Download Lecture 21 – hip and back pain in adults Should know differentials

Lecture 21 – hip and back pain in adults
Should know differentials of hip and back pain
anterior: osteoarthritis, psoas syndrome, patellafemoral syndrome
lateral: IT band syndrome, greater trochanter bursitis, meralgia paresthetica, “dead butt syndrome”
posterior: piriformis syndrome, spondyloysis, spondylolisthesis
Hip pain: sciatic nerve can cause hip and back pain from piriformis syndrome: sacralplexus directly beneath or
through the pirimormis muscle. Also lateral femoral cutaneous nerve can cause meralgia paresthetica: nerve
entrapment as it passes through inguinal ligament
Anterior Hip Pain
1. Psoas Syndrome “snapping hip”/iliopsoas
a. Origin: L1.L4 joints iliacus at ingunia and inserts on lesser trochanter
b. MOA: hip flexion, tendon bursa becomes inflamed in dancers gymnast complaining of anterior
pain/ groin pain.
2. Patellofemoral syndrome
a. MAO: most common knee pain, due to overuse, tight hamstrings, weak hip abductors
(g.medius,minimus muscles)
b. Worsens while squatting, walking up stairs, sitting and standing after long periods of time
Lateral Hip Pain
1. IT band
a. MAO: overuse syndrome common in runners
b. OBERS: abduct, extend hip and the knee wont dip down
c. In between the tensor fascia latae and glut. Maximus
d. O: lateral iliac crest inserts on the lateral tubercle of the tibia
2. Greater troachanter bursitis
a. “Hip pain” points laterally to hip
b. MAO: exaggerated movement of G.medius tendon/ tensor fascia over used by flexing of hip
c. Presentation: can radiate, lateral hip pain, point tenderness, seen in older people and gymnast.
3. Meralgia Paresthetica
a. MAO: mononeuropathy of lateral femoral cutaneous nerve due to excess weight/stress. Can get
entrapped near the inguinal ligament because it travels through the fascia latae so movement
between thigh and pelvis can stretch the nerve causing entrapment.
b. Test: tinnels test over inginual ligament or deep palpation to ASIS.
4. Dead Butt syndrome: gluteus medius tendonitis
a. Origin: external ilium and Inserts on greater trochanter
b. Symptoms: weakness of the g. medius/ with tight iliopsoas and weak abdominals
c. Test: Trendelenberg sign: hip goes down on one side, pain in abduction/rotation. They have
wobbly gait, point tenderness of Trochanter and positive test.
Posterior Hip Pain
a. Symptoms in sedentary patients with sciatic pain in butt down the leg. Worse with exercise and pain is
reproduce din adductions/IR. Helps with external rotation and abduction.
b. O/I: anterolateral sacrum, greater trochanter
c. Treat: piriformis counterstain
Spondylolysis Vs Spondylolisthesis
Spondylosis is weakness of stress fracture in on of the bony bridges that connects upper and lower facet joints
(usually L5) where spondylolisthesis is the sliding of vertebrae (L5-S1). Both are seen in young athletes with
continuous hyperextension (gymnast) but also in post menopausal, older men. You can see middle line
tenderness. With the spondylolistheses the x-ray will have a step off a neurological issues can occur via
impingement.
Lecture 22 – crystal arthropathies
Treatment for Gout
Pathophysiology: underexcretors (genetic) or overproducers (genetic, or environment)
Physical findings: spontaneous onset, chills, fever, malaise, podgra, coronary artery disease, topi
Diagnostics: negatively birefrngent crystals. Increase serum uric acid above 6.5 mg/dL. Urinary with low uric acid
points to underexcretor.
 Short term = NSAIDS, ice, colchicine, steroid (prednisone)
 Long term = allopurinol, febuxostat
Diagnosis for Gout with aspiration and synovial fluid culture. Would see negative birefringement syndrome
Rheumatory Arthritis
Diagnose RA via: rheumatory factor and anti-CCP in a blood culture
 PM&R: Exercise to match the ability and fitness level, heat or ice to make it feel better.
 Diagnose polymyalgia rheumatica by treating with steroids and should go away in 2 days.
o Make sure you taper down the steroids and slowly start with 10 mg.
Dermatomyositis –
Pathophysiology DM: T cells will build up in between the muscles and steroid
treatment will not work. In labs we will see these T cells between the muscles
and make sure you look for malignancies.
Clinical Findings: shoulder/hip black female*, pain in large muscles, malaise,
fatigue, weight loss. Higher in blacks and higher in males. Affects symmetrical
muscles* Prednisone wont work in these patients. Helotrophic rash,
polkilderma, gattron papules, sparing of periorbital folds
Diagnosis: diagnosis it via muscle biopsy but so we don’t have to do that we can see an elevated creatine kinase.
Watched for cardiac, pulmonary and GI muscle problems (because affecting muscles!)
Polymyalgia rhematica
Pathophysiology: does not affect the muscles. Increased ESR, anti CCP/R (T cells and increased IL-6)
Clinical findings: shoulder/hip, older in age (71), worse in the morning, are to get up from the chair, very
fatigued, bad range of motions, tender. Quickly start to steroids and watch for vasculitis and steroid side affected.
(Giant cell arthritis
Lecture 23 – rheumatic disorders.
 JIA – juvenile idiopathic arthritis: IL-6, IL-1,TNF alpha
Type
Age
Gender
Diagnosis
Complications
Joints affected
Systemic JIA
2-4 y/o
1:1
25% severe
destructive
joint disease
Polyarticular arthritis
in small to medium
joints follows fever
Oligioarticular
1-5 y/o
Girls 4:1
Fevers for at least 2
weeks with rash
hepatosplenomegaly,
lymphadenopathy,
serositis. Negative RF/
rarely positive ANA
70% ANA+ (higher risk
of uveitis)
Knee>ankle big joints
Persistent or Extended
Polyarticular
2-5 (ANA+)
or early
teenage
(RF+)
Girls
Uveitis or I
ridocyclitis
(cataracts,
synechiae,
glaucoma
leads to
blindness)
Blindness,
osteoporosis
RF (-): <10 ANA+
RF(+)/ Anti CCP: >10
rapid severe onset
RF-: knees, wrist
ankles
RF+: hands feet
Enthesitis
Psoariatic
9-12 y/0
Males
9:1
Arthritis and (2)
sacroiliac pain, HLAb27*, symptomatic
uveitis (pain), positive
FH
Chronic arthritis and
psoriasis or Arthritis
and 1* FH of psoriasis
plus dactylitis or
fingernail abnormal
HLA b-27*
Lower limbs and
spine, any number of
joints. Axial
involvement
Arthritis is
after psoriasis
Peripheral and or axial
arthritis asymmetric
small and medium
joints.
Complications: joint destruction and uveitis/glaucoma make sure you monitor these throughout. Also monitor for
spondyloarthrpathies
Diagnostic Criteria*: joint effusion plus two of the following pain, warmth, erythema, limited ROM. Presence has
to be at least one joint at least six weeks and onset before 16. For joint pain history is key! Pain, age and
precipitating factors
Treatment: stop synovitis to prevent joint destruction and blindness (not pain relief. 1 st line is NSAIds,
Glucocorticoids then DMARDS methotrexate (IL inhibitor, TNF alpha and IL-6 inhibitor)
JIA vs Septic Joint? Pain when you touch septic joint/wont be able to stand. Know by symptoms/joint aspiration.
JIA and septic arthritis all have warm, acute pain and severely painful ROM. In JIA we will see a bilateral arthritis
in comparison to septic. In RA biopsy we will see infiltrates of blood vessels, inflammatory cells, and lymphocytes
where in septic arthritis we will see these but it will also grow on culture
Lupus (SLE) – rash (butterfly/mallor/photosensitive), systemic symptoms. Need to ask heart block for maternal
history! Watch for renal problems and med toxicity. Kids will have more hematologic, fever and cutaneous signs.
Diagnose with anti-dsDNA (most specific), ANA 100% +, anti-smith is 30%
Pathophysiology = autoimmune (immune complexes)/autoimmune dysfunction. The immune complexes bind to
the mast cells African American woman* (non-white people know this). Cause immune complexes via histamine
and mast cells
Juvenile Dermatomyositis
Characteristics: heliotropic rash (with nasolabial sparing *lupus*), Gattrons papules (dorsum of hand, knees),
Calcinosis of muscle, nail bed changes
Diagnosis: Skin (Gattrons/helptrophic) plus 2 of progressive symmetrical proximal weakness or increase serum
muscle enzymes (CPK*,LDK,AST,ALT)
complications: calcinosis, cellulitis, pulmonary via treatment, liver failure, GI pleed from muscles.
Septic Arthritis vs Toxic Synovitis
Septic: refusal to bear weight 95% of the time*, high fever, elevated ESR/CRP/WBC, red hot swollen tender joint.
Hip is flexed abducted and externally rotated. Draw blood culture
Toxic: pain is limited ROM of the hip
Henock shlomlin perpura –abdominal pain, rash, musculoskeletal pain
MSK findings: arthritis/arthralgia, oligoarticular, usually lower extremity/large joints, no periarticular
swelling/tenderness, no effusion, redness, warmth
Complications = GI initial problems because intussception and we can screen via ultrasound which later goes
into renal disease so we need to monitor the blood pressure and urinary analysis (creatine kinase)
Lecture 24/25 – immune mediated musculoskeletal disorders
Rheumatory Arthritis
Diagnosis: rheumatoid factors (immune complex test for autoantibody to self IgM binding to self IgG FC
receptor), anti-CCP(most specific), ESR, CRP, ANA. Swann Neck (flexed DIP/hyperextended PIP), symmetrical,
progress to large joints, acute synovitis
Genetics: autoantibody binding to self-IgG FC receptor possibly genetic (HLA-DR4 and CTLA4 attacks the class
two to make a pannus). TNF alpha/IL-1 bring more cells to the area to make the vessels leaky! CD4+cells play
major role in B cell activation to make autoantibody and to activate Macs for more cytokines (Th17)
Environmental: smoking can cause in influx of cells as well (TNFalpha, IL-1))
Pathophysiology Early RA:
Initiation: in lymph node, macs make cytokines RF made in normal antibody making process. Breaking down the
tolerance of immune system (of the T and B cells/tolerance fails from antigen presentation, deletion, receptor
specificity, or differentiation to suppressive T lymphocytes).
Propagation: immune complex enters and makes macs to make more cytokines, histamine release, B cell
stimulation to make antibodies, tissue damage and pannus forms. This creates a type III hypersensitive reactions.
Complement activation and recruitment of immune cells. There can be a problem with complement but also with
phagocytosis (frustrated) so bad cleaning up of all the debris.
Tissue damage: by cytokines making synovial fibroblast, OC and ROS.
 Autoantigens are from a clearance problem of apoptotic cells
 CTLA4 usually kills bad B cells so if it is mutated it will cause the B cell to persist
 TNFalpha, IL-1, IL-17 are most common cytokines.
 T cell CD4+ plays major roll in B cell activation to make autoantibody and for Macs to make cytokines
 Th17 major T cell with destruction and formation of inflammatory cytokines
Reiter syndrome/Reactive Arthritis: conjunctivitis, urethritis, arthritis.
pathophysiology: from molecular mimicry of HLA-B27 (Class 1). The body now begins attacking itself. Binds to
other self and has to be initial insult and makes antibodies against it so it will begin to attack self. Needs infection
first (chlamydia, salmonella, Yersinia) .
Reactive arthritis: sausage fingers, coexisting articular infection. Asymmetrical peripheral large joints (weight
bearing). 1-4 weeks after initial infection. The T regs rail at doing their jobosteoclast
1. X-ray is none diagnostic. Inflammatory joint fluid without identifiable organism. You will see
conjunctivitis, UTI and skin infections! The links have to be close together.
Anklyosing Sponyloitis:
HLA-B27+, age less than 40 in males* (adolescent boys and young men), When we x-ray we look for sacroiliac
joints
Cardinal features: sacroilititis inflammation of SI joints, spondylitis inflammation of the spine, enthesitis
inflammation of tendon insertion sites, uveitis inflammation of the eye .
Systemic Lupus Erythematosus: no pearls on it but affects renal, CNS, vascular (Raynaud’s), cutaneous, pulmonary
(pleuritic), cardiac (Libman Sacks endocarditis* sterile vegetation’s on the valve leaflet on echo onset murmur) La
findings are titers of dsDNA antibodies. Need 4 of the 11 to have Lupus.
susceptibility: C4 deficiency, HLA-DR3-2, defective immune complex clearance, drugs (temporarily induced). The
autoantibody production is similar to RA. Immune complex clearance and apoptosis with C4 is similar problems. B
cells become hyperactive and continuously secrete auto-antibody and T regs aren’t shutting down the auto
immune response and cause production of pro inflammatory cytokines
cellular markers: LE cells on the peripheral
UV light, gender, infections, drugs, abnormal immune response, autoantibodies: DNA proteins (ANA/histones),
type 3 hypersensitivity (watch kidneys), damaged systems attacks entire body.
loss of tolerance to nuclear antigens (sle11, sel1b, sle1c), dysregulation (Far, TLR7) of immune system, disease
FCG receptors, adhesion macs (allows cells to come in)
treatment: NSAIDS, steroid, IV/oral steroids, hydroxychlorquine*, cyclophosphamide)
Scleroderma: chronic systemic disorder by thickening of skin and has variable internal organ involvement with
vasculitis and fibrosis of these organs.
CREST:
C-Calcinosis cutis
R-Raynauds: spasm of BV
to cold/stress
E-Esophageal dysmotility
S-Sclerodactylyl: thickening tightening of skin on the fingers
T-Telagenietasias: dialation of capillaries causing red
GI: esophageal dysmotility, reflux and watermelon
stomach* Diagnosis is clinical based!
marks on surface of skin
Renal Crisis: malignant hypertensions/rapidly
progressive acute renal failure (males, AA)
Lab: ANA, Scl-1 anti tropisomerase I (most specific) anti
centromere antibodies)’
Sjogren’s Syndrome: slowly progressive autoimmune disorder caused by lymphocytic infiltration of exocrine glands
(primary SICCA and parotid enlargement). Has more dry eye and mouth without the other symptoms. Associated
with HLA-B*8DRB1 (IFN alpha). You can have scleroderma with sjorgens but not vice versa. IFNalpha problems
Clinical: Sicca (dry eyes/mouth), middle age females, extra glandular (arthralgia’s, Raynaud’s (vascular), GI
(pancreatitis), lymphoma (higher risk)
Labs: labial biopsy focal lymphocytic infiltration, abnormal tear flow shcirmers test, anti-Ro/SSA/SSB* and AntiLA/S
Jacobasus lecture (26/27)
MCL sprain/tear
Testing in knee with 30 degrees of flexion and add
valgus stress
Mechanism: hyperextension and pushed valgus stress
MCL injures can be treated with a brace. 3 grades to the
injury.
LCL sprain/tear
testing with the knee in 30 degrees of flexion, you add varus stress, and you test by doing a figure 4
Mechanism:
ACL tear: occurs during noncontact deceleration event that produces a valgus twisting injury. Meniscus tears occur
with 50-75% of ACL tears.
Extraarticular knee pain: prepatellar bursitis (anterior to the patella, no
infectious aspirate/steroid injections and nsaids), Osgood-Schlatter (tibial
tuberosity, young boys affects who kneecap moves requires immboilization),
Bakers cyst (posterior, associated with meniscal tear)), cellulitis, skin infections
Pes ansare bursa = medial side of knee. Distal to joint line. Protecting 3 tendons
(Sartorius:femoral nerves, gracilis:obturator nerve, semitendinosus: tibial branch
of sciatic nerve). It is a common cause of knee pain in older females/runners
because the tendon insertion along the proximal tibial gest pulled out. There
are rehab programs to do. Inframedial joint line plane. They can do exercises to
help strengthen these muscles.
Hemarthrosis = intra-articular swelling, poke a needle in there and suck on some blood. Could be ACL tear* (most
are this) L tear, Tibial plateau fracture*, PCL, meniscal tear, intraarticular fractures, tear of joint capsule
Osteochondrosus deficans : (complications) focal injury to bone and overlaying cartilage cause by a disruption of
the blood supply
 Symptoms = adolescents and is extremely rare 15-30 people per 100,000. Micro fractures
 Signs = XRAYs show the size and location of the lesion on the femur
 Treatment = crutches, splinting or cast for a short period of time. If the lesion is separated or to large you
go to surgery. Osteoarticular transformer (results encouraging, cell viability incomplete but maintained
over time plugs, graft you need fresh chondrocytes
Knee dislocation: most dislocation will have ACL, PCL,
posterolateral corner and medial knee structures (MCL and
posterior oblique ligament), medial/lateral meniscus, articular
cartilage. Position of the tibia relative to femur gives us
classifications.
1.
2.
Anterior dislocation
Posterior: anterior/posterior force (dashboard
injury/high injury fall flexed knee)
3. Medial/lateral/rotatory
*high incidence of popliteal artery injury and maybe the
genicular artery, posterior tibial recurrent artery, sural artery.
*posterior articular branches of tibial and obturator nerves for a
posterior dislocation
*anterior branches of femoral, common peroneal* and saphenous
nerve
*Common fibular nerve (winds around fibular head which can be
injured during dislocation) *
sciatic nerve splits into the tibial and common peroneal above the
knee. Tibia nerve supplies the posterior side and common peroneal
supplies anterior side (10-40%) can be injured with varus
Lock-knee: meniscus tear. Meniscus only has blood supply to the periphery. Differential with posterior knee pain.
Meniscus. Probably needs surgical repair. Meniscal tears and they cant bend because the meniscus is stuck.
Extension located is a posterior tear of the meniscus. Cant bend it because of the severe pain and it gets stuck
from that meniscus.
posterior tear of meniscus: locked in extension
Indications for knee arthroplasty
1. limited walking
2. attempted physical therapy, tried NSAIDS, injection, walker
3. limitations on daily activities of daily living
4. Acceptable medical risk
Risk factors for tears
1. Age
2. Weight
3. Previous injury
4. Muscle imbalance in hamstrings and quads. The hamstrings decrease the ACL load by ruding the
quadriceps induced anterior tibia translation
5. Limb alignment
6. Notch width: is less an women than it is in men. The ACL width correlates with the notch so the smaller
the notch the thinner the ACL
Don’t operate if no meniscus tear, no cartilage injury, low activity level prior to injury. Development of
osteoarthritis as later complication of ACL deficient knees
Lecture 28 – osteoarthritis
Treatment (in order) *
 Reduction of Joint loading*: weight reduction, decrease in stressful activities, learning to work smarter,
using devices to help
 Exercise, physical therapy (strength, aerobic, range of motions, agility, neck and back strength)
 Drug therapy: acetaminophen (stay under 3000), tramadol, NSAIDS (can cause ulceration/renal
compromise), opioids
 Intraarticular therapies: corticosteroids, hyaluronic acid (Synvisc, Hyalgan)
Aspirate knee* : sterile, gram stain negative, no inflammatory cells
On x-ray*
 joint mice, joint narrowing in the medial compartment with subchondral
sclerosis and osteophytes
 fingers: DIP and PIP, gleno-humeral joints, base of thumb (spared wrist
elbow and ankle)
 Medial compartment will cause varus (bow leg) deformity
 Lateral compartment will cause valgus (knock knee) deformity
Osteoarthritis: joint failure which is pathologic hyaline articular cartilage loss with
increasing thickness and sclerosis of subchondral bony, osteophytes, stretching of articular capsule, mild synovitis,
weakness of muscles bridging the joints, muscle degeneration. (type to collagen)
Where is it? Knees, hips, C spine, L spine, first MTP joint, DIP/PIP, base of thumb wrist, elbow and ankle are spared.
Heberdens nodes, bouchards node which develop gradually.
Lecture 29
Disease
Gender,
Pathophysiology
Diagnosis/Symptoms/Complications
Age, Race
LCPD
Male 4:1, 3- Idiopathic osteonecrosis of proximal femoral
Stage 2: Crest sign (fracture of necrotic
10 yo,
epiphysis at secondary ossification center due subchondral trabeculae), and Gage sign (rat bite
Caucasian
to pressure changes in the capsule. Inc.
at femoral head)
pressure decreased blood flow to ischemia.
Stage 3: Coxa magna due to premature physeal
At sg 2 revascularization from periphery and
arrest and hypertrophy of epiphyseal cartilage.
as BF inc. areas are digested via granulation
Symptoms: pain is achy, gradual, without trauma,
tissue (cystic areas of bone). At sg 3 retender in hip and IR/ABd is restricted and painful,
ossification begins at epiphysis, and
antalgic gait. Galeazzi test (knees)
distortion of femoral head may occur. Sg. 4 is Imaging: Bone scan will detect earlier
remodeling resolution and new bone
SCFE
Male 1.5:1,
11-16 yo,
AA
Slipped capital femoral epiphysis, when
forces applied to the femoral head exceed
the strength of the epiphysis causing
slippage. Ray reveals posterior displacement
of femoral head. Can be bilateral.
Hip, medial thigh, knee pain, acute/insidious
onset (more pain associated)
Diagnosis: radiology: instability of proximal
femoral growth plate. Causes widening of
hypertrophic zone up to 80%
Classification: preslip, acute, acute on chronic,
chronic (most common, not joint effusion). Treat
with screw in hip.
Transient
Synovitis
Male 4:1, 310 yo,
Pain and lip most often seen after post
infection, allergic reaction, post trauma. Has
fever and ROM is limited
Xray shows widening of joint space. MRI used to
confirm diagnosis. Treat with limited activity,
NSAIDS. Can progress to LCPD in 1-2% of cases.
Can do ultrasound
Lecture 30/31
Knee Anatomy and Key coronal view of MRI of the Knee
Six main ligaments/cartilaginous structures (ACL/PCL/MCL/LCL/Lateral and medical meniscus). The menisci
stabilize against rotation forces. The muscles of the knee are the vastus lateralis/medialis/intermedius, rectus
femoris, biceps femoris, semitendinosus, semimembranosus, Sartorius, gracilis, IT bad, popilteus, and
gastrocnemius.
Popliteal fossa and popliteal artery gives off 5 genicular arteries (superior/inferior paired, middle). Collateral
circulation to the knee are lateral femoral circumflex and anterior tibial arteries. The genicular arteries cannot
compensate if a popliteal artery is ruptured. The tibial nerve joints the popliteal artery in the fossa but is not
tethered to the knee. The peroneal nerve passes around the proximal fibula just distal to fibular head.
Femoral head and neck injuries. Complication of femoral neck fracture = AVN
because of the strong fibrous hip capsule there is a high rate of nonunion and
avascular necrosis. Femoral head fractures are associated with posterior hip
dislocations. Due to blood supply and strong fibrous hip capsule there is a high rate
of a non union and AVN
The major artery is the medial femoral circumflex artery to the femoral head that
turns into its terminal branch the lateral epiphyseal artery
Posterior hip dislocation
can injure sciatic nerve. If the dislocation was anterior it would damage the femoral canal. Can be associated with
posterior wall acetebaular fractures as well.
Pelvic fracture complications
hemorrhage (blood loss) occurs in 75% of pelvic fracture patients, urogenital and muscular skeletal pain
Sacral Fractures:
Divided into 3 zones.
Zone 1: Vertical alar fractures. Osteoporotic stress fractures usually. The sacral ala up to
the lateral border of neural foreman 5.6% of neural deficits (L5 root)
Zone 2: Through the neural foramen has a 28.4% of neural deficits
Zone 3: Central point of the sacrum and the canal, it’s a 56.7% of neural deficits. In the
lumbar sacral plexus and neurological surgery
Insufficiency fractures: 5% of all sacral fractures and is common in osteoporosis patients (elderly females). Tibial
stress fractures occur because of fatigue fractures. The repetitive loading exceeds the bones capacity to remodel.
Muscles of pelvis and hip
Flexion: iliopsoas (Major/Minor
Psoas, Iliacus)
Extension: Glut max
Abduction: glut med/min
Adduction: add brevis, longus,
magnus, pectineus, gracillis
Ext rotation: in & ext obturator,
quadratus femoris, sup/inf
gemelli
Int rotation: glut med & min
Femoral Shaft fracture: vascular injury to femoral artery tether at adductor hiatus
Most Common Avulsion Sites
1. Ischium: hamstring/adductor muscles
2. Anterior Superior Iliac Spine: Sartorius
3. Anterior inferior iliac spine: rectus femoris
4. Iliac crest: abdominals
5. Lesser trochanter: iliopsoas
6. Greater trochanter: Gluteus medius, gluteus
minimus
Salter harris classifications
Type I Slipped: involves epiphyseal plate (only
epiphyseal plate SCFE)
Type II Above : involves epiphyseal, fracture of
metaphysis Most common
Type III Lower: fracture of epiphyseal plate and
epiphysis itself
Type IV Through : epiphyseal plate, fracture of
metaphysis and epiphysis. Needs to be taken care
of immediately
V Rammed: involves epiphyseal plate
Lecture 32/33
Developmental Dysplasia of the Hip: Increased ligamentous laxity of the hip capsule due to hormonal, mechanical
and genetic factors Breech Position in 25% of the children
Risks/Etiology: Crowding phenomenon, Congenital muscular torticollis, metatarsus adducts

Neonate Testing: if there is clicking it’s a positive test
o Barlow Tests: Barlow Barbarian. Dislocating the hip by adduction and applying
gentle posterior force to hip
o Ortolani Test: “Ortho-Ortolani”, reducing the hip by abduction and applying
gentle anterior force to posterior thigh.

Infant
o
Hip abduction test: baby on back up to 90 degrees. Under 60 is concerned and under 50 is
diagnostic
o Galeazzi Sign. Place the knees up and look at the height of the knees.
o Asymmetry of thigh and gluteal folds: Asymmetry of thigh/gluteal folds.
 Diagnostic Testing
o <4-6 months: Do ultrasounds as diagnostic testing and look at alpha angle
o >4-6 months Xray to look for shenton line.
 Clinical findings: in toeing and limping (number 1 misdiagnosed DDH), waddling gain, leg length
discrepancy, excessive lumbar lordosis
 Treatment
o <6 mo: immobilization in Pavlik Harness start at 4 wks and do for 6. If no reduction after 3 weeks
go to Spica
o >6 mo-2 yo: Spica cast done in general anesthesia. Use CT/MRI to check
o Surgery: If closed reduction fails. <2 y/o do open reduction no osteotomy. If >2 yo: do open
reduction and osteomoty.
 Complications: Avascular necrosis
Congential Disorders of Lower Extremity
Disorder
Age
Symptoms/Testing
Treatment
Internal Femoral Torsion
>2/yo W sitting, patella pointed inwards, internal
Observation
Femoral Anteversion
rotation. In Toeing
Test: Hip rotation degree angle lay on abdomen
and IR >70 degrees/limited external (10-20)
Internal Tibial Torsion
< 2 yo Patella’s say forward.
Resolve
Test: Thigh foot angle measure inward value. Will
spontaneously
have a negative angle. In Toeing
Genu Varum (Bowlegs)
Physiological: crowding. Same as ITT, no intoeing
Physiological: fixes
Blount’s Dz: abnormal growth of medial aspect of
itself
proximal tibial physis. Sloping, peaking, widening,
Physiological:
fragmentation. African Americans, adolescents
depending on age,
*Xray to differentiate. Blunts has asymmetric,
stage and nature.
abrupt sharp angulation and off angle
Osteomoty (op)
Genu Valgum (knock
3-5
Physiological
Resolution btwn 5knees)
yo
Rare causes: infection tumor, renal,
8 yo. Surgery if bad
osteodystrophy, cerebral palsy*
Ankle/Foot
Disorder
Metatarsal Adductor
Calcaneovalgus foot
Talipes Equinovarus
Club foot
Symptoms/Testing
Convex lateral foot concave medial foot. DDH test (2%)
Forefoot is adducted, midfoot and hindfoot are normal.
In toeing
Testing: finger V test, xray increased angle btwn 1-2 MT
Hyperdosiflexion, forefoot abduction, heel valgus
Xray differentiate from congenital vertical talus
(rockerbottom)
C: Cavus (planter flexion) (FF)
A: Adduction of forefoot/midfoot on hindfoot (FF)
V: Varus of hindfoot (HF)
E: Equnus of hindfoot (HF)
Multifactorial, family history
Congential: 75%, breech, AP/lateral 30 deg plantar flexion
Treatment
Depends on rigidity.
To neutral: stretch,
opposite shoes
Cannot to neutral: cast
Failure Surgery
Reassurance, stretching,
rare serial casting
Nonsurgical: casting
changed 1-2 weeks and
achieved by 3 months.
Followed by bracing
Surgery is easy if
needed (failure by 3 mo)
Congenital Vertical
Talus
Rocker bottom foot
40% neuroMSK/ 60% unknown
Talar head prominent at med border of midfoot, forefoot
and midfoot are dorsiflexed
*Trisomy 18 Edward Syndrome (overlapping fingers)
Tarsal Coalitions
2+ bones in mid/hindfoot are joined. Decreased joint
motion, pain, flat foot, ankle sprains
Talonavicular (3-5 y), Calcanonavicular (8-12y),
Talocalcaneal (12-15 y).
CT Scan!
Absence of arch. Medial longitudinal arch laxity.
While sitting arch is present when standing its gone.
(protonation)
Neuromuscular! Elevation of longitudinal arch
Pes Planus
Pes Cavus
Serial
manipulation/casting
after birth
Surgery at 6-12 mo
Casting then orthosis
postoperatively
Non-operative: shoe
inserts, casting
Surgical: arthritis
Resolution by 6 mo or
have rest of life. Use
shoe inserts
stretch