Orthopedic Surgery Flashcards
What is an intra-articular fracture
fracture line crossing articular cartilage and enters joint
What is a physeal fracture
Growth plate fracture
How do you describe a displaced fracture
for displaced fracture, displacement described as distal component relative to more proximal fracture fragment
What is a distracted fracture
fracture fragments separated by gap
How is an angulated fracture described
angulated fracture is described in terms of direction of fracture apex
How is a translated fracture described
translation described in terms of distal relative to proximal segment and percentage of overlapping bone at fracture site
In regards to fracture management, what is the xray rule of 2’s
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
Indication for reduction
Displaced fracture
How to perform closed reduction
apply traction in long axis of limb and reverse mechanism that produced fracture with IV sedation and muscle relaxation
Indication for open reduction
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
What are potential complications of open reduction
infection mal-union non-union implant failure new fracture
What are steps that should be completed post reduction
- re-check neuromuscular status
2. obtain post-reduction X-ray
How to maintain reduction post reduction
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
Fracture healing stages through time
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
Local, early general fracture complications
Compartment syndrome
Neurological injury
Vascular injury
Infection
Implant failure
Fracture blisters
Systemic early general fracture complications
Sepsis
DVT
PE
ARDS secondary to fat embolism
Hemorrhagic shock
Local late general fracture complications
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)
Compartment syndrome etiology
intra-compartmental causes
- fracture: tibial shaft fracture, pediatric supracondylar fracture, forearm fracture
- crush injury
- ischemia-reperfusion injury
extra-compartmental causes
- constrictive dressing: circumferential cast, poor positioning during surgery
- circumferential burn
Compartment syndrome pathophysiology
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
Compartment syndrome clinical presentation
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
- Pain out of proportion for injury and not relieved with analgesia
- Paresthesia -> 3. Pallor
- Paralysis
- Pulselessness
Compartment syndrome most important symptoms
pain out of proportion and with passive stretch of muscle are most important and early signs of compartment syndrome
Compartment syndrome complications
- Muscle / nerve necrosis
- Lactic acidosis
- Rhabdomyolysis
- Myoglobinuria -> renal failure
- Volkmann’s ischemic contracture (ischemic necrosis of muscle resulting in fibrosis and calcification resulting in muscle and joint contracture)
Compartment syndrome diagnosis
compartment syndrome is a clinical diagnosis based on history and physical exam
Compartment syndrome management
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
Open fracture management
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:
- operative irrigation and debridement within 6-8 hours
- open reduction and internal fixation (ORIF)
- traumatic wound left open to drain (delayed closure) or vacuum assisted closure dressing
- re-examination with repeat incision and drainage within 2 days, then repeat 2-3 days as necessary
What is the Gustilo Classification of Open Fractures
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
What are the motor tests that can test each of the following levels: C5, 6, 7, 8, T1
C5 = shoulder abduction, elbow flexion C6 = elbow flexion and wrist extension C7 = elbow extension and wrist flexion C8 = finger flexion T1 = finger abduction
What are the nerve roots, plexus and terminal branches that peripherally innervate the arm
C5-T1 -> brachial plexus -> 5 terminal branches MARMU = musculocutaneous, axillary, radial, median, ulnar nerve
Musculocutaneous nerve motor and sensory distribution
motor = biceps & brachialis (elbow flexion)
sensory = lateral forearm
Axillary nerve motor and sensory distribution
motor = deltoid (shoulder abduction) & teres minor
sensory = seargeant patch on lateral shoulder
What is a potential complication that can occur in a proximal humerus fracture
Axillary nerve have risk of being damaged in proximal humerus fracture
Radial nerve motor and sensory distribution
motor = triceps (elbow extension), all muscles in posterior compartment (extensors) of forearm (wrist extension, finger extension)
sensory = first web space of dorsal hand
What is a potential complication that can occur in a mid shaft humerus fracture
radial nerve have risk of being damaged in mid-shaft humerus fracture
Median nerve motor and sensory distribution
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
What is a potential complication that can occur in a supracondylar fracture
median nerve have risk of being damaged in supra-condylar fracture
Ulnar nerve motor and sensory distribution
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
What is a potential complication that can occur in a fracture involving the medial epicondyle
ulnar nerve have risk of being damaged in fracture involving medial epicondyle
Supracondylar fracture epidemiology
most common in children (peak age ~7 years)
Supracondylar fracture mechanism
95% cases due to extension injuries with falling onto outstretched hands
5% cases due to flexion injuries
Supracondylar fracture potential complications
neuromuscular compromise of median nerve, radial nerve, radial artery
Supracondylar fracture investigations
X-ray elbow: fracture line in distal humerus above condyles, commonly displaced posteriorly, may have fat pad sign at elbow
Supracondylar fracture treatment
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
Galeazzi fracture mechanism
falling onto outstretched hand with axial loading of pronated forearm
Galeazzi fracture clinical presentation
fracture at distal 1/3 of radius near junction of metaphysis and diaphysis
unstable or widening of distal radial ulnar joint (DRUJ)
Galeazzi fracture investigation
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
Galeazzi fracture treatment
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
Colles’ fracture epidemiology
most common wrist fracture
common in older adults age >40
risk factor: osteoporosis
Colles’ fracture mechanism
falling onto outstretched hand with wrist in extension
Colles’ fracture clinical presentation
swelling, tenderness and bruising at wrist
dinner fork deformity (dorsal angulation and displacement of distal radius)
Colles’ fracture investigation
X-ray wrist: distal radius fracture with dorsal displacement and angulation, may involve distal ulna
Colles’ fracture treatment
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)
Smith fracture mechanism
falling onto the back of a flexed hand
Smith fracture clinical presentation
swelling, tenderness and bruising at wrist
volar angulation and displacement of distal radius
Smith fracture investigation
X-ray wrist: distal radius fracture with volar displacement and angulation, may involve distal ulna
Smith fracture treatment
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
What are the most common complications following wrist fracture
- poor grip strength
- wrist stiffness
- radial shortening
Wrist fracture prognosis
80% cases have restored to complete normal function in 6-12 months
Wrist fracture early complications
difficult reduction, loss of reduction compartment syndrome extensor pollicis longus tendon rupture acute carpal tunnel syndrome finger swelling due to venous or lymphatic block
Wrist fracture late complications
mal-union, radial shortening painful wrist secondary to ulnar prominence frozen shoulder post-traumatic arthritis carpal tunnel syndrome complex regional pain syndrome
Scaphoid fracture epidemiology
common in young men
most common carpal bone fracture
Scaphoid fracture mechanism
falling onto outstretched hand with impaction of scaphoid on distal radius
Scaphoid fracture location
fracture at waist of scaphoid in 70% cases
fracture at proximal scaphoid in 20% cases
fracture at distal pole of scaphoid in 10% cases
Scaphoid fracture clinical presentation
anatomical snuff box tenderness
pain with wrist movement
Scaphoid fracture complication
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
Scaphoid fracture investigation
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
Scaphoid fracture treatment
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
Pelvic fracture mechanism
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
Pelvic fracture clinical presentation
local pelvic swelling or tenderness
deformity of lower extremity
pelvic instability
Pelvic fracture complication
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
Pelvic fracture classification
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
Pelvic fracture investigations
X-ray pelvis:
AP
Inlet & outlet view
Judet view (oblique)
CT pelvis: evaluation of posterior pelvic injury and acetabular fracture
Pelvic fracture treatment
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
Pelvic fracture indication for surgery
Indication for surgery includes any of the following:
- unstable pelvic ring injury
- disruption of anterior and posterior SI ligament
- symphysis diastasis >2.5cm
- vertical instability of posterior pelvis
Hip fracture epidemiology
common elderly
risk factors: osteoporosis
Hip fracture mechanism
young: fall from height, motor vehicle collision
elderly: fall from standing height, pathologic fracture
Hip fracture classification
intra-capsular: femoral head (capital) fracture and femoral neck (sub-capital, transcervical, basicervical)
extra capsular: inter-trochanteric and subtrochanteric
Hip fracture clinical presentation
acute onset hip pain unable to weight bear shortened and externally rotated leg painful hip range of motion bruising at back of upper thigh
Hip fracture complications
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
Hip fracture investigations
X-ray hip AP and lateral: fracture line, may have displacement or angulation of distal femur
Hip fracture treatment
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
What is the Garden Classification of femoral neck fractures
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
Patellar fracture mechanism
direct blow to patella: fall, motor vehicle collision
indirect trauma by sudden flexion of knee against contracted quadriceps
Patellar fracture types
Vertical
Comminuted
Displaced
Undisplaced
Lower/upper pole
Osteochondral
Transverse
Patellar fracture clinical presentation
patellar tenderness inability to extend knee or straight leg raise proximal displacement of patella palpable patellar deformity knee joint effusion, hemarthrosis
Patellar fracture complication
knee stiffness
non-union
infection
Patellar fracture investigations
X-ray knee AP, lateral, skyline
fracture line on patella
lipohemarthrosis (fat and / or blood) in pre-patellar pouch
Patellar fracture treatment
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
What normal variant can be confused with a patellar fracture
normal variant have bi-partite patella, but it has well corticated border where extra piece does not fit exactly into adjacent patellar defect
Tibial plateau fracture mechanism
axial loading: fall from height
femoral condyles driven into proximal tibia
Tibial plateau fracture clinical presentation
lateral fractures more common than medial fractures
medial fractures associated with concomitant vascular injuries
knee effusion and swelling
inability to bear weight
Tibial plateau fracture complications
ligament injuries, meniscal injuries, avascular necrosis, infection, osteoarthritis
Tibial plateau fracture investigation
X-ray knee AP lateral:
depression of tibial fracture
oblique fracture line from tibial plateau
lipohemarthrosis (fat and / or blood) in pre-patellar pouch
Tibial plateau fracture treatment
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
Ankle fracture mechanism
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
Ankle fracture classification
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
Ankle fracture clinical presentation
tenderness at medial or lateral malleolus
inability to bear weight
ankle joint effusion / swelling
complication: post-traumatic arthritis
Ankle fracture investigation
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
Maissoneuve fracture findings on imaging
fracture in proximal fibula (left) resulting in joint space widening especially in medial ankle joint and small bone avulsion
Ankle fracture treatment
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
Anterior shoulder dislocation epidemiology
shoulder is most commonly dislocated joint
95% shoulder dislocation cases are anterior dislocation
Anterior shoulder dislocation mechanism
blow to posterior shoulder
abducted arm that is external rotated or hyper extended
Anterior shoulder dislocation clinical presentation
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)
Anterior shoulder dislocation complications
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)
Anterior shoulder dislocation investigation
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
Anterior shoulder dislocation treatment
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)
What is a Bankart lesion
impaction fracture at inferior anterior glenoid rim
What is a Hill-Sach’s lesion
impaction fracture at superolateral aspect of humeral head
Posterior shoulder dislocation epidemiology
5% shoulder dislocation are posterior dislocation
Posterior shoulder dislocation mechanism
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
Posterior shoulder dislocation clinical presentation
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
Posterior shoulder dislocation investigation
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
Posterior shoulder dislocation treatment
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
What is a reverse Bankart lesion
impaction fracture at posterior glenoid rim
What is a reverse Hill-Sach’s lesion
impaction fracture at anterior aspect of humeral head
Hip dislocation epidemiology
risk factors: post total hip replacement with risk factors (neurological impairment, post-traumatic arthritis, revision hip surgery, substance abuse)
Hip dislocation mechanism
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
Hip dislocation clinical presentation
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
Hip dislocation complication
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
Hip dislocation investigations
X-ray hip AP and lateral: dislocation of femoral head from acetabulum
Hip dislocation treatment
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
What is the Rochester method
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
Knee dislocation mechanism
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
Knee dislocation clinical presentation
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)
Knee dislocation complications
unstable knee
knee stiffness
post-traumatic arthritis
Knee dislocation investigations
X-ray knee AP, lateral, skyline: dislocation of femoral condyle with tibial plateau
if suspected vascular compromise, then arteriogram
Knee dislocation treatment
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
Cervical spondylosis epidemiology
elderly patients
Cervical spondylosis pathophysiology
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
Cervical spondylosis clinical presentation
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)
Cervical spondylosis investigations
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
Cervical spondylosis management
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
Pancoast tumour pathophysiology
usually lung cancer located at lung apex that compresses on cervical nerves, which may include brachial plexus, sympathetic trunk, vagus nerve and phrenic nerve
Pancoast tumour clinical presentation
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
Pancoast tumour investigation
CT chest: tumor at lung apex
additional imaging as necessary for staging of cancer
Pancoast tumour management
management depend on disease stage
induction chemotherapy and radiotherapy followed by surgical resection if no metastases and no local progression
Thoracic outlet syndrome pathophysiology
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)
Thoracic outlet syndrome clinical presentation
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
Thoracic outlet syndrome investigations
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
Thoracic outlet syndrome management
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
Shoulder impingement syndrome pathophysiology
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)
Shoulder impingement syndrome clinical presentation
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
Shoulder impingement syndrome complication
adhesive capsulitis
Shoulder impingement syndrome investigation
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
Shoulder impingement syndrome management
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
What is the painful arc and the meaning of different findings
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
What is Hawkin test
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
What is Neer’s test
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
What is Empty Can test
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
Shoulder bursitis pathophysiology
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)
Shoulder bursitis clinical presentation
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
Shoulder bursitis investigation
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
Shoulder bursitis management
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
Bone tumour etiology
primary benign: hemangioma, cyst, lipoma, granuloma, giant cell tumor
primary malignant: osteosarcoma, Ewing sarcoma, chondrosarcoma
secondary: metastases
Bone tumour clinical presentation
symptoms: insidious and progressive localized pain (classically at night), swelling or tumour growth
signs: tumour solid growth, tenderness on palpation
Bone tumour complication
pathologic fracture
focal neurologic deficit
Bone tumour investigation
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)
Bone tumour management
management depend on benign vs. malignant and staging of cancer
benign tumor: surgical resection
malignant tumor: surgical resection, chemotherapy, and / or radiotherapy
Median neuropathy pathophysiology
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)
Median neuropathy clinical presentation
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
Median neuropathy investigation
EMG & NCS: conduction velocity slowing and conduction block, suggestive of demyelination, axonal injury in late stage
Median neuropathy diagnosis
clinical diagnosis based on history and physical exam
Median neuropathy management
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
What is Phalen’s test
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
Ulnar neuropathy pathophysiology
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
Ulnar neuropathy clinical presentation
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)
Ulnar neuropathy investigation
EMG & NCS: conduction velocity slowing and conduction block, suggestive of demyelination, axonal injury in late stage
Ulnar neuropathy diagnosis
clinical diagnosis based on history and physical exam
Ulnar neuropathy management
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
Radiculopathy definition
radiculopathy (aka sciatica): sharp shooting pain radiating down leg below knee with weakness or numbness in leg corresponding to nerve root distribution
Back pain investigations
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
- 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
- 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 - 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
When should you make a referral to neurosurgeon or orthopedist surgery specializing in back surgery for a patient with back pain
- cauda equina syndrome
- spinal cord compression: acute neurologic deficits in
patient with cancer and risk of spinal metastases - progressive or severe neurologic deficit
Back pain management
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
Lumbar disk herniation pathophysiology
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
Lumbar disk herniation clinical presentation
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
Lumbar disk herniation treatment
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
Cauda equina syndrome etiology
compression of cauda equina (containing L2 to S5) can be caused by any of the following herniated disc spinal stenosis vertebral fracture tumor
Cauda equina syndrome clinical presentation
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
Cauda equina syndrome investigations
urgent MRI to confirm compression of S2-4 nerve root and cause for compression
post-void residual >250cc to confirm urinary retention
Cauda equina syndrome management
urgent surgical decompression to preserve bowel, bladder and sexual function as well as prevent progression to paraplegia
Spinal stenosis pathophysiology
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
Spinal stenosis clinical presentation
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
Spinal stenosis investigation
spine MRI: visualize compression of spinal cord by nearby structures
MRI is necessary for diagnosis of spinal stenosis
Spinal stenosis treatment
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)
Epidural abscess epidemiology
risk factors: epidural catheter, IV drug use
source: contagious soft tissue or bone infection, bacteremia
Epidural abscess pathophysiology
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
Epidural abscess clinical presentation
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
Epidural abscess complication
irreversible paraplegia, sepsis -> death
Epidural abscess investigation
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
Epidural abscess treatment
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
Spinal bone metastasis epidemiology
most common malignancy with bone metastasis: lung, breast, prostate, thyroid, renal cancer
Spinal bone metastasis pathophysiology
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
Spinal bone metastasis clinical presentation
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
Spinal bone metastasis investigation
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
Spinal bone metastasis treatment
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
Pathologic vertebral fracture etiology
osteoporosis
bone metastasis
Pathologic vertebral fracture pathophysiology
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
Pathologic vertebral fracture clinical presentation
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
Pathologic vertebral fracture investigation
X-ray spine: compression fracture of vertebrae, lytic lesion if metastasis, osteoporotic changes if osteoporosis
if suspected spinal cord compression, then MRI spine
Pathologic vertebral fracture - treatment for osteoporotic fractures
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
Arthritis clinical presentation
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
Mono-arthritis
mono-arthritis involve 1 joint
Oligoarthritis
oligoarthritis involve 2-4 joints
Polyarthritis
polyarthritis involve >5 joints
Acute arthritis
acute arthritis last <6 weeks, usually develop only within a few days
Chronic arthritis
chronic arthritis last >6 weeks
Arthritis investigations
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
Arthrocentesis low WBC count (<2x109/L or <2,000/mm3 ) suggests
osteoarthritis, internal derangement
Arthrocentesis high WBC count (>2x109/L or >2,000/mm3) suggests
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
Arthrocentesis presence of fat droplets confirms
fracture
Arthrocentesis bloody synovial fluid need to be followed up with
MRI, arthroscopy or surgery to rule out fracture, internal derangement or tumor
Septic arthritis epidemiology and risk factors
~20% of all mono-arthritis
risk factors include age >80; diabetes; rheumatoid arthritis; prosthetic joint; joint surgery; skin infection; cutaneous ulcer; IV drug use
Septic arthritis pathology
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
Septic arthritis clinical presentation
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
- purulent arthritis (asymmetric polyarthritis usually knees, wrists or ankles) without skin lesions
Septic arthritis diagnosis
diagnosis based on high WBC >80,000 mainly >90% neutrophils and positive Gram stain or culture from joint aspiration
Septic arthritis management
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
Gout and pseudo gout epidemiology
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
Gout and pseudo gout pathology
gout and pseudo-gout are precipitation and deposition of crystals in joints causing inflammation
gout = monosodium urate crystals
pseudo-gout = calcium pyrophosphate crystal
Gout and pseudo gout clinical presentation
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)
Gout and pseudo gout diagnosis
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)
Management for gout
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
Management for pseudo gout
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
Developmental dysplasia of the hip epidemiology
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)
Developmental dysplasia of the hip pathophysiology
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
Developmental dysplasia of the hip clinical presentation
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
Developmental dysplasia of the hip physical exam
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
Developmental dysplasia of the hip investigation
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)
Developmental dysplasia of the hip treatment
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
Osteomyelitis pathophysiology
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
Osteomyelitis clinical presentation
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
Osteomyelitis investigations
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
Osteomyelitis treatment
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
Slipped Capital Femoral Epiphysis definition
type 1 Salter-Harris epiphyseal injury at proximal hip
Slipped Capital Femoral Epiphysis epidemiology and risk factors
most common adolescent hip disorder with peak incidence at pubertal growth spurt
risk factor: male, obese, hypothyroid
Slipped Capital Femoral Epiphysis pathophysiology
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
Slipped Capital Femoral Epiphysis clinical presentation
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
Slipped Capital Femoral Epiphysis investigation
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
Slipped Capital Femoral Epiphysis treatment
mild to moderate slip: stabilize physis with pins in current position
severe slip: ORIF or pin physis without reduction and osteotomy after epiphyseal fusion
Physeal fracture
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
Salter Harris classification
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
Physeal fracture management
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
