Download Lecture 15: Shoulder, Arm, Elbow, Forearm

CM-MSK Exam 2
Lecture 12 & Lecture 13
Lecture 14 Elbow and Forearm
I.
II.
Know the Growth Plates of the Elbow
a. CRMTOL (Come rub my tower of love) = Capetiluum, radial head, medial epicondly,
trochlea, olecranon, lateral epicondyle
Injury Patterns – Age Dependent
ADULT
ADOLESCENT
– MCL tear
- Medial epicondyle
– Medial epicondylitis
avulsion
– Ulnar neuropathy
– Medial epicondyle fx
– Valgus ext overload
– Medial epicondylitis
– Posterolateral rotary
– Olecranon apophysitis
instability
– OCD
– Lateral Epicondylitis
– Panners disease
III.
Mechanisms behind injury
a. Biomechanical demands of a sport  injury
b. Injury often occurs in acceleration; valgus torgue peaks
c. Patterns:
i. Medial tension overload
ii. Valgus extension overload
iii. Posterolateral rotary instability
iv. Lateral compression syndromes
IV.
Medial Injuries
a. Anatomy of Elbow (MCL = UCL)
i. Anterior bundle UCL = primary constraint to valgus instability
ii. Flexor-pronator group divides dynamic stabilization
b. Medial Tension syndromes in ADULTS
i. Medial Epicondylitis
1. Def = Chronic degenerative process of tendinous origin flexor-pronator
mass
2. Get it from repetitive eccentric contraction
3. An angiofibroblastic tendinosis, can have ulnar nerve involvement 50%
of the time
4. Exam = tender med epi, decreased grip strength, pain at rest =
tendinosis, provactive tests (flex/pronate wrist)
5. Tx = Rest/modify activity, NSAIDs, injection (he also mentioned
counterforce brace as well) to prevent muscle from maximally
contracting
6. Surgery = open debridement, removal of angiofibroblastic tissue, ulnar
nerve transposiion
ii. UCL injury (UCL aka MCL)
1. Where: originates at central 2/3 of epicondyle
2. At risk: those who’ve had an epicondylectomy or epicondyle Fx
3. Mechanics = every time you throw (right before peak mode of failure)
FCR and pronator teres help if your soft tissues are fatigued. They help
because the load gets dangerously high.
4. Hx of: medial pain w/ throwing, decreased accuracy and velocity
5. Dx:
a. Jobe’s Test (standing. Apply valgus force at 30 deg. Easier to
feel joint close w/ release of valgus)
b. O’Driscoll Test = same as Jobe’s but lying prone
c. Milking Maneuver(hand more supinated) or Defacing test
(hand pronated) to palpate for UCL tenderness
d. View stress on an x-ray
e. MRI w/ contrast to see UCL entirely in coronal sections
f. ***Arthroscopic Valgus Stress test at 70 deg flexion
(Andrews)  opening of more than 1 mm evidence of
ligament incompetence
6. Tx
a. Of MCL tear
i. Rehab is cornerstone of successful treatment
ii. Goals: relieve pain/inflammation, avoid cortisone
injections, plyometric strengthening for flexorpronators
b. Of UCL tear
i. Rehab: Pts w/ medial instability, decreased EMG of
flexor=pronator group, good potential for successful
rehab
ii. Surgery = Tommy-John (Jobe). A palmaris longus graft
in figure 8 fashion; combine w/ ulnar nerve
transposition. Return to sport in 15 months. I bet he
will ask about this one, there are a great many pics in
the slideshow
iii. Ulnar neuropathy
1. Traction or friction injury of:
a. Brachial plexus at coracoid
b. Medial epicondyle
c. Flexor-pronator insertion
d. Wrist extension
c. Medial Tension Syndromes in Adolescents
i. With kid pitchers, you see decreased pain w/ less than 300 or greater than
600 throws
V.
ii. Fusion of medial epicondyle occurs at 17 yo
iii. Medial epicondyle avulsion
1.
iv. Medial epicondyle fracture
1. What: occurs near skeletal maturity, kid hears a “pop” while throwing
2. Tx: nondisplaced in cast for 3 wks
3. Cautions: in young theltes, MCL is attached to the fragment; minimally
displaced Fx heal w/ fibrous union
4. DX
a. Use stress views for Xray
b. treat instability w/ ORIF (preserves flexor=pronator power)
5. prognosis is good, most return to sport. Few have degenerative
changes at maturity
Lateral Injuries
a. Anatomy
i. LUCL(lateral ulnar collat lig) = primary restraint against posterolateral rotary
instability
ii. Orientation same as anterior bundle of UCL
iii. Important UCL = MCL
b. Mechanism = FOOSH  partially flexed arm  dislocation
i. circular injury goes lateral to medial
c. Exam
i. Recurrent locking/catching after elbow dislocation
ii. Clunk after push off on the elbow from seated position
iii. + pivot shift test (disruption of LUCL produces pivot shift, radial head slides off
capitellum posterolaterally, elbow reduced w/ further flex-pronation)
iv. Check valgus stability (anterior UCL) in pronation post reduction
d. Tx
i. Hinged elbow brace
ii. Lateral capsular reefing
iii. Reconstruction of LCL w/ Palmaris graft
iv. Surgery if: flexorpronator rupture, widely incompetent UCL, bony instability
e. Lateral Epicondylitis (tennis elbow) = degeneration of ECRB origin
i. Microtrauma  micro tear  angiofibroblstic tendinosis
ii. Exam
1. Tennis elbow test
2. Rest or night pain = tendinosis
iii. Tx
1. * there’s little scientific evidence that nonoperative treatment alters
the natural history. Consensus =70-80% resolution at 1 year
2. Iontophoresis = transdermal admin of dexamethasone
a. Good short-term relief
b. No longterm benefit over other nonoperative tx (like bracing)
3. Counterforce bracing = decreases pull on ECRB orign, inhibits full
muscular expansion, decreased ECRB and ECD muscle activity w/ max
voluntary isometric contraction
f. Lateral Compression Syndrome = due to medial tension
i. Mechanism: acceleration phase happens, deceleration pahse creates shearing
force b/t radial head and capitellum w/ forearm pronation. Force primarily
absorbed by cartilage
g. Adolescent Lateral Compression Injury
i. Osteochondritis Dessicans (OCD)
1. 9-14 yo; delamination of cartilage from subchondral bone. Pain
localized laterally and relieved by rest
2. DX
a. MRI helps ID early lesion; find loose body not on x-ray. Defect
size correlates w/ outcome. Early DJD = poor prognosis
3. TC
a. Stable fragment (50% heal)  rest, nonoperative
b. Unstable, attached frag  surgery if mechanical Sx (option:
debridement, microfracture, ORIF)
c. Losse body  remove loose
ii. Panner disease = lesion of ENTIRE capitellum
1. Young athletes 7 – 12
VI.
Posterior Injuries
a. Olecranon Hypertrophy and Osteophytes
i. Later stages of apophysitis
ii. More common in older adolescents/adults
iii. Tx: removal of loose bodies or debridement of osteophyte if significant ¯ ROM
iv. Best time to prevent elbow injuries is at the beginning of the athletes career
when optimum mechanics can be taught
b. Radial head subluxation/Dislocation = Nursemaids Elbow
i. Occurs from sudden traction on extended and pronated arm
ii. Radial head slips under the annular ligament
iii. Most common <6 yrs old
1. Peak incidence 1-3 yrs old
iv. Sx: Child refuses to use arm, Holds it in flexed position against body, Often no
swelling or deformity
v. Tx: Almost never requires surgery, Arm sling for 2-3 days, then use as
tolerated
vi. Reduction of nursemaid’s elbow = supinate forearm, flex elbow, sling it
c. Olecranon bursitis (student’s elbow)
i. Not infected = inject w/ steroid? Infected = aspirate to check it out
d. Types of Tendinitis
i. Intersection Syndrome
1. between 1st (APL, EPB) and 2nd (ECRL/B) compartments
2. peritendinous bursal inflammation 2º repeated WF against resistance
3. pain 4-6 cm proximal to wrist
4. rowers, weightlifters
VII.
5. splint, injection
ii. DeQuervain’s Tenosynovitis
1. most common tendinitis
2. MOI: forceful gripping with ulnar deviation (use Finklesteins test)
3. golf, racquet sports, rowers
4. tenderness along 1st compartment
5. injection, thumb spica splint, decompression
NERVE INJURIES
a. Anatomy
i. Median Nerve- Passes through pronator teres
ii. Ulnar Nerve - Passes through the cubital tunnel
iii. Radial Nerve
1. Superficial (sensory) branch (sensory dorsolateral hand and 1st 3 digits)
and the deep (motor or posterior interosseous) branch(ECRB and
supinator)
2. The deep branch passes through the Arcade of Frohse (fibrous arch
formed by the proximal margin of the superficial head of the supinator
muscle)
b. Radial Tunnel Syndrome – goes w/ lateral epicondylitis
i. Nerve entraptment, pain on both sides of forearm, loss of finger strength,
hard to make twisting motions
c. Cubital Tunnel = ulnar nerve entrapment
i. Pain/numbness in last 2 digits
ii. Early Symptoms
1. Pain and Numbness Elbow (slept w/ fists clinched b/c its cold)
2. Night Pain
3. Tingling Ring and Small Finger
iii. Severe Symptoms
1. Weakness RF, SF
2. Decreased Pinch Thumb - Index Finger
3. Decrease Hand Grip
4. Muscle Wasting Hand
5. Claw like deformity Hand
iv. Tx
1. Smoking cessation (smoking slows healing, less O2 available)
2. Night time flexion blovk splint or towel
3. NSAIDS
4. 6 weeks surgery
d. Pronator syndrome = compression of median nerve by forearm muscles
i. Sx similar to carpal tunnel
ii. EMG NCS to rule out other compression syndromes
iii. Involves palmar cutaneous branch
iv. Pain with resisted pronation (between heads of pronator)
v. Pain with resisted supination (compression from part of bicipital aponeurosis)
e. Anterior Interosseous Syndrome
i. Weakness or loss of flexion of DIP joint of thumb index finger
ii. EMG/NCV
1. Technically difficult
2. False + if < 3weeks of onset
iii. Treatment
1. Lifestyle modification
2. Splinting
3. NSAIDS
4. PT
5. Surgical decompression if sx >6 months
iv. Anatomy = AIN: Gives muscle function to the FPL, FDP (Index finger, Middle
finger), Pronator Quadratus
f. Median Nerve Injury
i. Typically induced by blunt trauma, penetrating wounds
ii. Innervates the thenar muscles and 1st and 2nd Lumbricals. Pope hand with
attempted flexion.
iii. Motor and sensory loss to the thumb, index finger, and middle finger
g. Radial Nerve injury (wrist drop)
i. Mid-shaft humerus fracture
ii. Radial nerve divides into the superficial and the deep branch (posterior
interosseous nerve) at the lateral epicondyle
iii. The superficial branch is a purely sensory nerve (first dorsal web space)
iv. Injury proximal to the branching leads to wrist drop and sensory loss
h. Ulnar Nerve Injury
i. Innervates 3rd and 4th lumbricals, hypothenar muscles, dorsal and palmar
interossei, palmaris brevis and adductor policis
ii. Sensory loss is SF and RF
iii. Muscle wasting and atrophy of the first dorsal interosseous muscle are
present
iv. Ulnar claw most obvious with attempted extension.
v. Traumatic injury is the most common cause of ulnar nerve damage, although
leprosy is associated with ulnar nerve lesions
vi. Froment’s sign (make a fist, out a piece of paper b/t thumb and curled fingers)
(problem in Guyon’s tunnel)
Lecture 15: Shoulder, Arm, Elbow, Forearm
I.
II.
III.
IV.
Anatomy and Problems: Elbow, Radius shaft/head, Ulnar styloid/shaft/olecranon,
Monteggia, Humerus proximal/shaft/supracondylar
MOI for shoulder dislocation, AC joint injuries and clavicle fracture
a. MOI = fall on outstretched arm (FOOSH), fall on tip of shoulder, direct impact
b. Factoids on shoulder instability
i. History most productive
ii. Differentiate between long-term MDI vs. traumatic
iii. Rehab often 1st treatment option
iv. Growing trend toward early repair, especially in younger patients
c. Shoulder instability can be
i. AMBRI = Atraumatic, Multidirectional, Bilateral, Rehab, and (if surgery)
Inferior capsular shift
ii. TUBS = traumatic, unilateral, Bankart, Surgery
1. Look at # of dislocations, age, collision sports, sensation of instability
w/ ADL
Bankart and Hill-Sach’s lesions
a. Bankart
i. Defect of the inferior Capsulolabral complex
ii. Can be bony or non bony
iii. injury of the anterior (inferior) glenoid labrum of the shoulder due to
repeated (anterior) shoulder dislocation.[1] When this happens, a pocket
at the front of the glenoid forms that allows the humeral head to
dislocate into it. It is an indication for surgery and often accompanied by
a Hill-Sachs lesion, damage to the posterior humeral head.
b. Hill-Sachs - cortical depression in the posterolateral head of the humerus bone.
It results from forceful impaction of the humeral head against the
anteroinferior glenoid rim when the shoulder is dislocated anteriorly.
Diagnose common fractures of shoulder, arm, elbow and forearm. Utilize radiographs
to diagnose fractures.
a. HUMERUS Fx
b. Proximal Humerus Fx – Use NEER to classify
i. Look for “ice cream cone” on radiology. Nondisplaced doesn’t need surgery
(ice cream is ON the cone), displaced needs surgery (ice cream OFF the cone).
ii. Indications
1. 4part fractures = Older patients, Osteopenic bone, Anatomic neck
component
2. 3part fractures = Older/osteopenic patients
3. 2part fractures = Rare indication
4. Head-splitting fractures
iii. Indications for open tx of a humoral shaft fracture
1. Big one = Change in NV status with reduction maneuver
a. Explore nerve during ORIF
c. Humoral shaft
i. Can accept up to 30 degrees of angulation
ii. More deformity is tolerated in the plane of motion
d. Nerve Injury in humeral Fx = “ARM” Fx
i. Axillary Nerve = Humeral Head Fracture
ii. Radial Nerve = Humerus Mid Shaft Fracture
iii. Median Nerve = Humeral Supracondylar Fracture
e. Supracondylar Humerus Fx – Elbow
i. Ant humeral line, anterior sail sign, spinnaker
f. Lateral Condylar Humeral Fx – Elbow (green line is LCL)
g. Monteggia
V.
VI.
h. Fx of Scapula and Clavicle
i. Scapula Fx
1. Often do not need to be fixed
2. Associated with: Rib fractures, Mediastinal injuries, Pulmonary
contusion
3. Need surgery if: displaced glenoid fracture, Floating shoulder
i. Lots of pics of Adult Supracondylar Fx
Diagnose soft tissue injures (sprain, dislocations) of the elbow region
Predict treatment options for various injuries to the elbow and forearm
a. Elbow Dislocation
i. Types = post, ant, med, lat, divergent (Mostly posterior)
ii. Evaluation
1. Must document neurovascular exam before and after reduction
2. Must be suspicious of arterial injury – presence of radial pulse does
not exclude injury
3. Must evaluate triceps function after anterior dislocation
iii. Non-operative Tx
1. Closed reduction with elbow in flexion; entrap median nerve if
reduction performed in extension
2. After reduction – splint in 45 to 90 degrees of flexion; before splinting,
document stable ROM
3. Early motion is essential to good outcome
iv. Operative Tx
1. Indicated for soft tissue or bony entrapment
2. Large displaced coronoid fx requires ORIF
3. Ligamentous reconstruction in cases of recurrent instabilit
VII.
Recognize the indications for surgical treatment options of two-bone forearm fractures
and distal radius fractures
a. Radial Head Fx Classification
VIII.
Associate Neuropathic lesions and nerve compression injuries to the Forearm and
Wrist
Lecture 16: Elbow, Forearm, Wrist, Hand
I.
II.
III.
IV.
V.
Wrist and hand exam
a. Wrist joints
i. Radiocarpal (most flexion), radiulnar, intercarpal. RC provides MOST FLEX/EXT
b. Hand joints
i. Metacarpalphalangeal (MCP), proximal interphalangeal (PIP), distal
interphalangeal (DIP)
Palpation – know the diffs:
a. Bouchard’s nodes from degenerative joint disease/RA = palpate PIP
b. Heberden’s nodes = palpate DIP
Maneuvers
a. Motion testing
i. Wrist
1. Flexion = flexor carpi radialis and ulnaris
2. Extension = ext carpi radialis longus and brevis, ext carpi ulnaris
3. Adduction (ulnar deviation 30 deg) – flex carpi ulnaris
4. aBduction (radial deviation 20 deg) – flex carpi radialis
b. sensation – dermatomes
c. grip strength – put your fingers in their palm and they grip
d. Thumb movement = Finkelstien’s test. Pt puts thumb aginst palm then makes a fist,
moves wrist in ulnar deviation (like you’re casting when fishing/flick of the wrist) to
check for de Quervain’s tenosynovitis – inflamm of abductor pollicus longus and ext
pollicus brevis tendons and sheaths
e. Carpal tunnel = phalen’s or tinel’s test. Think: thenar atrophy
Innervation – he said to know where they cross
a. Median n. – crosses the elbow mediallt and passes thru the two heads of the
pronator teres, a potential site of entrapment
b. Ulnar n. – passes along the medial arm and posterior to the medial epicondyle thru
the cubital tunnel, a likely source of entrapment
c. Radial n. – descends the arm laterally, divides into the superficial (sensory) branch
and deep (motor or posterior interosseous) branch. Deep branch passes thru the
Arcade of Frohse, where it’s most susceptible to injury
Problems/Injuries Breakdown (the bare minimum)
a. RA
i. Granuloma formation causes hand deformities. Ulnar deviation. Hammer
fingers, Boutoinniare and Swan neck deformities. Wrist and MCP joints
commonly involved
b. Osteoarthritis – think ENTIRE joint, including nearby muscles, underlying bones,
ligaments, joint lining (synovium), joint capsule…progressive loss of cartilage
i. Could have bony nodule at DIP (Heberden’s) and PIP (bouchard’s)
ii. Wrist arthritis = may be osteoarthritis (DJD) or RA
1. w/ RA, you’d see swelling, tenderness and limited ROM, involvement
of MCP and PIP
2. DJD would be same but less involvement of other joints
VI.
VII.
iii. Thumb arthritis = idiopathic, women 30-60
c. Ganglion cyst
i. Soft tissue mass of hand/wrist. From tear in ligaments overlying the lining of
tendons
d. DIP joint injuries
i. Mallet finger – ie, a baseball guy slides into a base. A flexion deformity,
sudden forceful flexion of DIP. Image = distal part of finger hangs down.
e. DIP and MCP and PIP
i. Trigger finger – can’t open fingers. Can close them. A form of stenosing
tenosynovitis. From repetitive finger flexion.Nodule gets trapped behind
tendon sheath, finger stuck in flexed position.
f. Thumb MCP
i. Tear of the UCL (ulnar collateral ligament) = “Gamekeeper’s thumb” or
“Skier’s thumb” – hyperabduction of thumb MCP joint. Note that for X-rays
you’d do a stress test. If stress X-rays show greater than 20% of instability
compared w/ contralateral side, complete tear likely
g. Inflammation of tendons and synovial sheaths = DeQuervian’s Tenosynovitis
i. Dorsal compartment of wrist. Abd poll longus and ext poll brevis. Note a
positive Finkelstein’s test.
h. Depuytren’s Disease – insidious onset of thickening and contracture of palmar
fascia/skin on distal side of primary nodule is drawn up into a fold
i. Not a consequence of activity.
ii. Eventually fingeres become progressively flexed at MCP and PIP
iii. Note: can be genetic (Auto Dom) but also EtOH-induced liver disease,
diabetics, smokers.
iv. Use table top test of Hueston (positive = hand unable to go flat)
Nerve Entrapment Injuries
a. Carpal tunnel = tingling in fingertips, numbness/pain at night…all from compression
of median nerve. Phalen’s and tinels = +
b. Guyon’s Canal = ulnar nerve entrapment.
i. Know that ulnar nerve passes b/t pisiform and hook of hamate
On his “recap” slide is: RA, osteoarthritis, ganglion cyst, mallet finger, trigger finger, tumb
MCP-UCL, and DeQuervain’s
Lecture 17: Fx of Hand and Wrist
I.
Fractures of distal radius, scaphoid, hook of hamate, metacarpal, phalanx
a. Scaphoid most Fx’d
i. Tx
1. nondisplaced; thumb spica x 10-12 weeks
2. displaced; ORIF and immobilization x 6-8 weeks
3. ORIF if:
a. displacement > 1mm
b. scapho-lunate angle >60deg
4. protective splinting x 12 weeks
b. Wrist Fx
i. Kienböck’s Disease
1. AVN(avascular necrosis) of lunate 2º to fracture
2. seen in martial arts and volleyball
3. assoc. with ulnar negative variance
ii. Hook of Hamate Fx
1. racquet or club sports 2º direct pressure of handle
2. MOI: repetitive stresses or impact on hypothenar eminence
3. usually non-dominant hand in golf; dominant in racquet sports
4. diagnose clinically and with carpal tunnel view
5. racquet or club sports 2º direct pressure of handle
6. MOI: repetitive stresses or impact on hypothenar eminence
7. usually non-dominant hand in golf; dominant in racquet sports
8. diagnose clinically and with carpal tunnel view
iii. Triquetrum Fx
1. second most common fracture
2. fall on dorsiflexed, ulnar deviated wrist= impingement between
hamate and ulnar styloid
3. immobilize 4wks
iv. Distal Radius Fx
1. fall on outstretched arm-hyperextension & ulnar deviation
2. youth football, snowboarding, soccer, skating
3. nondisplaced; conservative treatment
4. 4-6 weeks in cast then splint
5. displaced; fix surgically
6. external/internal fixation, bone grafting
v. Iatrogenic nerve compression = median nerve compression
1. due to poor positioning and external compression; is a common
surgical complication
2. they always say, “crooked cast, straight bone.” Need 3 point
pressure for better casting. (Cast complication also is stiffness)
vi. Dorsal Impingement Syndrome
1. inflammation of dorsal joint capsule with repetitive wrist
hyperextension
2. chronic pain in gymnasts
3. treat with dorsal blocking splints
II.
Radiographic diagnosis of fractures of the distal forearm, wrist, hand and fingers
a. Scapholunate injuries – most common instability pattern
i. mech: excessive wrist extension, ulnar deviation with intercarpal supination=
fall on outstretched hand
ii. widening of the S-L space
iii. dorsal/radial pain with ROM and weak grasp
iv. Watson’s scaphoid shift test
<2 mm
b. DISI Deformity
i. SL injury and lunate pulled dorsally by triquetrum, scapholunate angle
increases beyond 60 degrees
ii. How to tell—scaphoid = hand falls forward, triquetrum = hand moves
backward
c. Scapholunate Instability
i. triquetrum cont. to exert extension moment on lunate DISI deformity
occurs
ii. leads to carpal collapsescapho-lunate dissociation with advanced collapse
(SLAC)
d. Lunotruqetral Instability
i. Dx: difficult; ulnar sided weakness/pain with click during loading; tenderness
at lunotriquetral joint
ii. Angle b/t scaphoid and lunate gets smaller
iii. Tx:
1. immobilization if no VISI (ligament healing 80%)
2. injection, NSAID’s
3. arthroscopic debridement
e. Perilunate Dislocations
i. dorsal dislocation of carpus with lunate left in fossa
ii. frequently missed injuries
iii. closed reduction attempted
iv. immobilization for 10-12 weeks
1. 6-8 weeks in cast
2. remainder in protective orthotic device
v. often requires open reduction and fixation
f. Gilula’s archs (used for alignment)
i. described on posteroanterior or anteroposterior wrist radiographs and
are used to assess normal alignment of the carpus:
1. first arc is a smooth curve outlining the proximal convexities of
the scaphoid, lunate andtriquetrum
2. second arc traces the distal concave surfaces of the same bones
3. third arc follows the main proximal curvatures of
the capitate and hamate
g. TFCC (triangular fibrocartilage complex) injuries
i. Affect ulnar side of wrist
ii. TFCC: TFC, articular disk (loosely attached to ulna), UCL, radioulnar lig,
ulnolunate and ulnotriquetral lig, ECU tendon sheath
iii. DRUJ capsule intimately related (DRUJ stabilizer)
iv. MOI:
1. axial loading with pronation and ulnar deviation
2. twisting and compression vectors
3. acute or over use syndrome
v. (+) ulnar variance =  loading of TFCC
vi. Diagnosis
1. tenderness between pisiform, FCU and styloid
2. MRI helpful; +/- arthrography
vii. Treatment
1. therapy, NSAIDS, splinting x 6 weeks
2. arthroscopic debridement +/- ulnar shortening
3. possibly repair and cast x 3-6 weeks
h. DRUJ (distal radial ulnar joint) Injuries
i. MOI:
1. FOOSH in pronation and ulnar deviation
2. dislocations typically occur dorsally in pronation
ii. Diagnosis
1. tenderness to palpation and rotation
2. palpable dorsal mass in pronation
3. x-rays sometimes helpful (comparison views, CT)
4. association with TFCC tears
i. Ganglion cysts (Bible bump)= fluidfilled sacks from S-L
j. Neuropathy types (check entire limb, many occur proximal to wrist)
i. Carpal tunnel – splint, NSAIDS, rest, injection, decompression
ii. Wartenburg’s syndrome (radial nerve) – superficial radial n. (sensory)
irritation.
1. Dx: pain shooting up thumb, paresthesia dorsal thumb, + tinel’s
2. From repeated pronation/supination, direct trauma
3. Tx: splint in supination, RICE/NSAIDS,
iii. Guyon’s canal (ulnar nerve)
1. Ulnar nerve (Guyon’s canal syndrome)
2. MOI:
a. direct compression inflamming tissues in canal
b. hamate hook fracture
c. prolonged hyperextension
3. cycling (common), racquet sports
4. Diagnosis = pain in small finger, (+) Tinel’s
5. TX: padding, splinting, rest, NSAIDS, decompression
iv. Hypothenar Hammer syndrome
1. repetitive trauma to ulnar artery and superficial palmar arch
2. common in martial arts, volleyball, lacrosse
3. Diagnosis
4.
palmar pain with cool digits
a. may radiate to forearm
b. doppler for spasm, thrombosis or aneurysm
5. Treatment: rest,  hand padding, surgery
v. Finger injuries
1. Jersey finger (FDP avulsion) – extension force against a flexing finger
(grab an opponent’s jersey), can be bony or soft tissue
2. Flexor Tendon infection
a. Use Kanavel’s signs
i. Volar digital tenderness
ii. Fusiform swelling (while finger)
iii. Pain with passive extension
iv. Finger held partially flexed
3. Mallet Finger (DIP flexion)- forcible flexion injury
a. Patterns = stretch, rupture, avulsion Fx
b. Tx:
i. acute : extension splint 6-10 wks
ii. avoid hyperextension
iii. Kwire for higher demand pts
iv. Chronic = poorer results, will always have some ext lag
v. May need Fowler release if swan neck present
4. Phalangeal Fx
a. TX must include early motion to prevent stiffness
b. Position of immobilization intrinsic plus
c. Extra-articular
i. nondisplaced, stable - buddy tape
ii. displaced, stable - immobilize
iii. unstable - CR, PCP vs ORIF
5. PIP Injuries
a. Collateral Injuries
i. RCL > UCL
ii. Stress views in 0 and 30 deg flexion
iii. acute tears - partial : buddy tape
iv. complete : ? Open repair
b. Dislocations
i. dorsal most common
ii. volar plate always injured, may block reduction
iii. closed reduction
iv. open only if complex
v. chronic instability may require reconstruction
c. Fracture dislocation of PIP
i. debilitating injury
ii. dorsal most common
iii. unicondylar vs pilon
iv. extension block splint, dynamic traction
v. compass hinge, volar plate arthroplasty
vi. fusion
vi. Metacarpal Fx
1. Neck Fractures
a. stable vs unstable
b. accept less angulation in IF and LF
i. 10-20-30-40
ii. SF Metacarpal 40-70 degrees acceptable
c. 90-90 reduction technique
d. hold with splint, unstable = PCP
e. <40 degrees, 5-10mm shortening acceptable
2. Bennetts Fx
III.
IV.
3. UCL injury MCP thumb = skiier’s/gamekeeper’s thumb
a. Dx : stress views
b. Don’t stress a nondisplaced boney gamekeepers thumb
c. Stener Lesion : interposed adductor aponeurosis
Predict treatment principles of hand injuries
a. Refer out for: deep penetrating wounds/ bites, high pressure injuries, extensive fost
tissue injury like finger deglovement
Indications for surgical intervention of hand injuries
V.
Recognize types of fixation, ex fix, pinning, IM
a. Interfrag screw fixation for spiral metacarpal fx
VI.
Predict the after care following surgery
a. RICE? Splint? Nsaids or pain meds as directed?
Lecture 18: Fractures of the Lumbar Spine
I.
Recall the clinical evaluation of a patient with a lumbar spinal fracture
a. Suspect TLS fracture in any patient with trauma & back pain/tenderness, neurologic
deficit, altered mental status or presence of other vertebral or pelvic fracture
b. Treatment priorities in patients with TLS injuries involve treatment of life threats
first while maintaining spinal immobilization until fracture excluded
c. Plain x-rays must be obtained if any pain / tenderness, neurologic dysfunction or if
unable to accurately evaluate clinically (altered mental status, alcohol, distracting
injury)
d. If any abnormality on plain x-rays or highly suspicious for injury and negative, x-ray,
obtain CT. Used to define bony anatomy…used if x-ray is abnormal
e. MRI indicated if any neurologic dysfunction. Use to see ligaments.
f. Must suspect LS injuries in: (b)
i. Victims of mvcs, falls, sport related injuries & other trauma who complain of
mid to lower back pain
ii. All trauma pts with suggestive mechanism of injury who cannot be clinically
assessed
g. Important! TLS fractures can also occur in the absence of trauma if:
i. Elderly secondary to osteoporosis
ii. Malignancy with bony metastasis
iii. Patients on chronic corticosteroids
II.
Distinguish between spinal vs neurogenic shock
a. Spinal Shock = A loss of sensation accompanied by motor paralysis with initial loss
but gradual recovery of reflexes following a spinal cord injury. Most often after
complete transection.
b. Neurogenic shock = Distributive shock resulting in hypotension
i. Disruption of the autonomic pathways within the spinal cord
ii. Hypotension occurs with decreased systemic vascular resistance
iii. Caused by severe nervous system damage(brain injury, cervical or high
thoracic)
Interpret the three-column concept of spinal stability
a. Spinal stability based on the “3 column” concept – instability is present if 2 or more
columns are disrupted
b. 3 Columns
1. Anterior
a. Anterior longitudinal ligament
b. Anterior annulus fibrosis
c. Anterior ½ of the vertebral body
2. Middle
a. Posterior longitudinal ligament
b. Posterior annulus fibrosis
c. Posterior ½ of the vertebral body
3. Posterior
III.
a. Posterior body arch – spinous process, lamina, facets and
pedicles
b. Posterior ligament structures – supraspinous ligament,
interspinous ligament, ligamentum flavum & facet joint
capsules
IV.
Identify and distinguish lumbar fractures including: compression fractures, Burst
fractures, fracture dislocations and seat –belt type injuries
i. All these fractures result from one or more of 3 mechanisms of injury: Axial
compression, Axial distraction, Translation
b. Compression fractures = think: smushed
i. Compression anteriorly along the vertebral bodies, often stable fractures.
S/Sx = pain/tenderness at the site. From axial load applied in flexion. Can
occur in elderly in absence of trauma. You need to use lateral view plain film.
Note the imaging on right looks like a ‘squished marshmallow’
1. Important to confirm that the posterior elements remain intact. Might
need a CT.
c. Burst fractures = think: pushed back
i. Fragments into column means an unstable fracture (could impinge on spinal
cord)
ii. Most common on T10-12. From axial loading.
iii. Has disk injury and bone framents can be retropulsed, destruction of the Ant
and middle columns (vs. compression fracture just have mostly post column
disruption)
iv. All burst fractures should be considered unstable
d. Flexion distraction injuries/Chance fractures = think: split open
i. Posterior elements, disks & ligaments are torn or avulsed
ii. Chance fracture extends into vertebral body, usually L1-L3.
e. Fracture dislocations/translational injuries Seatbelt type injuries = think: rips
everything else
LECTURE 18 – LUMBAR FRACTURES (Dr. Myles) - OBJECTIVES!
Recall the clinical evaluation of a patient with a lumbar spinal fracture.
Must consider vertebral column injury in patients with multiple injury!
 Injury may be overlooked due to more obvious or immediately life threatening injury – don’t
forget to check the spine for injuries if something else is gushing blood.
 33% TL fracture patients have altered level of consciousness – makes it harder to find out
exactly what happened and they may not tell you if the back was potentially injured
 Missed / delayed diagnosis results in a 7.5 fold increase in incidence of neurologic injuries.
 Make sure you’re careful when moving them. Further damage (spinal/neuro) can occur if
you don’t stabilize them.
Patients with traumatic injuries (car crash, falls, sports related) can present with spine injuries, but
fractures can occur without trauma
 Elderly secondary to osteoporosis
 Malignancy with bony metastasis
 Patients on chronic corticosteroids
Normally need X-rays to exclude fracture or other problem.
In order to clinically exclude an unstable thoracolumbar spine fracture, the following must be
present:
 Patient must be awake, alert and sober
 Patient must have no midline thoracic or lumbar back pain OR tenderness
If there is no tenderness on palpation or ecchymosis over the spinous processes, an unstable spine
fracture is unlikely. X-rays may not be needed in this case
Need to perform:
 Physical exam
o Sensitivity of clinical exam for TL fracture = 80%
o Specificity for TL fracture = 39.4%
 Inspection: simple observation – patient must be exposed
o Must maintain spinal precautions
o Visually inspect the back
 Contusions, lacerations, abrasions, visual deformity
o Other findings that are a clue to risk of spinal injury
 Scapular bruising, chest and abdominal markings (seatbelt, steering wheel
etc)
 Palpation of entire spine

o Tenderness, deformity or muscle spasm
o Step-off deformity may be palpated with severe subluxation (d)
o Widening of interspinous space
 Tearing in posterior ligament complex & potentially unstable spinal injury (d)
Perform neurologic examination
o Dorsal & ventral cord function
o Quantitative assessment of motor function / myotomes
 Muscle graded on 6 point scale from normal strength to paralysis
o Sensory testing including evaluation of the sacral dermatomes
o Evaluation of anal sphincter tone (I’d rather not, but ok).
Distinguish between spinal vs. neurogenic shock and spondylolysis vs. spondylolithesis.
Spinal shock – A loss of sensation accompanied by motor paralysis with initial loss but gradual
recovery of reflexes following a spinal cord injury.
 Usually after complete transection (severing of cord)
 Affects everything at the severed level and below.
Neurogenic shock – Distributive shock and disruption of the autonomic pathways within the spinal
cord resulting in hypotension
 Hypotension occurs with decreased systemic vascular resistance
 Caused by severe nervous system damage(brain injury, cervical or high thoracic)
 “Affects the entire body”
Spondylolysis – specific defect in the connection between vertebrae (in the pars interarticularis of
the vertebral arch.
 Causes the affected vertebrae to be unstable because it can’t articulate properly in proper
alignment with its neighbors.
 Most common in L5, but can be in all lumbar and in thoracic spine (3-6% of population).
 Causes back pain (common in adolescents that over-train.
Spondylolithesis – The anterior or posterior displacement of a vertebrae or the vertebral column in
relation to the vertebrae below.
 Most common cause is spondylolysis
 Two types
1. Dysplastic – rare congenital form  occurs due to malformation of lumbosacral joint
2. Isthmic – slip or fracture of the intravertebral joint
Interpret the three-column concept of spinal stability.
Spinal stability commonly assessed via the “three column” concept
 Stability based upon integrity of two of the three spinal columns (b)
 Instability = failure of 2 or more columns
3 Columns
 Anterior
o Anterior longitudinal ligament
o Anterior annulus fibrosis
o Anterior ½ of the vertebral body


Middle
o Posterior longitudinal ligament
o Posterior annulus fibrosis
o Posterior ½ of the vertebral body
Posterior
o Posterior body arch – spinous process, lamina, facets and pedicles
o Posterior ligament structures – supraspinous ligament, interspinous ligament,
ligamentum flavum & facet joint capsules
Identify and distinguish lumbar fractures including: compression fractures, Burst fractures, fracture
dislocations and seat –belt type injuries.
Compression fractures – compress and fracture the anterior column of a vertebrae
 Mechanism – axial load placed while spine is in flexion
 Fairly stable (posterior ligaments not messed up so everything is still held together).
 Neurologic deficits rare but associated with a high incidence of intestinal ileus
 S+S: Pain or tenderness at the site
 Can occur in the elderly in the absence of trauma.
 Get lateral X-ray
 Usually fine with no operative treatment
Burst fractures – disruption/fracture of the anterior and middle columns
 Most common location: T10 – T12 and from 2o falls & car crashes
 Mechanism – axial loading (compressive force) causing:
o Fracture of the endplate
o Often extensive disk injury at levels directly adjacent to fx (j)
o Danger: bone fragments can be retropulsed into spinal canal
 Unstable, unlike compression fracture
 Neurologic deficits are seen in 42-58% of these patients
 Get lateral X-ray

o Loss of anterior AND posterior vertebral height
o Distorted posterior longitudinal line
o CT scanning - generally recommended if vertebral compression > 50% or a burst
fracture suspected for any reason
o Causes actual DISPLACEMENT of the vertebrae
Treatment depends on severity of injury (j)
o May be operative or non-operative depending on several factors
 % of spinal canal compromise
 Degree of angulation at the site of injury
 Presence or absence of a neurologic deficit
o Management decisions should be made in conjunction with an orthopedic or spinal
surgeon
Flexion-distraction injuries (chance fracture) – fracture in the posterior and middle columns, with
the anterior column serving as the fulcrum
 Most common mechanism – car crash and patient isn’t properly wearing seatbelt (lap belt
only)
o Inertia causes severe flexion of lumbar spine and anterior column gets the brunt of
the pivoting force
o Can produce pure bony injury, pure ligamentous injury (including bilateral facet
dislocation) or a combination of injuries
 High incidence of associated intra-abdominal injuries (50%) including bowel rupture & liver
or spleen lacerations
 Unstable
 Symptoms may also include
o Ecchymosis of the lower abdomen
o Tenderness at the fracture site
 Lateral X-ray – key view
o Horizontal disruption through spinous process, laminae, transverse process, pedicles
& vertebral body (b)
o Height of vertebral body is INCREASED
o Distance between the spinous processes may appear to be widened
o May have anterior vertebral impaction with compression fractures
 Operative vs. nonoperative treatment
o Decision depends on bony vs. significant ligamentous injuries
 Fx through bone only - good prognosis for healing: (j) – nonoperative or
operative
 If significant ligamentous disruption - heal in less predictable fashion generally considered unstable & operative treatment
Fracture dislocations (translational injury) – failure of all three columns of the spine (most at T10L2)
 Mechanism – massive direct trauma to the back (combination of forces)
 Several patterns can occur (c)
o Rotational fracture-dislocations
o Shear injuries
o Pure vertebral dislocations




Neurologic injury common
o 60-80% of these result in permanent neurological deficits (b)
o Shear fractures & pure dislocations result in severe neurologic injury causing
complete paraplegia in nearly all patients
Clinical exam
o Usually reveals tenderness at the fracture site
o May have large contusions in the lumbosacral area due to direct trauma
o May have significant kyphosis and widening of the spinous process at the level of the
dislocation
o Due to massive trauma associated with complete vertebral dislocation, patients
invariably demonstrate neurologic deficits
Imaging
o Plain X-rays
 Dislocations appear as complete displacement of superior vertebrae relative
to the one below
 If rotational component present - distorted alignment of the spinous
processes
o CT scanning
 Usually indicated for both fx evaluation & detection of intra-abdominal
injuries
 Can detect fx fragments in the spinal canal & quantify extent of spinal cord
impingement
Most patients treated surgically
LECTURE 19 – BENIGN TUMORS OF THE MUSCULOSKELETAL SYSTEM (Dr Bhansaly)
Characteristics that favor benign diagnosis
o Asymptomatic
o Radiograph: well defined lesion with sclerotic well defined reactive margins
 Suggest a long standing process associated with slow growth
Characteristics that favor malignant diagnosis
o Pain
o Radiograph: permeative (spreading) lesion, with lytic destruction and poorly defined
margins
 Suggest rapid progression
 Many times – no further studies are needed for typical benign tumor
 Precise incidence is unknown because many benign bone tumors are NOT biopsied
 HOWEVER, benign tumors greatly outnumber malignant counterparts and most frequently occur
in the first 3 decades of life
 Malignant tumor is most likely in an elderly individual
Bone Forming Tumors
Osteoid osteoma – tumor with small radiolucent nidus (origin)
 < 1-1.5 cm
 Nidus – produces prostaglandins (cause nocturnal pain which aspirin alleviates)
 Males 10-20 years old
 Normally in cortex of proximal femur
 No treatment if pain is bearable; otherwise surgical resection
Osteoblastoma – tumor with larger radiolucent nidus (same as osteoid osteoma, just bigger).
 > 2 cm
 Pain; does not go away with NSAID’s – may have limp or neuro symptoms from nerve
compression
 Males 10-20 years old
 Normally in vertebrae (spinous process, lamina, pedicle)
 Treatment: curettage (scooping out the bad bone)  then bone grafting to fill in
 Good prognosis if completely removed; can recur up to 20% of cases
Vertebrae common, but different here.
Cartilage Forming Tumors
Osteochondroma – MOST COMMON BENIGN BONE TUMOR – cartilage capped bony spur on
external surface of bone  Looks like a cauliflower
Males 10-30 years old
 Normally located in metaphysis of distal femur (around knee) – sometimes proximal
humerus
 Can be solitary or multiple
o Hereditary multiple osteochondromas (2 or more) – autosomal dominant
 Small risk of progressing to chondrosarcoma (not good)
 Most can go untreated unless it bothers them
o Remove if irritation or concern for turning into something malignant
Enchondroma – cartilage tumor that develops in the medulla (marrow cavity) of diaphysis of long
bone
 Well circumscribed lucent lesion
o Risk of fracture
o If pain and absence of fracture, low grade chondrosarcoma must be ruled out
 Usually second decade, but any age really; Males = females
 Long bones of hand, then humerus and femur
 Distinctive “C” and “O” formations
Periosteal chondroma – (Rare) cartilage forming tumors that arise from the surface or cortex, deep
periosteum, and that erode into the cortex
 Kids and adults
 Usually in proximal humerus; also in long bones of hands and feet
 Pain at site of lesion (palpable hard mass)
o Small scalloped radiolucent lesions on outer cortex of bone
o Rim of sclerotic bone
 Treatment – curettage or en block excision
Chondroblastoma - Rare type of benign bone tumor that originates from chondroblasts
 Males 10-20 years old
 Found in epiphyses of long bones (particularly knee)
 Can continue to grow and destroy bone
 Patient has pain, impaired mobility, withered appearance of muscle, fluid accumulation in
nearest joint
 Surgical removal, bone grafting, and physical therapy
 Radiographs show cysts with spots of calcification
Chondromyxoid fibroma – rare, benign, cartilage-forming tumor of the tubular long bones.
 Males teens-20’s
 Proximal tibia or distal femur (knee), also in calcaneus in foot
 Pain and swelling
 Curettage & bone grafting to treat
 Radiographic findings:
o intramedullary, lobulated or bubbly lesion in the metaphysis
o it has a sclerotic border
o It typically is lucent, with a rare chondral matrix
Fibrous Lesions
Fibrous dysplasia – lesion in which portions of the bone are replaced by fibrous connective tissue
and poorly formed trabecular bone
 Males in teens-20’s
 Found in any bone; proximal femur, tibia, ribs, skull are most common
 Occurs in medullary cavity
o Caused by a postzygotic mutation in the guanine nucleotide stimulatory protein
(GNAS1) gene
o More of a skeletal dysplasia than a true neoplasm.
 Can occur in single or multiple bones
o Monostotic
o Polyostotic
 McCune-Albright syndrome (Albright syndrome)
 Associated with endocrine abnormalities and café-au-lait spots
 Mazabraud syndrome
 Associated with soft tissue myxoma
 Overlaps clinically with McCune-Albright syndrome
 Most asymptomatic, but localized pain and swelling with some
 “Shepherd’s crook” deformity of proximal femur
 Lytic lesion with “ground glass” appearance
Nonossifying fibroma – well circumscribed solitary fibrous proliferation usually discovered as
incidental finding on x-ray
 Two size classes
o Fibrous cortical defects - ~0.5 cm
o Nonossifying fibromas – 5 to 6 cm
 Males (usually children)
 Usually femur, followed by tibia
 Normally asymptomatic and regress spontaneously
 Radiographic finding:
o They are eccentric, multi-loculated sub-cortical lesions with a central lucency and a
scalloped sclerotic margin
o Serial x-rays show the lesion migrating away from the epiphyseal plate with time
Cystic Tumors
Aneurysmal bone cyst – expansive vascular lesions that consist of blood-filled channel
 May be primary or related to other benign bone lesions (e.g., giant cell tumor,
osteoblastoma, chondroblastoma)
 FEMALE adolescents
 Found in many bones; posterior spinal elements, femur, tibia – most common
 Pain, swelling, neuro symptoms; can inhibit growth of bone if it crosses growth plate
 Excision or curettage with bone grafting to fix
 Radiographic Findings:
o Aggressive, expansile, lytic metaphyseal lesions with an "eggshell" sclerotic rim
o Sharply circumscribed. They may have a "soap bubble" appearance secondary to the
reinforcement of the remaining trabeculae that support the bone structure
Other
Benign giant cell Tumor – Rare, benign but locally aggressive osteolytic skeletal neoplasm
 Reactive multinucleated giant cells resemble osteoclasts
 FEMALES 20-30 years old; more Asians
 Epiphysis of distal femur or proximal tibia (knee)
 Pain, swelling, limited ROM



To treat: curettage, marginal excision, en bloc resection (may need reconstructive surgery)
o If surgery isn’t feasible – may need radiation (need to make sure you get margins)
Prognosis:
o Reoccurrence varies
 May be as high as 50%
 Can get lung metastasis – benign lung implants
Radiographic finding:
o expansile eccentrically-placed lytic area, which is the result of intratumoral
hemorrhage
o involves the epiphysis and the adjacent metaphysis and there is frequent extension
to the subchondral plate, sometimes with joint involvement
LECTURE 20-21 – INFECTIOUS AGENTS OF THE MUSCULOSKELETAL SYSTEM (Dr. Gregg)
Recall the important key characteristics helpful in identifying the infectious agents responsible for
osteomyelitis and infectious arthritis.
Osteomyelitis – infection in a bone
Hematogenous – comes in through the blood supply
 Affects Children and adults differently
o Children – long bones affected  each bone metaphysis has its own blood supply,
and the blood slows while changing directions within the bone
 Trauma to the bone can cause occlusion of blood flow and slow it even more
– increasing likelihood of microbe colonization.
 Usually in single bone
 Symptoms – Fever/chills, localized pain and swelling, restricted ROM
o Adults – vertebrae affected  microbes access vertebral bodies via spinal arteries
 Sources of bacteremia:
– UTI (esp. men >50 y)
– Dental abscesses
– Soft tissue infections
– Contaminated IV lines
 Symptoms – neck, back, chest, abodomen, extremity pain; fever & chills
PRIOR to onset of pain
 Common microbes by age class
o Neonates – 95% cases caused by single microbe
 Strept. Agalactiae (group B strept)
– gram (+) “chains”
– Catalase (-)
 E. coli
– Gram (-) “clusters”
– Catalase (+)
– Oxidase (-), also ferments lactose
o Children (prepuberty)
 Staphlyococcus aureus – common  50% of all cases
– Gram (+) clusters – often tetrads
– Catalase (+)
– Coagulase (+)
 Streptococcus pneumoniae
– Gram (+) encapsulated chain
– Catalase (-)
o Adults
 Staph aureus
 E. coli – 25% of cases
o IV Drug users
 Pseudomonas aeruginosa
– Gram (-) motile baccili
– Oxidase (+)
– Blue (pyrocyan) pigment
 Candida albicans
– Yeast – hyphal & pseudohyphal fungus
Contiguous focus – comes from a neighboring infection
 Fever, pain, redness/tender
 May not be apparent for weeks to months
 Diabetic Patients
o Diabetic neuropathy exposes foot to frequent trauma & sores
o Patient may be unaware that infection has spread to bone
o Poor tissue perfusion impairs normal wound healing
o Promotes anaerobic infections
o Bone palpable during exam of ulcer base = osteomyelitis
 Microbes responsible
o Staphylococcus aureus
 >50% of cases
o Additional microbes:
 Staphylococcus spp. – Postoperative
 Gram-negative bacilli (GNB) – Mandible, pelvis, small bones
 Pseudomonas aeruginosa – Punctures
 Pasteurella multocida – Animal bites
 Anaerobes – Facial, pelvic, sacral & bites
Infectious arthritis – infection in a joint
 Hematogenous route is the most common route of infection in all groups
 Neonates
o S. aureus, Candida, GBS, Neisseria
 Children
o S. aureus, Streptococcus ssp.
 Adults (15-40)
o Neisseria
 Adults (over 40)
o S. aureus
 Knee is most common joint affected
o Swelling
o Fever/chills
o Limited ROM
 Diagnosis
o Obtain synovial sample – will contain microbes (normally a pretty sterile
environment)
 Look for crystals to rule out gout
o Two types
 Gonnococcal – can use Thayer-Martin agar; PCR for Neisseria DNA
 Nongonococcal – 75% are S. aureus
o Other less common types/origins
 Borrelia burgdorferi (tick bite)
 Treponema pallidum (syphilis)
 Gram (-) motile spirilla
 Mycobacterium tuberculosis



50% of cases (thoracic & lumbar spine)
1% cases – granulomatous arthritis
Acid fast stained
Identify the means by which the pathogens gain access to the target tissues and any discussed
pathogenic factors that perpetuate disease.
Bites, puncture wounds, open fractures, surgery, transfer from other infections in body, sexual
activity (gonoccocal)
 Osteomyelitis often precedes infectious arthritis
Identify from values in the table and general characteristics of the microbes the causative agents in
clinical cases.
Lecture 22: Osteoporosis

Define osteoporosis
1. A reduction in bone strength with an increased risk of fractures
 Loss of bone tissue results in a deterioration of skeletal microarchitecture
 Increased “porosity” of bone
 Bone density 2.5 standard deviations below the mean of same gender, young healthy
adults (WHO): T-score < -2.5
2. Diff from Osteopenia = Low bone density is diagnosed in postmenopausal women at lower
end of young normal range: T-score < -1.0

Discuss causes of osteoporosis
1. Bone repairs itself by actively remodeling

bone resorption (osteoclasts)

bone formation (osteoblasts)
2. The remodeling cycle may become unbalanced


after menopause

with aging in both men and women

bone resorption excedes bone formation

net bone loss is predominantly cancellous (vertebral) bone
Discuss sequela (after effect of disease) of osteoporosis
1. Hip fractures
2. Vertebral fractures
3. Wrist fractures
4. Most any fracture you can think of (pelvis, head of the humerus, etc.)
5. Incidence doubles q5 years after age 70.
6. Only ⅓ have a full recovery.
7. 20% live in a nursing home lifelong.
8. Hip Fx Complications
 Deep venous thrombosis
 Pulmonary embolism
 5 – 20% mortality rate
 66% suffer permanent mobility loss
 Doubles risk of future fractures.
9. Vertebral Crush Fx
 Asymptomatic; height loss, kyphosis, back pain
 Thoracic compression fractures = Restrictive lung disease (lungs smaller)


Lumbar compression fractures = abdominal distention, early satiety, constipation
(tummy is smaller)
Discuss treatment for osteoporosis ( a lot is preventive too)
1.
2.
3.
4.
5.
Most imp part is Dx
Weight-bearing exercise: lifelong
Smoking cessation: lifelong
Ethanol moderation: lifelong
Calcium and vitamin D: dietary, sunlight, lifelong
 Calcium and vitamin D maintain or increase bone density in postmenopausal
women & help prevent hip and nonvertebral fractures in all older adults.
 Calcium has no benefit on fracture rate used alone.
 Vitamin D: NNT = 45 to prevent a hip fracture over 3 years.
 1200 mg / day of calcium: men 65 years and older & postmenopausal women.
 1000 IU / day of vitamin D3: regardless of sunlight exposure to offset skin changes
that  efficient use of UV light to synthesize vitamin D precursors. (I start with 4000
units qd.)
6. Estrogen replacement
 Estrogen produces bone loss protection.
 All benefit is lost in 10 years if stopped.
 It’s a wash.
7. Bisphosphonates
 Impair osteoclast function.
 Poorly absorbed
 incorporated into bone matrices where resorption is active.
 Reduce osteoclast number by apoptosis
8. Selective estrogen receptor modulators
 Tamoxifen reduces bone turnover and CA breast, but it increases uterine CA.
 Raloxifene reduces vertebral collapse as well as CA breast.
9. Calcitonin
 Nose spray
 Possible analgesic effect
10. Hip pads = worn over greater trochanters, prevents hip fractures (NNT=7)

Discuss prevention of osteoporosis
1. Osteoporosis Risk factor reduction: Glucocorticoids can be titrated to minimal effective
doses.
-Thyroid hormone doses need to be as low as needed to normalize TSH.
Smoking cessation.
2. Fall risk factor reduction: Ethanol avoidance. Reduce or eliminate sedating medications.
Protect against orthostatic hypotension. Address nocturia. Fix environmental hazards: wires,
rugs, furniture, socks. Vision correction.
3. Exercise





Decrease in physical activity or immobilization  decline in bone mass
Walking, a weight-bearing exercise, can be recommended for all adults
Adult initiated exercise  2% bone mass increase at best.
Start slowly and gradually increase the number of days and time spent walking each
day (at least 3 days weekly)
Improves coordination, balance, and strength.
***He really likes DOE, POE, NNT, NNH. Also he hates drugs and says hip pads are best.