Download ORTHOPEDIC SURGERY – Pediatric/Oncology

Section 10
ORTHOPAEDIC SURGERY STUDY GUIDE
FOR
MEDICAL STUDENTS, R1s and R2s
July 5, 2011
Jeffrey J. Eckardt M.D. – Professor and Chair, Orthopaedic Surgery
Joshua G. Bales M.D. - Resident
Trauma
Fractures:
 Definition: a fracture is a structural break in continuity of bone
 Location in the bone: diaphysis, metaphysis, epiphysis, intra-articular
 Extent: complete or incomplete (hairline, buckle, greenstick fractures)
 Configuration: transverse, oblique, spiral, butterfly
 Simple fractures have 1 fracture line and 2 fragments. Comminuted fractures have more
than 1 fracture line and more than 2 fragments.
 Relationship of fracture fragments to each other: nondisplaced: fragments remain in
anatomic alignment. Versus displaced fractures: nonanatomic alignment.
 translated
 angulated
 rotated
 distracted
 overriding
 impacted
 Relationship of fracture fragments to the environment closed (not exposed to the
environment) versus open (exposed to the environment via a break in the soft tissues)
 Gustillo Classification
 Type I  1 cm wound
 Type II > 1 cm wound with moderate soft-tissue damage
 Type III extensive soft-tissue damage
A: adequate coverage, without periosteal stripping or vascular injury.
B: bone exposed with periosteal stripping, plastics consulted needed for soft
tissue coverage of defect
C: with vascular or nerve injury, vascular surgery consulted needed for vessel
injury
 Fracture healing
 Union - complete and timely healing
 Delayed union – healing that takes longer than expected
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Nonunion – healing has not occurred within 1 year (time is fracture site dependent)
Malunion – healing with residual angular deformity
Closed Fracture - treatment
 Closed reduction (realignment of fracture fragments) with immobilization
 Closed reduction and percutaneous fixation
 Open reduction and internal fixation (ORIF) operative realignment with rods,
plates, and screws for fixation
 External fixation operative realignment with external device to hold fixation. may
be used for extensive soft tissue injury, extensive comminution or a grade III open
fracture
Open Fracture - treatment
 Complete neurovascular examination
 Align and splint fracture, monitor neurovascular status post manipulation
 Culturing the wound is controversial (not performed routinely at UCLA).
 Cover wound, consider pressure dressing if oozing blood, take emergently to the
OR. If unable to control hemorrhage (arteriogram vs. Vascular surgery consult if
pulses absent)
 Begin antibiotics in the ER - ASAP. This is the only Level 1 evidence we have for
open fractures. Ancef 1g IV q8 h., which is good for gram positive organisms.
Add Gentamicin IV 1mg/kg q8 for gram negative coverage for Type III and some
Type II fractures depending on attending preference.
 Tetanus prophylaxis: If patient has not been immunized for tetanus, then tetanus
immune globulin 1g 250 units IM and tetanus toxoid 0.5cc IM at separate sites. If
pt previously immunized for tetanus, then tetanus toxoid 0.5cc IM.
 Never irrigate or debride in the ER. Always irrigate and debride in the controlled
environment of the operating room.
 In the OR remove all foreign material, irrigate and debride wound: “The solution
to pollution is dilution”.
 In terms of fracture management, consider IM nail for tibia/femur. Spanning
external fixator for contaminated fractures/intra-articular fractures/unstable patients
Orthopedic Emergencies

Primary trauma assessment ABCs
 Airway, Breathing, Circulation, Disability, Evaluation
 Open fracture: needs to be in the OR within 6 hours (controversial, also depends on
type, contamination, etc). Some type I fractures can wait overnight if needed.
 Compartment syndromes need fasciotomy
 Clinical exam, pain out of proportion to physical exam. Compartment pressures
within 30 mmHg of the diastolic pressure.
 Herniated disc or spine fracture with impending neurological loss; Cauda Equina
Syndrome: needs admission, neurologic exam, MRI or CT myelogram, and
decompression of the neurologic structures
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Dislocated joint. For example, dislocated knee: risk of popliteal artery rupture and
danger of a compartment syndrome.
Hand infections. Tenosynovitis of one finger may spread to palm and other fingers via
common tendon sheath, and therefore need emergent antibiotics and possible I&D.
Septic joint: risk of cartilage destruction, post infectious arthritis, and even total loss of
the entire femoral head with subsequent leg length discrepancy.
Fat embolism following long bone fracture or reaming, rodding or manipulation of the
medullary canal of a long bone.
Orthopaedic complications
A: Compartment Syndrome
Important Points
 abnormal increase in pressure within an anatomic compartment
 Snake Bite: rare cause of compartment syndrome, treat via stabilization and antivenom.
Presentation
 4 Ps
 Pain out of proportion to injury, pain with passive motion
 Paresthesia
 Paralysis
 Pulselessness
Evaluation
 This is a clinical exam, pain out of proportion and tense compartments signal a need for
emergent fasciotomy
 Measure intracompartmental pressures
 Compartment pressures greater within 30 mmHg of diastolic blood pressure
 Normal pressures usually around 4-8 mmHg in a compartment.
Treatment
 Emergency fasciotomy
Complications
 Volkmann’s Contracture due to untreated compartment syndrome of the forearm.
 Associated with a supracondylar fracture in a child.
 May also occur in open fractures
 Compromise of the brachial artery leading to ischemia, muscle death, and necrosis of
the flexor muscle groups in the forearm
 Severe flexion contracture of the forearm, wrist and fingers
B: Pulmonary Emboli
Important Points
 emboli occluding pulmonary artery, arteries; clot usually originates in the deep veins of
the thigh and pelvis and not in the calf
 Risk Factors: bedridden, hypercoagulable states (i.e. cancer; medications such as oral
contraceptives; surgery – may present 2-3 wks after surgery)
Presentation
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difficulty breathing, shortness of breath, tachypnea, sinus tachycardia, delirium (due to
hypoxia), cough, hemoptysis, anxiety, “impending sense of doom,” coma, pleuritic
chest pain - ischemic necrosis sets up inflammatory response between the visceral and
parietal pleura, may hear rub over the area.
Evaluation
 Chest X-ray – Look for the wedge, area of lung infarct caused by emboli.
 Arterial blood gas – PO2 < 70mmHg; decreased O2 saturation.
 EKG – sinus tachycardia; right heart strain (2O to saddle emboli – right heart pumping
against saddle embolus in pulmonary arteries, emergent)
 V-Q scan – many false positives and false negatives
 Doppler – looking for DVT’s, noninvasive
 Venogram – gold standard, best way to locate emboli in veins
 Spiral CT – useful at diagnosing pulmonary embolism
 Pulmonary angiography – high risk, infrequently performed
Treatment
 Reduce hypoxia, stabilize clot, prevent more clots and emboli
 Oxygen – via mask
 Intubation- if mask not effective
 Add PEEP to ventilator settings
 Anticoagulants- stabilize/dissolve clot. In general if the diagnosis is phlebitis,
anticoagulate for 3 mos. If the diagnosis is PE, anticoagulate for 6 mos.
 Heparin – IV 5,000 – 10,000 units (or 80 units/kg) bolus followed by a continuous
infusion (18 units/kg/hour) titrated to a PTT between 1.5 –2.5 times normal for 510 days.
 Coumadin – while giving heparin start coumadin titrated to an INR of 2-3 times
normal for 6 months or longer depending on patient and etiology.
 Streptokinase 1.5 million units IV over 60 min. Administer directly into involved
vein to dissolve clot. (Not performed routinely may be done by IR)
 IVC Greenfield filter – prevent clots from entering right heart. Indicated if there is
risk or evidence of more emboli.
C: Fat Embolism
Important Points
 Diffuse pneumonitis in the lungs secondary to the embolization of fat and marrow
debris.
 Can result from trauma, fracture, reaming a canal, impaction of a prosthesis, or
pressurization with cement.
Presentation
 Cardiovascular, respiratory, and neurologic symptoms due to occlusion and therefore
hypoperfusion of tissues. Increased heart rate, increased respiratory rate, fever. may see
petechiae under eyes, in axillary folds, and in nail beds. Progressive hypoxia may lead
to a delirious patient.
Evaluation
 Lab Work-Up – ABG – decreased PO2, Pulse Ox – decreased SpO2,
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CXR – diffuse pneumonitis, (vs. pulmonary thromboemboli – local pneumonitis),
whited out lungs
Treatment
 Oxygen. Intubate if indicated with PEEP
 Steroid bolus with 100 mg solumedrol (controversial but appears to be effective)
 Heparin contraindicated
Pediatric Orthopaedics
Pediatric Diseases
A. Arthrogryposis – Multiple rigid joints, no skin creases, teratologic hip dislocation,
sensation is intact and these patients have normal intelligence
B. Duchenne’s Muscular Dystrophy – sex linked recessive, elevated CPK, absent dystrophin
protein, most patients die at age 20; Becker’s muscular dystrophy has an abnormal
dystrophin gene and is not as morbid as Duchenne’s
C. Cerebral Palsy – Nonprogressive upper motor neuron disease; injury to the immature
brain, onset before 2 years of age; constellation of symptoms include spasticity, toe
walking, crouched gait, scoliosis; types include spastic, athetoid, ataxic, mixed
D. Myelodysplasia – Failure of neural tube to close, patient’s functional level is lowest
functioning nerve root, risk factors include maternal hypothermia, maternal insulindependent diabetes, valproic acid, folate deficiency; most patients have a latex allergy,
clubfeet, vertical talus, hip dislocation
E. Adolescent idiopathic scoliosis – right thoracic is the most common, curve progression
most closely associated with peak growth velocity; bracing controversial but most will
brace above 25 degrees, most will perform surgery above 40 degrees
The Limping Child The Five Major Causes
A.
B.
C.
D.
E.
Toxic transient synovitis
Septic arthritis
Developmental dysplasia of the hip (DDH)
Legg-Calves-Perthes disease (LCPD)
Slipped capital femoral epiphysis (SCFE)
F. Don’t forget other causes!
1. Trauma
2. Child abuse
3. Infection: osteomyelitis
4. Arthritis: juvenile rheumatoid.
5. Tumor:
Rhabdomyosarcoma: Muscle (0-5years)
Ewings Sarcoma: Round cell (5-15 years)
Osteosarcoma: Spindle cell (5-80years, 17 yr. Median)
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A: Septic Arthritis of the Hip, Knee, Foot, Wrist, Elbow and Shoulder Joint
Important Points
 bacterial infection of a joint hip of particular concern as a medical emergency
 Untreated may quickly lead to destruction of joint cartilage and avascular necrosis of
femoral head due to decreased blood supply
 Caused by hematogenous spread of infection, often no known source
Presentation
 Child with high fever, limp, pain with passive motion of hip, may lie with hip
externally rotated, slight hip flexion
Evaluation
 Labs: elevated WBC, C-reactive protein and ESR, blood cultures often negative
 Radiology:
 Bone scan: focal area of increased uptake
 X-ray : may show joint effusions
 diagnosis: MUST aspirate joint, send fluid for cell count, gram stain, culture and
sensitivity (certain aspirations may need fluoro guidance)
Treatment
 To OR for immediate irrigation and debridement, must take a sample of the synovial
lining as well
 Open washout is standard but in select cases may perform an arthroscopic washout
 followed by IV antibiotics for 2-8 weeks (per organism and ID recommendations)
 Empiric treatment with Ancef 1g IV q8 h (do NOT give any antibiotics until
cultures are taken!!!)
 Modify according to culture results and bacterial sensitivity
 followed by 2-4 months of oral antibiotic, in consultation with ID
Organisms
 Staph aureus: most common organism.
 Gonorrhea in pediatric and adult populations
 Cocci: in the Southwest USA
B: Toxic Synovitis: Important Points
 Viral inflammation of the hip
 Presentation similar to septic arthritis of the hip
 Diagnosis of exclusion
Presentation
 Child with low fever, limp of in lower extremity, pain with active and passive motion,
increased warmth of joint
Evaluation
 Labs: WBC and ESR often normal, blood cultures negative
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Radiology:
 bone scan: may or may not show focal area of increased uptake
 X-ray: may show joint effusion
 MUST aspirate joint if high index of suspicion for septic arthritis of hip, send fluid for
cell count, gram stain, culture and sensitivity
 Diagnosis of exclusion: MUST rule out septic arthritis of the hip
Treatment
 gradual return to activities as tolerated
 bed rest  longitudinal traction in select cases
C: Developmental Dysplasia of the Hip (DDH)
Important Points
 progressive condition with abnormal development of hip structures
 indicates hips that are unstable, subluxated, dislocated and/or have malformed acetabula
 formerly congenital dysplasia of the hip but may not be evident at birth
 3 characteristic components:
 abnormal slope of acetabulum
 excessive hip joint laxity
 abnormal rotation of upper end of femoral shaft
 3 stages
 head of femur located within inadequate acetabulum
 head of femur slightly subluxed and moved away from medial aspect of
acetabulum
 head of femur dislocated
 Risk factors for DDH:
 positive family history for DDH, female sex, breech presentation, primaparity,
oligohydraminiosis
 Associated with:
 congenital muscular torticollis, skull and facial abnormalities, congenital
hyperextension of the knee, metatarsus adductus, clubfoot deformities
 Definitions
 dislocated hip: no contact between femoral head and acetabulum in resting position
 Dislocatable hip: in reduced position at rest. Can be dislocated with stressed
flexion and abduction
 Subluxable: in reduced position at rest. Can be dislocated with stressed flexion and
abduction hip can be subluxed (partial contact between femoral head and
acetabulum)
 Dysplastic - no signs of instability but femoral head and acetabulum are
abnormally shaped. Hips may/may not become unstable with continued
development
 Teratologic dislocation of the hip – secondary to another disease process
 occurs early during intrauterine development
 stiff , high-riding, irreducible with severe dysplasia of joint at birth
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usually associated with neuromuscular abnormalities arthrogryposis,
myelodysplasia
Presentation (according to age at diagnosis):
 Newborn:
 if unilateral: asymmetrical skin folds on proximal thigh (not sensitive or specific)
of affected side and + Galeazzi
 if hip is already dislocated, - Barlow, +/- Ortolani (depending on whether
reducible)
 if hip is subluxable or dislocatable, + Barlow, + Ortolani
 6 month with DDH and dislocated hip
 often asymptomatic
 unilateral: positive Galeazzi, + leg length discrepancy, asymmetric skin folds on
proximal femur, trochanter displaced upward, broadened perineum on affected side
asymmetric abduction >10%discrepency
 bilateral: negative Galeazzi, no leg length discrepancy, symmetric abduction but
less than 60% each side
 2 year old child with DDH and dislocated hip
 unilateral: limp with tendency towards Trendelenberg sway due to weak hip
abductors on affected side, unilateral toe walking, examination may reveal
shortening of thigh, multiple skin folds, broadened perineum, prominence of
trochanter, decreased distance trochanter to iliac crest
 bilateral: waddling gait
Evaluation
 all tests must be performed on a completely undressed child supine on a flat
examination table
 a child’s hips MUST be examined with each examination from birth until walking with
normal gait (usually 2-3 years of age)
 Galeazzi test: assess apparent femur length
 Hips flexed to 90 adducted to midline with knees in flexion, child’s knees do not
line up suggesting femur length discrepancy (positive test) indicative of apparent
femur shortening on affected side due to femoral head in abnormally cephalad
position.
 often associated with asymmetric skin folds on affected proximal thigh
 dysplastic hip must be compared to normal
 Note: negative Galeazzi test in patient with bilateral DDH
 Ortolani test: assess passive subluxation or dislocation
 Thumb on medial side of thigh, middle and index fingers over greater trochanter,
knees flexed to 90, sequentially, each hip is brought from midline in 90 degree of
flexion and abducted, gentle anteriorly directed force on greater trochanter.
palpable clunk when femoral head is seated into acetabulum (positive test)
indicates a dislocated but reducible femoral head
 Note: irreducibly dislocated hip will have negative Ortolani test
 Note: hip clicks - audible high pitched sounds without palpable clunk - on hip
examination likely caused by iliotibial band moving over greater trochanter or
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iliopsoas tendon sliding over iliac crest. normal and usually disappears within 4-6
months.
 Barlow test: stress test to assess potential for hip subluxation or dislocation
 Thumb on medial side of thigh, middle and index fingers over greater trochanter,
knees flexed to 90, sequentially, each hip is placed in 90 flexion in neutral
adduction with gentle force directed posteriorly. Sensation of displacement of
femoral head posteriorly out of acetabulum is positive test. Normal (negative test),
no instability. Found. degree of displacement (positive test) indicates subluxable or
dislocatable
 Note: will be negative if the hip is already in a dislocated position
Radiologic evaluation
 Ultrasound: less than 6 months - ultrasound may help delineate configuration and
position of femoral head and acetabulum - cartilaginous structures not seen on XR.
Static or dynamic in conjunction with Barlow test. High degree of interobserver
variability. Has not been shown to be reliable as screening test (high false + at
birth)
 XR: AP with hip extended and lower extremities in neutral rotation and frog leg
views. Most reliable after age > 4-6 months when femoral head has begun to
ossify. Normal femoral head: below ilium pointing towards triradiate cartilage.
Intact Shenton’s line (curve made by femoral neck and an anterior rami. normal
acetabular angle)
Treatment (depends on age of presentation, degree of DDH)
 Pavlik harness
 treatment of choice for child with dislocated, subluxable, dislocatable hip
identified as newborn to 5-6 months
 consist of suspenders with chest cerclage, anterior flexion straps, posterior
abduction straps providing suspension for two stirrup boots
 maintains hip in 90-100 flexion, and limits adduction thus helping child’s
musculature to hold hip in reduced position and while allowing for some
movement in a safe range of reduction stability to encourage normal hip
development
 continued for 8-12 weeks, followed radiographically
 successful in 90-95% cases
 bilateral dislocations, late diagnosis (beyond 6-7 weeks) irreducible at presentation
likely to fail
 Complications: femoral nerve palsy, secondary to hyperflexion, failure to
recognize persistent dislocation of hip - posterior dislocation and malformation of
posterior acetabulum, growth disturbance of proximal femur, osteonecrosis of
femoral head
 Reduction and spica casting – performed in operating room
 Treatment for child diagnosed at 6 month, failed Pavlik harness treatment
 Closed reduction, then spica casting
 May require period of traction to be able to place hip opposite acetabulum
 Examination under anesthesia, with possible arthrogram to confirm position
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Casting in “human” position with hips flexed 90-100 and abducted to 45-60
Confirm placement with post-reduction CT
Cast worn for as many months as child is old or 6 months, changed at 4-6 week
intervals to account for growth
 For child older than 18-24 months of age, inability to achieve closed reduction,
open reduction with iliopsoas and adductor tenotomies +/- femoral shortening
procedure, capsulorrhaphy may be necessary followed by spica casting
 Osteotomies
 Various osteotomies have been developed to reshape acetabulum and or femur to
improve femoral head coverage and joint movement
Complications
 Untreated unilateral DDH leads to leg length discrepancy, Trendelenburg gait due to
poor force direction across hip joint and pain due to degenerative arthritis
 Bilateral DDH: hyperlordotic and waddling gait, pain due to degenerative arthritis
 May be treated with total hips arthroplasty or hip fusion
D: Legg-Calve-Perthes (LCPD)
Important Points
 Idiopathic avascular necrosis of the femoral head
 Male to female ration 4:1
 Associated with abnormalities of thrombosis (protein S or C deficiency)
 Age at onset predicts outcome: younger age at onset (age 4-6) = better prognosis
 10% bilateral hip involvement
 4 stages
 Initial: femoral head is dense. intermittent synovitis with hip pain and limp which
increase with activity, decrease with rest
 Fragmentation: femoral head is soft and deforms. loss of range of motion,
particularly decrease in internal rotation and abduction
 Healing: new bone grows into femoral head. gradually symptomatic improvement
 Residual: femoral head is healed with residual deformity. minimal symptoms
Presentation
 Usually presents ages 4-9
 4-5:1 male: female ratio
 Classic patient profile: small thin active male child
 Child with limp, occasional hip or knee pain for weeks to months
 Mild limp, decreased range of motion of hip with limited internal rotation
Evaluation
 AP and lateral XR of pelvis: increase in density of affected femoral head compared to
normal. May be negative early in disease. during later stages progresses through
fragmentation, healing and residual stages
Treatment
 Observation and restriction from sports with rest and NSAIDs, restricted weight bearing
if symptoms severe
 Abduction casting, abduction bracing
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Complications
 Patients generally do well with very mild to no symptoms during adolescence and
adulthood
 ½ patients develop degenerative arthritis by 5th decade
 Older age at onset, more severe disease may need femoral or pelvic osteotomy
E: Slipped Capital Femoral Epiphysis (SCFE)
Important Points
 Separation of the proximal femoral growth plate with displacement of proximal femoral
epiphysis on femoral neck. displacement generally posterior
 30% bilateral hip involvement
 Defined as acute or chronic (2 weeks or more)
 Defined as stable or unstable. This is more important. Unstable, or painful hips where
the child cannot bear weight due to discomfort, require immediate surgery
Presentation
 Usually presents ages 8-16, males>females
 2 classic patient profiles: obese, adolescent male, very tall thin adolescent male
 Adolescent with limp, pain in hip, groin, thigh, or knee
 Rarely may be associated with trauma
 Pain in hip, may be referred to knee, limp, external rotation of limb, limited internal
rotation and abduction of hip
Evaluation
 AP and lateral of pelvis: “ice cream falling off of cone” femoral epiphysis displaced
posteriorly. Be sure to evaluate both hips radiographically
Treatment
 Stabilization of slippage via in-situ percutaneous pinning
 May require realignment osteotomy for moderate to severely displaced chronic slips
Complications
 Problems with gait, sitting, or appearance due to abnormal relationship between femoral
head and neck
 Osteonecrosis due to disruption of vascular supply to femoral head leading to
degenerative osteoarthritis
HAND
A. Flexor tendon injuries
a. Zone I: Distal to FDS insertion
b. Zone II: FDS insertion to distal aspect of A1 pulley (most difficult repair)
c. Zone III, IV, V; no associated pulleys, easier to repair
d. Repair should include a 4 core sutures and an epitendinous repair
B. Hand infections
a. Flexor tenosynovitis – emergency, needs to have I and D. Kanavel sign’s, affected
finger held in flexion, pain with passive extension, fusiform swelling, tenderness
to palpation along flexor tendon sheath
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C. Compression neuropathies
a. Carpal tunnel syndrome – compression of the median nerve, paresthesias in the
radial three digits and the radial aspect of the ring finger; weakness of the thenar
muscles. May respond to night splinting but surgery is the only disease modifying
treatment
b. Ulnar neuropathy – most common at the cubital tunnel, paresthesias in the ulnar
two digits and weakness of the hand intrinsics. Also may respond to splinting in
extension but release may be necessary although does not have as good results as
carpal tunnel release
D. Perilunate fracture/dislocations
a. Frequently missed diagnosis after a fall on an outstretched hand. May see a
disruption of alignment of the carpal bones along with carpal bone fracture/distal
radius fracture. Must release carpal tunnel if acute carpal tunnel syndrome occurs.
E. Replantation
a. Needs to be done before 6 hours of warm ischemia time. Order is thumb, middle,
ring, small, and index. Most always replant thumb and almost anything in
children. Expect 10 mm of 2 point discrimination and 50% decrease ROM.
SPORTS MEDICINE
Shoulder – Easiest to stratify based upon age
A. Young patients 15-30s
a. Most often instability issues
b. TUBS – Traumatic unilateral bankart surgery
i. Classic athlete with acute single direction dislocation + apprehension and
relocation tests
ii. Age is most important, younger patients will most likely dislocate again
iii. Most often perform surgery after 2nd or 3rd dislocation
1. Surgery is arthroscopic bankart repair (anterior inferior portion of
the labrum is torn)
c. AMBRI – Atraumatic multidirectional bilateral rehab inferior capsule shift
i. Classic picture is a swimmer with multidirectional instability
ii. Treatment is rehab rehab and rehab
iii. Surgery only rarely indicated (capsular shift)
B. Middle age 40-60s
a. May have instability or arthritis depending on presentation but…
b. Most often have impingement (hawkin’s sign and neer’s sign)
c. Rehab first
d. May need subacromial decompression
C. Older patients >60
a. Rotator cuff tears, arthritis
b. Arthritis (see below) but may eventually need total shoulder arthroplasty
c. Rotator cuff tears (beware of an older patient dislocating, this will commonly have
a component of cuff tear as well)
i. May do an open or arthroscopic repair
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ii. If rotator cuff tear and arthritis – bad problem, may need reverse total
shoulder arthroplasty but this is only for low demand elderly patients
A. Knee injuries
a. ACL tear
i. Common noncontact, twisting injury. In the young healthy patient it
should be reconstructed with autograft (your choice hamstring vs bone
patellar bone) rehab important; no return to sport for 6-8 months
b. PCL tear
i. Can be sports related or posterior force directed to tibia with foot plantar
flexed. Mostly treated with rehab, if repaired tibial inlay is best
c. MCL/LCL injury
i. Can be associated with other injuries. Most often nonoperative treatment
for isolated injuries.
d. Posterolateral corner
i. Repair corner acutely with possible staged repair of ACL or PCL
depending on injury. + Dial test
e. Knee dislocation
i. Ortho emergency, check vascular status, reduce, then check vascular status
again, may require post reduction angiogram then knee immobilizer
FOOT AND ANKLE
A. Ankle sprain
a. Primary stabilizer is the deltoid ligament
b. Anterior talofibular ligament prevents anterior translation
c. Begin with immobilization then gradual return to activity
d. Surgery includes repair of affected ligaments or possible reconstruction
B. Achilles tendon
a. Tendonitis or tendonosis – treatment with eccentric strengthening
b. Achilles tendon tear – treated either plantar flexed cast or surgical repair
C. Plantar fasciitis
a. Therapy includes stretching, injection, and rarely surgery. Normally a self-limited
condition
D. Hallux Valgus
a. Maternal predisposition
b. Normal MTP angle is < 9 degrees and abnormal if > 15
c. Abnormal intermetatarsal angle is > 9 degrees
d. Surgery may include distal or proximal osteotomy, soft tissue release, fusion or
resection arthroplasty depending on patient and degree of hallux valgus
E. Diabetic foot
a. Diabetic ulcers should always be taken seriously to prevent amputation
b. Test ABI should be above 0.45
c. Transcutaneous oxygen should be above 30 mmHg
d. Toe pressures should be above 40 mmHg
e. Serum albumin should be >3.5 mg/dL
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f. Total lymphocyte should be > 1500
F. Flatfeet
a. Weakness or deficiency of the posterior tibial tendon
b. Test by having patient do a single heel lift on the affected side
c. Cast/splint/orthosis if flexible, no deformity and only slight pain
d. FDL transfer, medial calcaneal displacement osteotomy with Achilles lengthening
for flexible deformity
e. Triple arthrodesis if fixed deformity
TUMORS
A. Benign or malignant
a. In general benign processes do NOT have cortical destruction or a significant soft
tissue component
B. Always perform a thorough H&P as most bony tumors are metastasis
a. Pain at night, weight loss, previous history or cancer are all worrisome
C. Labs include CBC, Comprehensive metabolic profile including alkaline phosphatase,
ESR, CRP, and CEA; may need protein electrophoresis if myeloma is suspected
D. Radiographs are a must with CT and MRI most always needed as well
E. Bone scan and PET scan to detect metastasis
F. Biopsies should be longitudinal incisions with good hemostasis
a. Always send to pathology and culture if concern of infection
b. Resection may be intralesional (through the tumor), marginal (through the reactive
zone), wide (en bloc removal), radical (entire compartment removed).
ARTHRITIS
A: Osteoarthritis
Important Points
 Non-inflammatory disorder of joints characterized by deterioration of articular cartilage
and new bone formation at joint surfaces and margins
 Degeneration and loss of articular cartilage surface on weight-bearing areas, eburnation
of bone, subchondral cyst formation, osteophyte formation
 Associated with obesity, hereditary, occupation, endocrine disorders
 90% of all people have some degenerative changes in weight-bearing joints by age 40
 Osteoarthritis is NOT the same as age related changes to the joint
Presentation
 pain, increased with joint motion relieved by rest, limitation of joint motion due to pain,
early AM stiffness, eventual loss of ROM due to contractures
 localized joint tenderness
Evaluation
 Labs: ESR, CBC, RF, calcium, alkaline phosphatase usually within normal limits
 Synovial Fluid: noninflammatory with minimal increased WBCs, normal viscosity and
glucose, no crystals or bacteria
14

Radiographically: loss of joint space, subchondral cysts, osteophytes, loose bodies,
deformity and malalignment
Treatment
 Rest, assistive devices (cane, crutch), NSAIDs, physical therapy, bracing, intra-articular
steroid injections or injections of hyaluronic acid (synvisc/euflexa)
 All of these modalities do not change the natural history of OA, they only temporize
the patient before definitive treatment which would be a total joint arthroplasty
 Total joint arthroplasty: commonly performed to increase joint mobility, decrease pain,
increase stability
 Arthrodesis: uncommonly performed, improves joint stability with decreased motion
 Resection arthroplasty: uncommonly performed. provides good motion with decreased
stability
Complications
 Untreated OA: subluxation, joint deformity, bony fusion of joint, intrarticular loose
bodies, leg length discrepancy
 Total joint arthroplasty: Infection, leg length discrepancy, damage to the nerves,
arteries, blood vessels, stiffness, need for revision surgery, pulmonary embolus, and
medical complications of undergoing surgery with advanced age +/- comorbidities
B: Rheumatoid Arthritis
Important Points
 Symmetric inflammatory arthritis involving small and large joints of at least 6 weeks
duration
 Must have 4/7 criteria
 AM stiffness
 Arthritis of at least 3 areas > 6 weeks
 Arthritis of hand joints > 6 weeks
 Symmetrical arthritis > 6 weeks
 Rheumatoid arthritis
 Serum rheumatoid factor
 Radiographic changes
Presentation
 Insidious slow onset week-months, may have fatigue, malaise, anorexia, arthralgias,
myalgias, AM stiffness
Evaluation
 Radiographically, bony erosions
Treatment
 Narcotic analgesics, NSAIDs, corticosteroids, disease-modifying agents (plaquenil,
methotrexate, parenteral gold), monoclonal antibodies (rituxan) have changed the RA
disease processes preventing many of the severe deformations of RA
 Incomplete or complete synovectomy
 Total joint arthroplasty: commonly performed to increase joint mobility, decrease pain,
decrease stability
 arthrodesis: uncommonly performed, improves joint stability with decreased motion
15

Resection arthroplasty: uncommonly performed. provides good motion with decreased
stability
Complications
 Untreated RA: subluxation, joint deformity, bony fusion of joint, intrarticular loose
bodies, leg length discrepancy
 Total joint arthroplasty: Infection, leg length discrepancy, damage to the nerves,
arteries, blood vessels, stiffness, need for revision surgery, pulmonary embolus, and
medical complications of undergoing surgery with advanced age +/- comorbidities
 C: Crystalline Arthopathies
Important Points
 Gout: monosodium urate arthropathy
 Pseudogout: calcium pyrophosphate deposition disease
Presentation
 Acute inflammatory arthritis or chronic erosive tophaceous arthritis
 Typically, acute onset of painful, swollen, warm and tender joints with systemic fever
Evaluation
 Labs: may have elevated WBCs, ESR
 Joint aspirate: polarized crystals (negative birefringence gout, positive birefringence
pseudogout, negative cultures)
 WBC in an aspirate of a native joint. WBC 30,000-50,000 gout; infection normally
present with greater than 80,000 WBC. The cutoffs are debatable and the gram stain,
percentage of neutrophils in the joint, blood WBC, presence or absence of crystals
should help dictate treatment.
Treatment
 Anti-inflammatory therapy with colchicine, indomethacin, allopurinol; never give
allopurinol acutely
Orthopaedic Infection
OSTEOMYELITIS
Important Points
 Bacterial or fungal infection of the bone
 generally develops hematogenously, but may occur after open fracture or orthopedic
procedure
 Definitions:
 Acute versus chronic
 Brodies abscess: small local infection of bone walled off by the body with sclerotic
tissue
 Involcrum – dead bone with new bone formation around it
 Sequestrum – dead bone in the middle of sclerotic bone
 Most common causes of osteomyelitis
 Most common – S. aureus
 IV drug users – P. aeruginosa
 Sickle-cell disease – S. aureus and Salmonella
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
Sexually active – Gonorrhea (always a USMLE, OITE, or board question but I
have yet to see this!)
Barnyard injury – Clostridia
Fungal – Coccidiomycoses
Joints – Tuberculosis



Presentation
 Pain, fever, erythema, swelling, drainage through sinus tract
Evaluation
 Acute appears on XR as rarefaction of bone with permeative destruction takes at least
10 days of infection before the periosteal reaction is present on plain radiographs
 Chronic appears on XR as sclerotic bone, with increased thickening of cortices,
increased lucency of bone
Treatment
 Irrigation and debridement (repetitive, radical debridement). Drill cortical window in
bone, curette out medullary bone, liberal saline lavage.
 Antibiotics – 2 months of IV antibiotics, followed by oral antibiotics for 2-4 mos.
 Prevent/protect from bone fracture
 Possible bone graft – after 2 mos. of IV antibiotics.
Complications
 Infection can spread from the bone into an adjacent joint and cause a septic joint.
Infection can spread into the skin, draining outside, causing chronic draining sinus (with
increased risk of squamous cell cancer of the draining tract after draining over many
years this is also known as carcinoma in-situ (Bowen’s disease)
Appendix
Sedimentation Rate: Erythrocyte Sedimentation Rate




0-20
20 – 40
>40
80-120
Normal
consider a benign or malignant tumor
consider infection
consider rheumatologic conditions such as RA, Lupus etc.
METASTASIS TO BONE
Lytic/Blastic
Lung
Breast
Thyroid
Renal
Prostate
Myeloma
L
L/B
L
L
B
L
Hormone sens.
Rads sens
+
+
+ steroids
+
I131
+
+
Most common metastatic disease to bone is myeloma.
The most common primary malignant bone tumor is myeloma.
17
Chemo sens
+
+/+/+
Life
Expectancy
6 - 12 mo.
2-4 yr.
2-4 yr.
2 yr.
2 yr.
10 yr.