
long term management = physiotherapy rehabilitation focus on restoring mobility, stability and strength training

2) Orthopaedic surgery
indication for orthopaedic referral: failure of 3 months conservative treatment, suspected alternative diagnosis requiring surgery (e.g. rotator cuff tear)

procedure: debridement of rotator cuff or labrum; acromioplasty with debridement, rotator cuff repair

145
Q

What is the painful arc and the meaning of different findings

A

patient abduct arm from 0 to 180 degrees

pain at 60-120 degrees indicate supraspinatus tendinitis or subacromial bursitis

pain at 120-180 degrees suggest acromiovlavicular problem

146
Q

What is Hawkin test

A

patient start with forearm in front as if shielding
examiner grasp patient forearm, support patient’s forearm and internally rotate

positive test is shoulder pain, which suggest anterior impingement

147
Q

What is Neer’s test

A

examiner internally rotate patient’s arm and passively forward flex patient’s shoulder until biceps touch ear

positive if action reproduces arm pain

positive test is indicative of impingement of tendons or bursa

148
Q

What is Empty Can test

A

patient abduct arm to 90 degrees, thumb pointing to floor, arm forward by 30 degrees
examiner put hands on patient wrist pushing down on patient arm while patient resists
positive if pain or weakness, which suggest involvement of supraspinatus tendon

149
Q

Shoulder bursitis pathophysiology

A

aetiology: direct injury, trauma, overuse / strenuous activity, crystal arthropathy, inflammatory arthritis, infection

subacromial bursitis = inflammation of subacromial bursa (fluid filled sac structure lining synovial membrane)

150
Q

Shoulder bursitis clinical presentation

A

acute bursitis: tenderness over sub-acromial bursa, elicited by shoulder movement

impingement syndrome: pain along anterior and superior aspects of shoulder referred to insertion of deltoid muscle (10cm down outer arm) present at rest, shoulder weakness, loss of active range of motion, loss of passive range of motion, shoulder stiffness

physical exam: pain at 80-120 degrees on arc test, positive Speed’s test, positive Neer’s test

associated with rotator cuff tears, impingement syndrome, adhesive capsulitis

151
Q

Shoulder bursitis investigation

A

imaging usually not necessary, because subacromial bursitis can be diagnosed clinically based on history and physical exam

ultrasound: inflammation and swelling of subacromial bursa, can rule out rotator cuff tear

shoulder MRI: inflammation and swelling of subacromial bursa, can rule out rotator cuff tear

152
Q

Shoulder bursitis management

A

acute management = pain control: ice, heat, rest, initial immobilization with NSAID

steroid injection of bursa if persistent disabling pain lasting >3 days

long term management = rehabilitation: physical therapy including strengthening and range of motion exercises to aid in recovery

153
Q

Bone tumour etiology

A

primary benign: hemangioma, cyst, lipoma, granuloma, giant cell tumor

primary malignant: osteosarcoma, Ewing sarcoma, chondrosarcoma

secondary: metastases

154
Q

Bone tumour clinical presentation

A

symptoms: insidious and progressive localized pain (classically at night), swelling or tumour growth
signs: tumour solid growth, tenderness on palpation

155
Q

Bone tumour complication

A

pathologic fracture

focal neurologic deficit

156
Q

Bone tumour investigation

A

1) X-ray: sclerotic / lytic lesion, laminated periosteal reaction, short axis growth, wide zone of transition
2) bone biopsy (operative biopsy, needle biopsy, FNA biopsy, core biopsy): confirms definitive diagnosis

biopsy of suspected primary bone tumour should be carefully planned and done by orthopaedic surgeon to avoid compromise the oncologic outcome

operative biopsy and core biopsy usually required for most primary bone tumours

3) staging including MRI (tumor size and extent), PET scan (screening for bone and other metastases), CT chest (screening for lung metastases)

157
Q

Bone tumour management

A

management depend on benign vs. malignant and staging of cancer

benign tumor: surgical resection

malignant tumor: surgical resection, chemotherapy, and / or radiotherapy

158
Q

Median neuropathy pathophysiology

A

median neuropathy usually due to local structural compression of median nerve

anterior interosseus neuropathy: compression of anterior interosseous nerve branch in region of elbow

pronator teres syndrome: entrapment of median nerve in proximal forearm where nerve passes through pronator teres

carpal tunnel syndrome: compression of median nerve within carpal tunnel formed by transverse carpal ligament (flexor retinaculum)

159
Q

Median neuropathy clinical presentation

A

pronator teres syndrome: forearm pain, paresthesia / anesthesia in entire lateral palm especially thenar eminence)

carpal tunnel syndrome: pain and paresthesia in median nerve territory (first 3 digits and radial half of 4th digit), weakness and atrophy of thenar and hypothenar muscle, positive Tinel’s sign (pain with tapping along carpal tunnel), positive Phalen’s sign

anterior interosseus neuropathy: weakness of flexor of flexor pollicus longus, deep flexor of 2nd & 3rd digit, pronator quadratus

160
Q

Median neuropathy investigation

A

EMG & NCS: conduction velocity slowing and conduction block, suggestive of demyelination, axonal injury in late stage

161
Q

Median neuropathy diagnosis

A

clinical diagnosis based on history and physical exam

162
Q

Median neuropathy management

A

indication for surgery decompression: persistent sensory loss with evidence of axonal injury, severe muscle weakness / wasting

pronator trees syndrome:
1st line = activity limitation, NSAID for pain, steroid injection
2nd line = decompression of nerve within pronator teres

carpal tunnel syndrome:
1st line = conservative therapy (wrist splinting, steroid injection into wrist)
2nd line = surgical release of flexor retinaculum

163
Q

What is Phalen’s test

A

Patient place backs of hands together with wrist flexed at 90 degrees and hold for 30 seconds, where positive = pain, numbness or tingling in 1-4th finger, which suggest carpal tunnel syndrome

164
Q

Ulnar neuropathy pathophysiology

A

ulnar neuropathy usually due to local structural compression of ulnar nerve

elbow ulnar neuropathy: compression of ulnar nerve at medial cubital tunnel

wrist ulnar neuropathy: compression of ulnar nerve under Guyon’s canal at wrist

165
Q

Ulnar neuropathy clinical presentation

A

elbow ulnar neuropathy:
anesthesia / paresthesia over 4th & 5th digits
weakness of interosseous muscle (weak digit abduction & adduction, weak grip)
elbow pain
weakness of wrist & finger flexion
positive Tinel’s sign (pain / paresthesia with tapping along medial cubital tunnel)

wrist ulnar neuropathy:
anesthesia / paresthesia over 4th & 5th digits
weakness of interosseous muscle (weak digit abduction & adduction, weak grip)

166
Q

Ulnar neuropathy investigation

A

EMG & NCS: conduction velocity slowing and conduction block, suggestive of demyelination, axonal injury in late stage

167
Q

Ulnar neuropathy diagnosis

A

clinical diagnosis based on history and physical exam

168
Q

Ulnar neuropathy management

A

indication for surgery decompression: persistent sensory loss with evidence of axonal injury, severe muscle weakness / wasting

elbow ulnar neuropathy:
1st line = activity limitation, physiotherapy, elbow splint
2nd line = surgical decompression of nerve with anterior transposition or medial epicondylectomy

wrist ulnar neuropathy:
1st line = activity limitation, physiotherapy
2nd line = surgical decompression

169
Q

Radiculopathy definition

A

radiculopathy (aka sciatica): sharp shooting pain radiating down leg below knee with weakness or numbness in leg corresponding to nerve root distribution

170
Q

Back pain investigations

A

most patients with low back pain do not require further lab test or imaging

Laboratory Tests
routine laboratory for patients with red flags include CBC, ESR and CRP
urinalysis if suspected UTI
ALP and Ca if suspected bone condition

Imaging

  1. lumbar X-ray indicated if low back pain and:
    - risk factors for cancer: history of cancer, multiple risk factors for cancer, strong suspicion of cancer
    - minor risk factor for cancer: age >50, unexplained weight loss
    - minor risk factor for ankylosing spondylitis: morning stiffness, buttock pain, night pain
    - risk factor for vertebral compression fracture: osteoporosis, glucocorticoid use, trauma, older age
    - >65 years for men or >75 years for women
    - failing 4-6 weeks of therapy

for patients with radiculopathy, spinal stenosis or another specific spinal cause, MRI is preferred over CT

  1. MRI indicated in patients with acute low back pain and any of the following
    - risk factor for spinal infection: fever, IV drug use, recent infection
    - cauda equina syndrome
    - severe or progressive neurologic deficit
  2. MRI indicated in patients with low back pain failing 4-6 weeks of therapy with any of the following
    - nerve impingement: radiculopathy corresponding to L4 / L5 / S1 distribution, positive straight leg raise
    - spinal stenosis: radiating leg pain, older age, pseudo-claudication

MRI may be considered in patients with low back pain for >12 weeks

for non-specific low back pain, lumbar X-ray indicated only if low back pain persist more than 4-6 weeks

171
Q

When should you make a referral to neurosurgeon or orthopedist surgery specializing in back surgery for a patient with back pain

A
  1. cauda equina syndrome
  2. spinal cord compression: acute neurologic deficits in
    patient with cancer and risk of spinal metastases
  3. progressive or severe neurologic deficit
172
Q

Back pain management

A

Analgesia
typical pain ladder as required

1) Tylenol 650mg PO (and NSAID Toradol 30mg IV if no contraindication and young patients)

2) opioid (1-2mg Hydromorphone SC or PO)
usually patients receive opioids to maximize ability of patient for physical exam

no evidence supporting use of muscle relaxants, which have anti-cholinergic side effects and should definitely be avoided in elderly

2) Specific Work-Up and Investigations
treat underlying cause

173
Q

Lumbar disk herniation pathophysiology

A

vertebral disc herniation, compression onto spinal nerve as they exit from spinal cord

classically, lateral herniation of disc between 2 vertebral level will affect the spinal root associated with the lower vertebral level

e.g. a L5-S1 disc herniation will impinge the S1 spinal root

174
Q

Lumbar disk herniation clinical presentation

A

radiculopathy (aka sciatica): sharp shooting pain radiating down leg below knee, with weakness or numbness in leg corresponding to nerve root distribution

motor symptoms: weakness, decreased reflex at affected spinal nerve root level

sensory: paresthesia, anesthesia at affected spinal nerve nerve level

positive straight leg raise: reproduction of radiculopathy with straight leg raise between 30-70 degrees

175
Q

Lumbar disk herniation treatment

A

conservative treatment: analgesia (NSAID, opioid, gabapentin, pregabalin, amytriptylline), muscle relaxant, corticosteroid spinal injection, head or ice, physiotherapy, short term bracing for lower back, other therapy (traction, ultrasound, electrical stimulation)

indication for surgery (discectomy): cauda equina syndrome, progressive neurological deficit (weakness, anesthesia, paresthesia), difficulty standing or walking

176
Q

Cauda equina syndrome etiology

A 
compression of cauda equina (containing L2 to S5) can be caused by any of the following
herniated disc
spinal stenosis
vertebral fracture
tumor
177
Q

Cauda equina syndrome clinical presentation

A

acute onset

motor: weakness and paresis in multiple nerve root distribution (L2 to S5), decreased deep tendon reflexes (knee or ankle)
sensory: radicular pain radiating to legs (sciatica) aggravated by Valsalva and sitting, bilateral sensory loss or pain in lower limbs, saddle anesthesia (S2-S4)

autonomic (S2-4): urinary retention -> urinary incontinence, fecal incontinence (loss of anal sphincter tone), sexual dysfunction

important findings of S2-4 suggestive of cauda equina syndrome includes saddle anesthesia, urinary incontinence, fecal incontinence, loss of anal sphincter tone on DRE

178
Q

Cauda equina syndrome investigations

A

urgent MRI to confirm compression of S2-4 nerve root and cause for compression

post-void residual >250cc to confirm urinary retention

179
Q

Cauda equina syndrome management

A

urgent surgical decompression to preserve bowel, bladder and sexual function as well as prevent progression to paraplegia

180
Q

Spinal stenosis pathophysiology

A

degenerative spine disease mainly spondylosis degenerative arthritis, progressive disc degeneration & protrusion, facet joint arthropathy & osteophyte and ligamentous flavour hypertrophy all contribute to narrowing of central spinal canal

181
Q

Spinal stenosis clinical presentation

A

neurogenic claudication (radicular pain with walking & standing, relieved with sitting & lying)

neurologic deficits: anesthesia, paresthesia, weakness, decreased deep tendon reflexes of bilateral legs

cauda equina syndrome

182
Q

Spinal stenosis investigation

A

spine MRI: visualize compression of spinal cord by nearby structures

MRI is necessary for diagnosis of spinal stenosis

183
Q

Spinal stenosis treatment

A

1) Conservative management
physiotherapy: stretching, strengthening and aerobic fitness
analgesia: NSAID, acetaminophen
epidural corticosteroid injection

2) Surgery
indication for surgery: cauda equina syndrome, severe or progressive neurologic deficits, bladder dysfunction
procedure: decompressive laminectomy (with lumbar fusion for spondylisthesis)

184
Q

Epidural abscess epidemiology

A

risk factors: epidural catheter, IV drug use

source: contagious soft tissue or bone infection, bacteremia

185
Q

Epidural abscess pathophysiology

A

1) bacterial infection invading epidural space from hematogenous spread or contiguous extension from nearby tissue or direct introduction into spinal cord

common bacterial pathogen: Staphylococcus aureus, gram negative bacilli, streptococcus

2) bacterial infection and inflammation extend longitudinally into epidural space forming an abscess

186
Q

Epidural abscess clinical presentation

A

classic triad of fever, spinal pain and neurological deficit

systemic symptoms: fever, chills, malaise
pain: focal severe back pain, neuropathic shooting pain in distribution
neurologic deficit: weakness, paresthesia, anesthesia of legs, bladder or bowel dysfunction

187
Q

Epidural abscess complication

A

irreversible paraplegia, sepsis -> death

188
Q

Epidural abscess investigation

A

blood work: CBC, ESR, CRP
CBC may show leukocytosis
ESR and CRP may be elevated from systemic elevation
blood culture and CSF culture, which can be positive

imaging: MRI spine with IV contrast to visualize abscess (ring enhanced lesion) and compression of spinal cord, which is necessary for diagnosis

CT with IV contrast may be an alternative to MRI

189
Q

Epidural abscess treatment

A

1) Source control
indication for surgery: neurologic deficit, no known organism from culture and aspiration

surgical decompression and drainage within 24 hours

2) Antimicrobial therapy
empiric IV antibiotic therapy of Ceftriaxone + Vancomycin + Metronidazole

narrow antibiotic therapy with culture and susceptibility results

total antibiotics for 6-8 weeks with follow up MRI in 4-6 weeks to ensure improvement

190
Q

Spinal bone metastasis epidemiology

A

most common malignancy with bone metastasis: lung, breast, prostate, thyroid, renal cancer

191
Q

Spinal bone metastasis pathophysiology

A

malignancy with hematogenous spread to bone, which lead to osteoclastic and / or osteoblastic reactive changes and continues to grow

bone metastasis growth may compress on spinal cord

192
Q

Spinal bone metastasis clinical presentation

A

history of prior or current malignancy

pain: pain of spine, which is insidious and progressive, classically worse at night

neurologic deficits: may have weakness, paresthesia, anesthesia of legs, bladder or bowel dysfunction, ataxia

193
Q

Spinal bone metastasis investigation

A

blood work: ALP, Ca
ALP and Ca may be elevated in bone metastasis

spine X-ray: sclerotic or lytic lesions in vertebrae, compression fracture

if neurologic deficit or new compression fracture, then spine MRI: vertebral involvement, impingement of spinal cord

if unknown primary, then bone biopsy for pathology and diagnosis of cancer

194
Q

Spinal bone metastasis treatment

A

1) Treat underlying cancer
cancer treatment with surgery, chemotherapy, and / or radiotherapy
chemotherapy and hormonal therapy may contribute to reducing tumor bulk at bone metastases sites

2) Specific treatment for bone metastasis
if asymptomatic, then observation

if pain, then analgesia with WHO analgesic ladder (acetaminophen -> NSAID -> opioid)

if lytic lesions with risk of pathologic fracture or compression, then osteoclast inhibitors (Bisphosphonates, Denosumab, ZOledronic acid)

if symptomatic, then radiotherapy (external beam or stereotactic)

indication for surgery or urgent radiotherapy: impending pathologic fracture, neurologic deficit signifying spinal cord compression, unstable vertebral column

surgical procedure: surgical decompression of spinal canal if spinal cord compression; vertebroplasty and kyphoplasty to improve mechanical spine stability and prevent compression fracture

195
Q

Pathologic vertebral fracture etiology

A

osteoporosis

bone metastasis

196
Q

Pathologic vertebral fracture pathophysiology

A

weakened vertebrae due to osteoporosis or bone metastasis fail under normal forces, resulting in usually compression fracture

pathologic fracture may cause spine instability and also cause compression of spinal cord

197
Q

Pathologic vertebral fracture clinical presentation

A

history of osteoporosis or malignancy

spine deformity

pain: sudden onset pain, worsened with axial loading

neurologic deficits: may have weakness, paresthesia, anesthesia of legs, bladder or bowel dysfunction, ataxia

198
Q

Pathologic vertebral fracture investigation

A

X-ray spine: compression fracture of vertebrae, lytic lesion if metastasis, osteoporotic changes if osteoporosis

if suspected spinal cord compression, then MRI spine

199
Q

Pathologic vertebral fracture - treatment for osteoporotic fractures

A

1) Symptomatic management
analgesia with acetaminophen, NSAID, and / or opioid
exercise to improve bone mineral density

2) Surgery
indication: intolerable pain not controlled with medical management, neurologic deficit, gross spine deformity, unstable spine

procedure: vertebral augmentation with kyphoplasty or vertebroplasty

3) Prevention of new osteoporotic fractures
treatment of osteoporosis: calcium supplement, vitamin D supplement, Bisphosphonates

200
Q

Arthritis clinical presentation

A

arthritis is inflammation of joint characterized clinically by pain located within joint aggravated by movement

limited range of motion (active and passive)

erythema

joint swelling

201
Q

Mono-arthritis

A

mono-arthritis involve 1 joint

202
Q

Oligoarthritis

A

oligoarthritis involve 2-4 joints

203
Q

Polyarthritis

A

polyarthritis involve >5 joints

204
Q

Acute arthritis

A

acute arthritis last <6 weeks, usually develop only within a few days

205
Q

Chronic arthritis

A

chronic arthritis last >6 weeks

206
Q

Arthritis investigations

A

X-ray of joint if history of trauma

routine laboratory test: CBC, electrolytes, ESR, uric acid level

culture depending on symptoms (blood if septic, throat if sore throat, urethral if urinary symptoms, rectal if GI symptoms)

Arthrocentesis
joint aspiration for definitive diagnosis
joint aspiration sample can be sent for stain & cell, culture and crystal

207
Q

Arthrocentesis low WBC count (<2x109/L or <2,000/mm3 ) suggests

A

osteoarthritis, internal derangement

208
Q

Arthrocentesis high WBC count (>2x109/L or >2,000/mm3) suggests

A

inflammatory arthritis including septic arthritis, crystal arthropathy and rheumatologic arthritis (RA, SLE, spondyloarthropathy)

high WBC count is septic arthritis until proven otherwise
positive stain or culture confirms septic arthritis

209
Q

Arthrocentesis presence of fat droplets confirms

A

fracture

210
Q

Arthrocentesis bloody synovial fluid need to be followed up with

A

MRI, arthroscopy or surgery to rule out fracture, internal derangement or tumor

211
Q

Septic arthritis epidemiology and risk factors

A

~20% of all mono-arthritis

risk factors include age >80; diabetes; rheumatoid arthritis; prosthetic joint; joint surgery; skin infection; cutaneous ulcer; IV drug use

212
Q

Septic arthritis pathology

A

most common pathogen include

1) Staphylococcus aureus
2) Streptococcus pneumoniae
3) Gonococcal infection, especially in young sexually active adults

coagulase-negative Staphylococcus in joint replacements

gram negative bacteria usually in immune compromised host with GI infection

213
Q

Septic arthritis clinical presentation

A

acute mono-arthritis, commonly affect knee (50% septic arthritis cases) or hip

20% septic arthritis are oligo-articular, usually in patients with rheumatoid arthritis

constitutional symptoms: fever, chills, rigor

physical exam: inability to bear weight, localized arthritis (pain, erythema, warmth, swelling), pain on active and passive ROM

vital signs: sepsis / septic shock

laboratory findings: leukocytosis

gonococcal infection can present with either of the following:
1. triad of tenosynovitis (wrist, finger, ankle, toes), dermatitis (painless vesiculo-pustular) and polyarthralgia without purulent arthritis

  1. purulent arthritis (asymmetric polyarthritis usually knees, wrists or ankles) without skin lesions
214
Q

Septic arthritis diagnosis

A

diagnosis based on high WBC >80,000 mainly >90% neutrophils and positive Gram stain or culture from joint aspiration

215
Q

Septic arthritis management

A

1) stabilize patient

2) investigations
joint aspiration, blood culture
laboratory test: CBC, ESR, CRP
X-ray to rule out osteomyelitis and as baseline

3) IV antibiotic
consider empiric antibiotics pending culture if septic arthritis suspected where Gram stain showed no organisms but WBC cell count >2,000/mm3 and patient exhibits signs of infection (fever, leukocytosis, sepsis)

1st line empiric antibiotic:
vancomycin IV 15-20mg/kg/dose Q8-12H
if immunocompromised or IV drug use or traumatic bacterial arthritis, add 3rd generation cephalosporin (see below)

for suspected gonococcal infection, 1st line empiric antibiotic Ceftriaxone IM / IV 1g daily for 14 days plus Azithromycin 1g PO 1 dose (for Chlamydia)

usually antibiotics guided based on Gram stain

if Gram positive cocci, vancomycin IV 15-20mg/kg/dose Q8-12H

if Gram negative bacilli, 3rd generation cephalosporin (any of the below)
Ceftazidime IV 1-2g Q8H
Ceftriaxone IV 2g daily
Cefotaxime IV 2g Q8H
add Gentamicin IV 3-5mg/kg daily if Pseudomonas suspected

definitive antibiotics based on culture results

usually narrow antibiotic coverage with culture results

antibiotic duration usually 14 days on IV followed by 14 days oral

4) joint drained (surgical or aspiration)
for small joints, needle aspiration, serial if necessary until sterile
for major joint (knee, hip, shoulder), surgical decompression and drainage

216
Q

Gout and pseudo gout epidemiology

A

prevalence of 2%

gout commonly occur in older male (onset age 40-60)
risk factors for gout include alcohol, meat, obesity, diabetes

pseudogout usually occur in elderly

217
Q

Gout and pseudo gout pathology

A

gout and pseudo-gout are precipitation and deposition of crystals in joints causing inflammation

gout = monosodium urate crystals

pseudo-gout = calcium pyrophosphate crystal

218
Q

Gout and pseudo gout clinical presentation

A

80% cases are mono arthritis, 20% cases are oligo-arthritis

commonly affect lower extremity joints, classically great toe MTP or knee
gout classically affect great toe MTP (aka Podagra); pseudo-gout classically affect knee

may extend beyond confines of original joint, giving impression of contiguous arthritis

recurrent gout may occur in almost any peripheral joints including wrist, finger, elbow, shoulder, hip, sternoclavicular joints

intense inflammatory symptoms: severe pain, redness, swelling, limited ROM

usually peak in several hours with complete resolution within days to weeks

usually history of flares

later gout flares may present as acute polyarthritis

chronic recurrent gout may present with tophi (yellow or white deposits in soft tissue or bone)

219
Q

Gout and pseudo gout diagnosis

A

gout and pseudo-gout definitively diagnosed based on crystal visualized from joint aspiration samples

gout = negative bright yellow bire-fringent needle cystals (monosodium urate)

pseudogout = negative bire-fringent crystals (calcium pyrophosphate dihydrate)

220
Q

Management for gout

A

A) treat acute gout flare
start treatment as soon as possible and stop within 2-3 days of resolution of attack
treatment usually last 5-7 days

1st line = NSAID including Ibuprofen, Indomethacin
Naproxen 500mg PO BID
Indomethacin 50mg PO TID
Celecoxib 400mg PO BID

2nd line = Colchicine only if within 3 days of onset of gout attack
Colchine 0.6mg PO TID

3rd line = oral / IV / IM systemic glucocorticoid for >2 joints; glucocorticoid injection for 1 or 2 joints
glucocorticoid injection Trimacinolone Acetonide
oral glucocorticoid Prednisone 30-50mg PO daily
systemic glucocorticoid require tapering over course of 7-10 days after resolution of flare

B) prophylaxis to prevent future gout flare

1st line = lifestyle modification (weight control, diet modification, decrease alcohol intake)

2nd line = urate lowering therapy
indication include
frequent and disabling attacks of gout (>3 attacks per year)
clinical or radiographic signs of chronic gout joint disease
tophaceous deposits in soft tissue or subchondral bone
gout with renal insufficiency
recurrent uric acid nephrolithiasis
urinary uric acid >1100 mg/day in men age <25 years or pre-menopausal women
goal of therapy = serum urate concentration <6 mg/dL (<357 mmol/L)
urate lowering therapy usually started >2 weeks after acute gout attack and continued indefinitely
1st line = Allopurinol 300mg daily
2nd line = Febuxostat 40mg daily
2nd line = Probenecid 250mg PO BID
initiation of urate lowering therapy should be concomitant with Colchicine 0.6mg PO daily or BID or Indomethacin 25mg PO BID prophylaxis for <6 months to decrease short term risk of gout flare with urate lowering therapy

221
Q

Management for pseudo gout

A

A) treat acute flare
rest and immobilization for all patients
same pharmacological treatment as gout

B) prophylaxis to prevent future pseudo-gout flare
indication for prophylaxis include:
>3 pseudo-gout attacks per year

1st line = chronic Colchicine
Colchicine 0.6mg PO BID

2nd line = chronic NSAID
Naproxen 500mg PO BID
Indomethacin 50mg PO TID

222
Q

Developmental dysplasia of the hip epidemiology

A

most common hip disorder in children: 1/1,000 live births and 1% of unstable hips

5 risk factors (5 F’s): 
Family history of ligament laxity
Frank breech
leFt hip
First born
Female

associated with congenital muscular torticollis (wry neck) and metatarsus adducts (bean shaped foot)

223
Q

Developmental dysplasia of the hip pathophysiology

A

multifactorial disease

early developmental dysplasia of hip due to lax joint capsule

later developmental dysplasia of hip due to capsular constriction, muscle contractors or bone deformity

224
Q

Developmental dysplasia of the hip clinical presentation

A

dysplasia of hip can present as congenital (before or at time of birth) or developmental (after birth or neonatal period in childhood)

developmental dysplasia of hip encompass any manifestation of hip instability including dislocatable, subluxated or dislocated hip

4 variants from mild to severe
1) Unstable (dislocatable) hip (mild)
femoral head reduced in true acetabulum, but it is dislocatable
hip can be dislocated and relocated with provocative maneuvers (Barlow)
2) Acetabular dysplasia (mild)
shallow acetabulum
femoral head can be dysplastic, subluxated or normal
3) Subluxated hip (medium)
femoral head contacts only portion of true acetabulum
femoral head do not articulate with medial portion of acetabulum
4) Dislocated hip (severe)
femoral head does not articulate with any portion of acetabulum
may or may not be reducible

in neonates, hip dysplasia present as dislocated hip on posture or hyper laxity of hip joint

complication: re-dislocation of hip, inadequate reduction, stiffness, avascular necrosis of femoral head

225
Q

Developmental dysplasia of the hip physical exam

A

on inspection, hip may be already sub-luxated or dislocated, resulting in lower limb asymmetry, affected leg shortening (asymmetry in skin folds and gluteal muscle, wide perineum),
limited abduction of flexed hip <60 degrees

Barlow to screen for dislocatable hip dysplasia; Ortolani to screen for dislocated hip that can be reduced

Barlow test shows that hips are dislocatable by attempting to dislocate the femoral head
1) infant lies supine while examiner flex infant’s hips and knees at 90 degrees while abducting hips and knees
2) examiner stabilize infant’s contralateral hip while adducting the ipsilateral hip (bring thigh together) while pushing hip posteriorly
positive sign = femoral head come out of acetabulum posteriorly resulting in palpable clunk

Ortolans test shows that hips are already dislocated by reducing an already dislocated hip
1) infant lies supine while examiner flex infant’s hip and knees to 90 degrees
2) examiner grasp infant’s thigh and lift the greater trochanter anteriorly while abducting the hip
positive sign = femoral head slides back into socket, resulting in palpable clunk

Galeazzi’s sign for children 1-2 years showing that hip is dislocated
hips and knees flexed, where dislocated hip will present as knees at unequal heights with lower knee on dislocated hip side

226
Q

Developmental dysplasia of the hip investigation

A

in infants (children <3 years of age), ultrasound of hip to diagnose suspected hip dysplasia

in children >3 years of age, X-ray hip: false acetabulum, acetabular index >30 degrees, broken Shenton’s line, femoral neck above Hilgenreiner’s line, ossification centre outside
inner lower quadrant (intersection of Hilgenreiner and Perkin’s line)

227
Q

Developmental dysplasia of the hip treatment

A

treatment depend on age of presentation

at 0-6 months of age, hip dysplasia treated with Pavlik harness that keep hip in abduction and knee in 90 degree flexion

Pavlik’s harness stabilize baby’s hips and every time baby kicks in harness, the femoral head is pushed into acetabulum stimulating acetabulum to grow in depth

at 6 months to 2 years, preliminary traction to loosen contracture and closed reduction -> hip spica cast

at >2 years, open surgical reduction with femoral or pelvic osteotomy

228
Q

Osteomyelitis pathophysiology

A

source: hematogenous (bacteremia) or exogenous (open fracture, surgery, local infected tissue) spread

most common pathogen: Staphylococcus aureus, Salmonella typhi in sickle cell disease, Gram negative bacilli in neonates and immunocompromised

osteomyelitis = infection of bone

229
Q

Osteomyelitis clinical presentation

A

history of prior infection such as soft tissue infection or respiratory infection

common sites: long bones in children and vertebrae in adults

MSK: localized extremity pain, skin erythema and swelling

constitutional symptoms: fever, chills

230
Q

Osteomyelitis investigations

A

blood work: CBC, ESR, CRP
CBC shows leukocytosis
elevated ESR and CRP suggestive of systemic inflammation

blood culture, which may be positive

bone aspirate culture, which may be positive

X-ray: findings usually not seen until 10-12 days after onset of infection, soft tissue swelling, lytic bone destruction, periosteal reaction

bone can: increased uptake within 24-48 hours after onset of infection suggestive of inflammation

MRI: most sensitive and specific for diagnosis of bone infection, which shows bone marrow inflammation, edema in marrow and soft tissue, penumbra sign, necrosis or abscess

231
Q

Osteomyelitis treatment

A

1) Source control
indication for surgery: abscess on MRI, failure to improve after 36 hours of IV antibiotics, sequestra that can be excised, contiguous foci of infection that can be debrided
procedure: bone decortication and drainage with insertion of antibiotic beads locally
serial incision and drainage
if ascending infection, then consider surgical amputation

2) Antibiotic therapy
empiric IV antibiotic therapy
children <3 months: Ceftriaxone + Vancomycin
children >3 months: Cefazolin or Cloxacillin
IV antibiotics therapy can be narrowed based on culture and susceptibility results, which can be stepped down to PO therapy after clinical improvement
total antibiotic therapy for minimum of 4 weeks

3) Rehabilitation
splint limb for several weeks followed by protective weight bearing of limb

232
Q

Slipped Capital Femoral Epiphysis definition

A

type 1 Salter-Harris epiphyseal injury at proximal hip

233
Q

Slipped Capital Femoral Epiphysis epidemiology and risk factors

A

most common adolescent hip disorder with peak incidence at pubertal growth spurt
risk factor: male, obese, hypothyroid

234
Q

Slipped Capital Femoral Epiphysis pathophysiology

A

multifactorial disease from any of the factors

genetic predisposition

cartilage physis thickening rapidly under growth hormone effects

sex hormone secretion stabilization of physis has not begun in early puberty

trauma and overweight can cause stress

235
Q

Slipped Capital Femoral Epiphysis clinical presentation

A

acute presentation: sudden severe ipsilateral hip pain with limp

chronic presentation: limp with ipsilateral medial knee or anterior thigh pain, positive Trendelenburg sign on affected side due to weakened gluteal muscle

physical exam: tenderness over hip joint capsule especially at extremes of ROM, restricted hip ROM (internal rotation, abduction, flexion), Whitman’s sign (obligate external rotation of hip with hip flexion)

complication: avascular necrosis, chondrolysis (loss of articular cartilage result in narrowing of joint space), premature osteoarthritis, loss of hip ROM

236
Q

Slipped Capital Femoral Epiphysis investigation

A

X-ray hip AP, frog leg, lateral: disruption of Klein’s line, normal or widened growth plate, posterior and medial slip
Klein’s line = line along lateral aspect of femoral neck which should intersect through femoral head
X-ray hip to confirm diagnosis and grade severity of SCFE

237
Q

Slipped Capital Femoral Epiphysis treatment

A

mild to moderate slip: stabilize physis with pins in current position
severe slip: ORIF or pin physis without reduction and osteotomy after epiphyseal fusion

238
Q

Physeal fracture

A

physeal fracture involve the physis (growth plate), which can be caused by crushing, vascular compromise, bone growth bridging from metapysis to epiphysis

damage to growth plate may result in premature closure of growth plate and / or interfere with symmetric growth of growth plate, resulting in progressive angular deformity, limb-length
discrepancy or joint incongruity

most physisial injuries heal within 3 weeks, which provide limited window for reduction of deformity

239
Q

Salter Harris classification

A

physeal fractures classified by the Salter-Harris classification system based on X-ray

Salter-Harris classification predict prognosis of premature closure of growth plate, limb shortening and deformity

higher classification types = worse prognosis

“SALTER”
Type 1 = “S” = slipped, 5-7% cases, fracture plane passes straight through growth plate not involving bone, good prognosis

Type 2 = “A” = above growth plate, 75% cases, fracture passes across most of growth plate and up through metaphysis, good prognosis

Type 3 = “L” = lower, 7-10% cases, fracture plane passes some distance along growth plate and down through epiphysis, poorer prognosis due to interruption of proliferative and reserve zones

Type 4 = “TE” = through everything, 10% cases, fracture plane passes through metaphysis, growth plate and down through epiphysis, poor prognosis due to interruption of proliferative and reserve zones

Type 5 = “R” = rammed, 1% cases, crushing type injury that does not displace growth plate but directly compresses it, worst prognosis

240
Q

Physeal fracture management

A

SH 1 and 2 - closed reduction and casting / splinting, then re-examination in 7-10 days to evaluate maintenance of reduction

SH 3 and 4 - anatomic open reduction and internal fixation with pins (ORIF)

SH 5 - usually diagnosed in retrospect

3rd year - Surgery (13 decks)

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