Week 9 CAD Questions Graham Healy

CHIR12007

Clinical Assessment and Diagnosis

Portfolio Exercises Week 9 & 10

Exercise 1

Differential Chart

Please create a chart that lists as many differential diagnoses for hip pain as you can, including but
not limited to the following conditions

Osteoarthritis

Avascular necrosis

Bursitis’

Tendinopathies

Strains

Infection

Piriformis S

Lumbar disc disease

Radiculopathies

Osteoarthritis
Definition: History:
degeneration (wear and tear) of articular *insidious onset of deep ,achy pain in the groin
cartilage in the acetabulum & head of ,buttock,thigh or knee
femur , in more advanced stages *morning stiffness (first 30 min)
accompanied by osteophytes ,narrowing of *pain is better with rest & mild activity but worse after
joint space ,sclerosis or hardening of bone excessive weight bearing activity
at joint surface & joint deformity. *prior hip trama/overuse/strain
*Snapping or popping (crepitus) may be noted with motion
Extremity manual Viziniak p208-9 Physical :
possible altered gait (antalgic)
Palpation :
within Normal Limits , possible myospasm around hip
(gluteal ,hip flexors, adductors)
*Often decreased ROM with normal muscle strength
*Crepitus with motion common , possible limited ROM due
to pain or tissue contracture
Neurovascular :
Within normal Limits
Differential diagnoses:
*transient hip synovitis

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*septic arthritis
*visceral pain referral or bursitis
*Trochanteric bursitis
*gout/Rheumatoid arthritis
Special Tests :
+ Scour test
+ anvil test
+Patrick FABERE

Avascular necrosis History:

Definition : look for potential risk factors
death of the femoral head cortical bone and *gradual onset of dull achy hip or groin pain is the most
marrow secondary to a disruption of blood common presenting symptom , usually worse with weight
supply , bone structure then collapses bearing & impact activities .
causing deformation –early diagnosis is key *pain may refer down to Knee
to improved prognosis *initially may be asymptomatic , possible incidental finding
on diagnostic imaging
*remember occurs bilateral 55% of the time
Extremity manual Viziniak p210 Physical :
inspection : possible antalgic gait + trendelenbery
*no bruising/swelling
*Possible short leg with femoral head collapse
Palpation :
possible tenderness around hip with occasional muscle
spasm
Motion:
AROM & PROM may be restricted & painful with possible
crepitus with motion
*RROM usually WNL (within Norm limits)
Neurovascular :
Usually WNL in advanced cases muscle wasting maybe
noted secondary to disuse
Differential diagnoses:
*Osteoarthritis/rheumatoid arthritis
*Septic arthritis
*Hip synovis/capsuilitis/groin strain /hip bursitis
*Neoplasm
*pain referral (Pyeonephritis/renal colic/regional
ileitis/appendicitis/salpingtitis
Special tests
+ scour (Quadrant )tests
+ Anvil test
+Patrick (FABERE)
+Laguerre

Bursitis’ History:
Definition : *pain usually a dull ache over post/lateral thigh
Inflammation of bursa around Hip & great *Pain may radiate down lateral thigh but rarely past knee
trochanter-most commonly trochanteric * Pain is worse with activity (getting up from low chair or
bursa (may also include ,ischial bursa, toilet)ar lining on affected side

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iliopsoas bursa, subgluteous minimus/or *Snapping Hip may be noted at time of injury patient may
subgluteus medium bursa ) Bursitis is found recall details of impact trama
secondary to other pathology or trama *Patients with past history of local surgery (1.4% of cases of
arthoscopic surgery of hip)
Extremity manual Viziniak p206 *in one study 75 patients with trochanteric bursitis, 67%
had a history of chronic lower back pain ,20% had ipsilateral
osteoarthritis of the hip
Physical :
Inspection -
Observe gait (antalgic limp or short leg gait)
*swelling is not usually seen due to soft tissue
*possible ecchymosis/abrasion at site of impact
Palpation :
POINT TENDERNESS OVER BURSA IS HALLMARK SIGN
*possible myospasm of gluteal muscles or TFL
Motion:
*AROM & PROM usually WNL , increased pain with external
rotation
*RROM increased pain with muscle testing structures that
ride over top of bursa
*Trochanteric bursitis –resisted abduction
*Iliopsoas bursitis –resisted hip flexion
*ischiogluteal –resisted hip extension
Neurovascular :
Evaluate muscle strength, DRTs, sensation & dural stretch
maneuvers (straight –leg-raise)
Differential diagnoses:
*Osteoarthritis of Hip
*lumbar radiculophy (herniation, DJD)
*Iliopsoas tendonitis or muscle strain
*Septic arthritis or bursa infection
*Meralga paraesthesia (lateral femoral nerve compression
–more common in obese patients )
*ITB syndrome
Special Tests :
+ Thomas test (flexion contraction of iliopsoas muscle)
+Obers test
+Patric FABRE
Tendinopathies
Definition : History:
Tendinopathy, also known as tendinitis or Pathophysiology[
tendonitis, is a type of tendon disorder that
results in pain, swelling, and impaired As of 2016 the pathophysiology is poorly understood;
function. The pain is typically worse with while inflammation appears to play a role, the relationships
movement. among changes to the structure of tissue, the function of
also known as tendinitis or tendonitis, is a tendons, and pain are not understood and there are several
type of tendon disorder that results in pain, competing models, none of which had been fully validated or
[16][17]
swelling, and impaired function.
[3][1]
The pain falsified. Molecular mechanisms involved in
[6]
is typically worse with movement. It most inflammation includes release of inflammatory cytokines like
commonly occurs around the shoulder IL-1β which reduces the expression of type I collagen mRNA
(rotator cuff tendinitis, biceps tendinitis), in human tenocytes and causes extracellular matrix
[18]
elbow (tennis elbow, golfer's elbow), wrist, degradation in tendon.
hip, knee (jumper's knee), or ankle

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[3][7][2]
(Achilles tendinitis).

https://en.wikipedia.org/wiki/Tendinopathy Physical :
Treatment
Treatment of tendon injuries is largely conservative. Use
of non-steroidal anti-inflammatory drugs (NSAIDs), rest,
and gradual return to exercise is a common therapy.
Resting assists in the prevention of further damage to the
tendon. Ice, compression and elevation are also
frequently recommended. Physical therapy, occupational
therapy, orthotics or braces may also be useful. Initial
recovery is typically within 2 to 3 days and full recovery is
within 3 to 6 months.[2] Tendinosis occurs as the acute
phase of healing has ended (6–8 weeks) but has left the
area insufficiently healed. Treatment of tendinitis helps
reduce some of the risks of developing tendinosis, which
takes longer to heal.
There is tentative evidence that low-level laser
therapy may also be beneficial in treating
tendinopathy.[33] The effects of deep transverse friction
massage for treating tennis elbow and lateral knee
tendinitis is unclear.[34]

Palpation :
Motion:
Neurovascular :
Differential diagnoses:
Diagnosis]

Diagram illustrating tendonitis and tendon rupture

Symptoms can vary from aches or pains and local joint

stiffness, to a burning that surrounds the
whole joint around the inflamed tendon. In some cases,
swelling occurs along with heat and redness, and there
may be visible knots surrounding the joint. With this
condition, the pain is usually worse during and after
activity, and the tendon and joint area can become stiff
the following day as muscles tighten from the movement
of the tendon. Many patients report stressful situations in
their life in correlation with the beginnings of pain which
may contribute to the symptoms.

https://en.wikipedia.org/wiki/Tendinopathy

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Special Tests :
Strains History:
Definition : *ask about mechanism of injury
Example Groin strain *forced hip adduction ?
stretch or tear (partial or full) of the thigh *medial thigh pain ,better with rest ?
adductor muscles in order of occurrence *Acute injuries described as ripping or stabbing pain in the
*adductor longus (62% of cases) aductor groin (may hear snap or tear) –intense pain lasts for a few
magus .brevis ,pectineus, or gracillis seconds and then becomes a dull ache
*chronic injuries are usually a diffuse dull ache
Extremity manual Viziniak p202 *Affects daily Living depends on grade of tear
Grade 1 walking ok but change of direction notice pain
Grade 2 pain & weakness when trying to squeeze legs ,
running not possible together
Grade 3 Full rupture may be less painful then grade 2
however will demonstrate marked muscle weakness ,loss of
function &altered gait
Physical :
Inspection –possible altered gait in more severe injuries
*swelling & ecchymosis may be observed
Palpation :
TENDER TO PALPATION OVER DAMAGE TISSUE
*Defect may occasional be palable
Motion:
AROM pain during adduction or flection
*PROM usually pain free until muscles are stretched
RPOM pain & muscle weakness with resisted adduction
Neurovascular :
WNL within normal limits
Differential diagnoses:
*30-90% of all patients with groin strain injury have one or
more other injuries that are missed & untrested –look for
other pathologies
*Mernia
*Avulsion fracture /Ostetis pubis
*Iliopsoas bursitis
*children legg-valve-perthes-slipped capital femoral
epiphysis
*Obturator neuropathy
Lower back or GI pain referral
Special Tests
+ resisted hip adduction & weakness
+Pain on stretch of hip adductors
History:
Physical :
Palpation :
Motion:
Neurovascular :
Differential diagnoses:
Special Tests
History:
Physical :

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Palpation :
Motion:
Neurovascular :
Differential diagnoses:
Special Tests
Piriformis S History:
definition: chronic pain in buttock that may radiate down leg
neuromuscular disorder that occurs when *worse with walking & squatting or hip internal rotation or
the sciatic nerve is compressed/irritated by adduction
the piriformis muscle causing pain ,tingling *low tolerance for sitting
& numbness along the distribution of the *505 of patients with piriformis syndrome will have history
sciatic nerve (pseudosciatica) of buttocks, lower back or hip injury
*true piriformis syndrome is thought to be Physical :
rare and is often misdiagnosed of another Antalgic gait with externally rotated hip on affected side
pathology . *when supine or standing affected side may show 45
degrees externally rotated foot due to lateral rotation of
the hip
Palpation :
KEY SIGN FOR DIAGNOSIS IS TENDERNESS & MYOSPASM
OVER GLUTEAL REGION & PIRIFORMIS
*direct deep palpation of piriformis muscle should
reproduce symptoms
Motion:
*Lumbar spine ROM is normal (unless co-existing
pathology)
*limited internal rotation of the hip may be noted
Neurovascular :
*WNL usually
Differential diagnoses:
*Lumbar radiculopathy (disc dernation)
*sacroiliac injury or subluxation
*hamstring strain
*lumbar facet syndrome , spondylisthesis
*lumbosacral sprain/strain
Special Tests
+Frebergs maneuver (forcefull horizontal adduction of the
flexed thigh –pain indicates piriformis syndrome (streteches
muscle)
Stretch knee across and over pelvis flexed at 90 degrees
+Hibbs test
patient prone , examiner grabs patient ankle and internally
rotates femur.
Lumbar disc disease History:
definition: Physical :
See Cmap chat at bottom of Page Palpation :
Motion:
Neurovascular :
Differential diagnoses:
Special Tests

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(where possible, note those factors that help to differentiate the condition – historical, physical
finding, specific testing or any other factor that may be helpful

Exercise 2

Osteonecrosis will be presented in lecture in week 10 however, this can occur in locations other than
the hip.

Please create a table/ chart that lists the locations where Osteonecrosis can occur.

https://orthoinfo.aaos.org/en/diseases--conditions/osteonecrosis-of-the-hip
Osteonecrosis of the Hip
Osteonecrosis of the hip is a painful condition that occurs when the blood supply to the head of the
femur (thighbone) is disrupted. Because bone cells need a steady supply of blood to stay healthy,
osteonecrosis can ultimately lead to destruction of the hip joint and severe arthritis.

Osteonecrosis is also called avascular necrosis (AVN) or aseptic necrosis. Although it can occur in any
bone, osteonecrosis most often affects the hip. More than 20,000 people each year enter hospitals for
treatment of osteonecrosis of the hip. In many cases, both hips are affected by the disease.

Anatomy

Your hip is a ball-and-socket joint. The socket is formed by the acetabulum, which is part of the large
pelvis bone. The ball is the femoral head, which is the upper end of the femur (thighbone).

The surface of the ball and socket is covered with articular cartilage, a smooth, slippery substance that
protects the bones and enables them to glide easily across each other.

Osteonecrosis of the hip occurs in the femoral head, which is the ball of ball-and-socket hip
joint.

Cause

Osteonecrosis of the hip develops when the blood supply to the femoral head is disrupted. Without
adequate nourishment, the bone in the head of the femur dies and gradually collapses. As a result, the
articular cartilage covering the hip bones also collapses, leading to disabling arthritis.

Osteonecrosis can affect anyone, but is more common in people between the ages of 40 and 65. Men
develop osteonecrosis of the hip more often than women.

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In osteonecrosis, the bone in the head of the femur slowly dies.

Risk Factors

It is not always known what causes the lack of blood supply, but doctors have identified a number of
risk factors that can make someone more likely to develop osteonecrosis:
 Injury. Hip dislocations, hip fractures, and other injuries to the hip can damage the
blood vessels and impair circulation to the femoral head.
 Excessive alcohol use. Overconsumption of alcohol over time can cause fatty deposits
to form in the blood vessels and can elevate cortisone levels, resulting in a decreased
blood supply to the bone.
 Corticosteroid medicines. Many diseases, including asthma, rheumatoid arthritis, and
systemic lupus erythematosus, are treated with steroid medications. Although it is not
known exactly why these medications can lead to osteonecrosis, research shows that
there is a connection between the disease and long-term corticosteroid use.
 Medical conditions. Osteonecrosis is associated with other diseases, including Caisson
disease (diver's disease or "the bends"), sickle cell disease, myeloproliferative
disorders, Gaucher's disease, systemic lupus erythematosus, Crohn's disease, arterial
embolism, thrombosis, and vasculitis.

Symptoms

Osteonecrosis develops in stages. Hip pain is typically the first symptom. This may lead to a dull ache
or throbbing pain in the groin or buttock area. As the disease progresses, it becomes more difficult to
stand and put weight on the affected hip, and moving the hip joint is painful.

It may take from several months to over a year for the disease to progress. It is important to diagnose
osteonecrosis early, because some studies show that early treatment is associated with better
outcomes.

https://orthoinfo.aaos.org/en/diseases--conditions/osteonecrosis-of-the-hip

Exercise 3

There are 4 major conditions that can affect the paediatric hip and may present with hip pain. Please list these,
nothing the main clinical features and identify those features which may help to differentiate these.
Developmental dysplasia of the hip (DDH)

DDH used to be known as Congenital Dysplasia of the Hip, but we now know that many children develop
this problem in their early months and years rather than only being born with the condition.

Hips affected by DDH are easily able to dislocate, or slip in and out of the socket or cup. This causes the
“clicky hips” often picked up by Child and Maternal Health Nurses or Family Doctors on screening new
babies. Other signs that are looked for are uneven thigh creases and different leg lengths. These factors
warrant further examination with an Ultrasound to see if the hips are enlocated and assess the shape and
size of the femoral head (ball) and the acetabulum (cup) of the hip joint. Older babies will need an X-ray
to fully examine the hip joint.

DDH affects girls six times more frequently than boys and predisposing factors include family history and
breech position in pregnancy. One third of children with DDH will have both hips affected.

Many babies respond very well to being braced and will then have normal hips. Some kids will need an
operation to help align the hip joint and some will go on to need more surgery. If not found and treated
early, children with DDH may have delayed walking and may limp. Without appropriate management,
DDH can develop into early onset osteoarthritis.

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Mr Loh’s philosophy about treating DDH is that an early concentric reduction gives the hip the best chance
of developing normally. Normal development of the hip requires the ball (femur) to press against the
socket (acetabulum) to create a congruent joint. The sooner we can achieve this, the better.

During your consultation, Mr Loh will discuss all the options for your child and explain his decision -
making process in detail with you and your family.
https://brianloh.com.au/hip-conditions-in-kids

Neuromuscular Hip

The hip is commonly involved in patients with neuromuscular disorders. As a result of muscle imbalance,
the hip joint is “pulled out” into a subluxated or dislocated position. This can result in joint inflammation
and ultimately, premature joint degeneration and intractable pain.

Whilst the method of treatment will depend on the cause of the pain and the state of the hip joint, Mr Loh
will weigh up the options with you and your family. His aim is always to provide the most reliable and
least traumatic solution for your child.
https://brianloh.com.au/hip-conditions-in-kids

Legg-Calve-Perthes Disease of the Hip

Often called Perthes Disease. Perthes is caused by a disruption to the blood supply to the head of the
femur (the ball of the thigh bone). This lack of blood supply causes the bone to degrade and eventually
die. As it does it changes shape.

It affects males more than females and typically children between 4 and 8 years of age. It presents as an
ache and the child will limp. The hip will often be stiff on abduction (out to the side) and internal
rotation. On X-ray we see changes in the joint space and the femoral head. As the disorder progresses,
there are more advanced changes in the femoral head as it progressively collapses. It can often affect both
hips.

Kids with Perthes do best when referred quickly to a surgeon. The aim of treatment is to stop the the head
of the femur from flattening. The mainstay of treatment is to keep of the hip and be non-weight
bearing. Sometimes surgery is required to contain the head within the socket and to preserve range of
motion at the hip.

Without appropriate management, Perthes Disease can lead to early osteoarthritis.

https://brianloh.com.au/hip-conditions-in-kids

Slipped Capital Femoral Epiphysis

The femur is made up of a ball, or head attached by a thin “neck” of bone to the main shaft. In children
there is a growth plate between the head and the neck. In a SCFE the head or ball of the femur slips down
off the neck. This can then lead to a disruption of the blood supply and avascular necrosis or “bone death”
can occur. As for so many conditions, the earlier a SCFE is found and the earlier management occurs, the
better the results.

SCFEs present as hip and knee pain in adolescents aged 10-15 who are often obese. The child will have a
limp and an irritable hip on movement. They often complain of knee pain. In 20% cases both hips are
involved.

Management involves immediate cessation of weight bearing. The head of the femur then needs to be
realigned and pinned in place through surgery.

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https://brianloh.com.au/hip-conditions-in-kids

Exercise 4

Self directed learning:

Please research ‘Myositis ossificans’ and present the history, clinical findings and
importance of this condition. Note: this does not solely apply to the hip!

Myositis ossificans
Dr Henry Knipe◉◈ and Dr Saqba Farooq et al.

Myositis ossificans (MO) is a benign process characterized by heterotopic ossification usually within
large muscles. Its importance stems in large part from its ability to mimic more aggressive
pathological processes. Myositis ossificans is one of the skeletal “don’t touch” lesions.

1
There are some conditions that are related to, or share a similar name to, myositis ossificans :

 myositis ossificans circumscripta: refers to new bone that usually appears after trauma
 myositis ossificans progressiva: a rare, inherited disorder characterized by fibrosing and
ossification of muscle, tendon and ligaments of multiple sites that are disabling and ultimately fatal
 panniculitis ossificans: similar to MO but occurring in subcutaneous tissues
 fibro-osseous pseudotumor of the digits: variant of MO occurring in the fingers and toes
The remainder of this article focuses on the former. Myositis ossificans progressiva, panniculitis
ossificans and fibro-osseous pseudotumor of the digits are discussed separately.

Epidemiology
Most cases of myositis ossificans occur as a result of trauma, and thus, the primary demographic is
1
young adults . Another group which is especially prone to myositis ossificans are paraplegics, usually
2
without evidence of trauma .

Clinical presentation
Typically presents as a painful, tender, enlarging mass, which in 80% of cases is located in large
muscles of the extremities, often following recognized local trauma, although a definite traumatic
1,3
event is not always recalled . In the case of paraplegics, recognized episodes of trauma are often
2
absent, and the disease occurs particularly around the knees and hips .
https://radiopaedia.org/articles/myositis-ossificans-1

Pathology
Myositis ossificans is essentially metaplasia of the intramuscular connective tissue resulting in
extraosseous bone formation (without inflammation).

1
It has a zonal organization :

 peripheral, well-organized mature lamellar bone

 intermediate osteoid region
 central immature non-ossified cellular (fibroblasts) focus
Unfortunately, the histologically of myositis ossificans can appear similar to osteosarcoma, and thus,
can lead to inappropriate management.

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Radiographic features
The typical radiographic appearance of myositis ossificans is circumferential calcification with a lucent
center and a radiolucent cleft (string sign) that separates the lesion from the cortex of the adjacent
bone.

Plain radiograph
Calcification usually begins to become apparent on plain radiographs within 2-6 weeks, and the lesion
reaches the classic well-circumscribed peripherally calcified appearance by two months. Over the
1,3
following 4 or so months, they typically become smaller and denser .

The cleft between it and the subjacent bone may be difficult to see on plain radiographs.

CT
CT appearances are similar to those of plain radiography, demonstrating mineralization proceeding
from the outer margins towards the center. The cleft between it and the subjacent bone is usually
visible.

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The peripheral rim of mineralization is usually visible within 4-6 weeks .

MRI
MRI appearances change with the age of the lesion.

Early features can be misleading because the peripheral calcification is not well seen, and edema in
the soft tissues may extend beyond the often inapparent calcific rim.

 T1
o ill-defined isointense to muscle mass
 T2
3
o periphery: high signal (edema) seen up to 8 weeks
o central: heterogeneous high signal, due to high proliferating cellularity and cartilaginous
3
components
1,3
o fluid-fluid levels have been reported and attributed to previous hemorrhage
 T1 C+ (Gd): enhancement is often present
1,3
Late features mimic bone :
https://radiopaedia.org/articles/myositis-ossificans-1

 T1
o periphery: low signal (mature lamellar bone)
o central: intermediate to high signal (bone marrow)
 T2
o periphery: low signal (mature lamellar bone)
o central: intermediate to high signal (bone marrow)
 T1C+(Gd): usually none in mature lesions

Nuclear medicine
Non-specific increased bone scan uptake on flow and blood pool images is seen early on in the
2
development of the lesion and gradually decreases as the lesion matures . Increased uptake on
delayed phase is typical.

5
FDG PET can demonstrate intense uptake mimicking high-grade lesions .

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Treatment and prognosis

Myositis ossificans is benign and there is no compelling evidence that malignant degeneration ever
1
occurs . As such treatment is reserved for symptomatic lesions, and surgical resection is usually
curative.

Differential diagnosis
Imaging differential considerations include:

 parosteal osteosarcoma: calcifies in the center and continues towards the periphery
 soft tissue sarcomas including
o malignant fibrous histiocytoma
o synovial sarcoma
If fluid-fluid levels are present, then a different differential should be entertained (see differential of
fluid-fluid level containing bone lesions).

https://radiopaedia.org/articles/myositis-ossificans-1

Lumbar disc disease

Radiculopathies
refer the C-map charts I have done up below regarding Lumbar Disc Disease &
radiculopathies :

Radiculopathies

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Concept map by Graham Healy

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Lumbar disc disease

by Graham Healy (Next page)

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