Hip Condition Physiopedia

Hip conditions
TRAUMA
A pelvic fracture is a disruption of the bony structures of the Pelvis. The pelvis consists of the ilium,
ischium and pubis. These form an anatomic ring with the sacrum. Disruption of the ring requires a lot of
energy. Because in most of the cases pelvic fractures are caused by high impact, it is possible that organs
in the bony pelvis are affected. Trauma to extra-pelvic organs is common. They are often associated with
severe hemorrhage due to the extensive blood supply to the region. [1][2] Pelvic fractures are associated
with a high morbidity and mortality. Emergency care with primary aim reducing blood loss is always
necessary. [3][4]
Image 1. Diagram of pelvis and sacrum with bony landmarks identified
Classification
There are two classification systems who are used most commonly to describe pelvic fractures:
Classification of pelvic fractures by Tile is based on the integrity of the posterior sacroiliac complex. [5][4]
Type A: rotationally and vertically stable, the sacroiliac complex is intact. Mostly managed
nonoperatively.
A1: avulsion fractures
A2: stable iliac wing fractures or minimally displaced pelvic ring fractures
A3: transverse sacral or coccyx fractures
Type B: rotationally unstable and vertically stable, caused by external or internal rotational forces, results
in partial disruption of the posterior sacroiliac complex.
B1: open-book injuries
B2: LC injuries
B3: bilateral type B injuries
Type C: rotationally unstable and vertically unstable, complete disruption of the posterior sacroiliac
complex, result of great force.
C1: unilateral injury
C2: bilateral injuries in which one side is a type B and the controlateral side is a type C injury
C3: bilateral injury in which both sides are type C injuries

Classification of pelvic fractures by Young and Burgess is based on mechanism of injury: lateral
compression, anteroposterior compression, vertical shear or a combination of forces. [1][3][6]
Grade I: associated sacral compression on side of impact. Associated widening of pubic symphysis or of
the anterior sacroiliac joint, while ligaments remain intact.
Grade II: associated posterior iliac fracture on side of impact. Associated widening of the anterior SI joint
caused by disruption of the anterior SI, sacrotuberous and sacrospinous ligaments, posterior ligaments
remain intact.
Grade III: associated controlateral sacroiliac joint injury. Complete SI joint disruption with lateral
displacement and disrupted anterior SI, sacrotuberous, sacrospinous and posterior SI ligaments.
Epidemiology/ etiology
Pelvic fractures have an incidence of 37 cases per 100000 person-years in the United States. The
appearance of pelvic fractures is the greatest in people aged between 15-28 years. In persons younger
than 35, pelvic fractures occur more in males than females. In persons older than 35, pelvic fractures
occur more in females than males. In younger people pelvic fractures occur mostly as result of high-
energy mechanisms, in older people they occur from minimal trauma, such as a low fall. Elderly people
with Osteoporosis have a higher risk factor. Low- energy fractures are usually stable fractures of the
pelvic ring. High-energy pelvic fractures occur most commonly after motor vehicle crashes, motorcycle
crashes, motor vehicles striking pedestrians and falls. This are mostly avulsion fractures of the superior
or inferior iliac spines or with apophyseal avulsion fractures of the iliac wing or ischial tuberosity. [5][3]
Clinical Presentation
Patients with low-energy injuries usually present with a history of trauma like a fall from a standing or
seated position onto a bony prominence or excessive strain on a muscle that inserts onto the Pelvis.
Swelling, pain, ecchymosis, erythema and focal tenderness may also be present. With avulsion injuries
there is often pain associated with contraction of the involved muscles. [7]
Patients with high-energy injuries present usually after motor vehicle accidents, falls and crush injuries.
In severe cases, this patients complain of pain in the pelvis, lower back pain, buttocks and/or hips.
Usually they are unable to stand. Concomitant distracting injuries or intoxication may limit the reliability
of the history. In patients with altered mental status or spinal neurologic deficits the presence of pelvic
fractures should be assumed until it can be excluded. Physical findings include abnormal position of the
lower limbs, pelvic deformity or Pelvic instability, swelling and ecchymosis. The abdomen, perineum,
genitals, rectum and lower back must be examined very carefully. [7] High-energy fractures are often
associated with severe injuries of other organs. [2]
Physical Therapy Management
Low-energy injuries are usually managed with conservative care. This included bed rest, pain control and
physical therapy. [7]. Physical therapy include gait training, stabilization exercises and mobility training.
[8]. Early mobilization is very important. The patient must get out of the bed as soon as possible.
Prolonged immobilization can lead to a number of complications including respiratory and circulatory
compromise.
The intensity of the rehabilitation depends on whether the fracture was stable or unstable. The goals of
the physical therapy program should be provide the patient with an optimal return of function by
improving functional skills, self-care skills and safety awareness. [9] In people with surgical treatment
(ex: ORIF), after 1 or 2 days of bed rest physical therapy is initiated to begin transfer and exercise
training. The short-term goals are independence with transfers and wheelchair mobility. After leaving the
hospital it is easier for the patient that the physical therapist comes at home for an exercise program.
The time to achieve this goals are from 2 to 6 weeks, depending on de medical status of the patient. The
home exercise program include basic ROM and strengthening exercises intended to prevent contracture
and reduce atrophy. The patient performs isometric exercises of the gluteal muscle and quadriceps
femoris muscle, ROM exercises and upper-extremity resistive exercises (eg. Shoulder and elbow flexion
and extension) until fatigued. The number of repetitions varied with every patient. The patient is still in
an non-weight-bearing status. [10]
Once weight-bearing is resumed, physical therapy consisted of gait training and resistive exercises for the
trunk and extremities, along with cardiovascular exercises (eg. Treadmill or bicycle training).
Aquatherapy is also good and helpful when available
Definition/Description
A hip fracture is a condition in which the proximal end of the femur, near the hip joint, is broken. It’s also
possible to have a fracture in the pelvis or acetabulum. Such a fracture is a serious injury that occurs
mostly in elderly people over 65 years and complications can be life threatening. [1](level of evidence
A1)
The femur is the largest and strongest bone in the body, so it requires a large or high impact force to
break. Most femur fractures are the result of a high energy trauma, such as a motor accident, gunshot
wound, or jump/fall from a height. [1]
However, in an older population a simple fall may cause a femoral fracture due to reduced bone mineral
density. A femoral fracture is a very serious injury and needs 3-6 months to heal. [1]
High mortality, long-term disability and huge socio-economic burden are the main consequences of a hip
fracture. [1]
The biggest risk factors for running up a hip fracture are osteoporosis and cognitive impairment. [1]
Clinically Relevant Anatomy
The hip joint is a ball and socket joint, formed by the head of the femur and the acetabulum of the
pelvis. [2]
The head of the femur is almost ( for ¾ ) shaped like a sphere. The acetabulum is formed by the three
parts of the os Coxae. It is a fusion of illium, ischium and pubis. [2]
Through this fusion the acetabulum is shaped like an hemisphere (the inner section of a sphere). [2]
Thereby the acetabulum is not covering the entire head of the femur. [2]
The convex head fits perfectly in the concave socket of the acetabulum forming a synovial joint. [2]
From an osteological viewpoint, the proximal end of the femur in four major parts, namely: femoral
head, femoral neck, greater trochanter and the lesser trochanter. [2]
These parts are most often and most closely involved with hip fractures. The hip joint is a very sturdy
joint, due to the tight fitting of the bones and the strong surrounding ligaments and muscles. [2]
So a hip luxation will less likely take place. [2]
Hip fractures can be classified into intracapsular (femoral neck) fractures and extracapsular fractures .
The intracapsular fractures are contained within the hip capsule itself. Those fractures are subcapital
neck fracture, and transcervical neck fracture.
The extracapsular fractures are intertrochanteric and subtrochanteric fracture. You also have a greater
and lesser trochanter fractures. (figure1) [3]
The pelvic ring is composed of the sacrum. The hip bone is formed at maturity by the fusion of three
ossification centers:
 The ilium
 The ischium
 The pubis
The transversely placed ligaments withstand rotational forces and incorporate the short posterior
sacroiliac. The vertically placed ligaments withstand vertical shear and incorporate the long posterior
sacroiliac, sacrotuberous and lateral lumbosacral ligaments.
Muscles (19)
The hip joint consist of 27 muscles with each their own function. A few important ones:
Posterior
 M gluteii
 M gluteus maximus
 M gluteus medius
 M gluteus minimus
 powerful muscles
 stabililzation
 stabilize the femoral head in the acetabulum
 accelerate the standing position
 strong hip extensors
 external rotators
 hip abductors
 M piriformis
 external rotator
 weak abductor
 weak flexor of the hip
 provide postural stability while walking or standing
Anterior
 M iliopsoas
 M iliacus
 M psoas major
 M psoas minor
 most powerful hip flexors
Epidemiology /Etiology
Etiology: Risk factors for hip fractures[6][9]:
Bone density: Decreased bone density is dangerous for causing hip fractures
Muscle mass: Decreased muscle mass is also dangerous, it could contribute with other causes to cause a
hip fracture
Sex: From all the hip fractures, 70% of them occurs women, so that’s a significant lot more than by men.
It’s common after the menopause that the bone density of women decreases very fast, so that’s a main
cause for hip fractures
Fall: All the reasons witch can make you fall: dizziness, vision problems, deaf persons,…
Medications: Some medications can cause a decrease in bone density like cortisone.
Nutrition: It is well known that calcium and vitamin D increase bone mass, so a lack of it can cause
several fractures, including hip fractures. Some eating disorders like anorexia and bulimia can weaken
your bones, zo you become more fragile to have a hip fracture.
Age: the older you get, the higher the risk is for hip fractures. 90% of these fractures occur in persons
over 70 years old.
Alcohol and tobacco: These products can reduce the bone mass, causing a higher risk to have a hip
fracture
Medical problems: Endocrine disorders can cause fragility of the bones

Physical activity: Physical activity is very important for the muscle mass and the bone mass, so if you
practice enough sports you will have less risk to have hip fractures.
Stroke disease → high risk factor for falls who can cause a hip fracture.
Parkinson’s disease → high risk factor for falls who can cause a hip fracture. [6][9]
Causes: [7]
Trauma or laesion in the femur ( around 10% )
Local pathologies ( 1% ): example: metastatic malignancy ( A tumor who can affect the bone marrow, it’s
a very dangerous disease)
Fall ( Most of the hip fractures are caused by falls)
Hip fractures without injuries ( < 5% )
Osteoporosis: Osteoporosis is a multifactorial, chronic disease that may progress silently for decades
until characteristic fractures occur late in life. [7]
Causes of Acute fracture:
After extreme muscle contraction-> avulsion fracture
After extreme sports -> stress fracture due
Osteoporosis or hip osteoarthritis often cause complaints in older people.
Causes of Stress fracture:
As a result of fatigue fracture:
As a result of fatigue fracture of the bone because of repeated stress
Athletes have an increased vulnerability due to high training load
In endurance runners/ athletes the pelvic region is frequently
By decrease in bone density.
A fracture at the femoral neck is hard to determine -> A femoral neck fracture by fatigue may be due to
lower shock absorption of the muscles and a lower load limit.
Because there are no symptoms prior to fracture, relatively few people are diagnosed in time for
effective therapy to be administered (Johnston et al. 1989). [7]
Consequently, a large number of individuals experience hip fracture-related pain, expense, disability, and
decreased quality of life. [7]
This number is increasing because fracture incidence rates rise dramatically with age, and populations
are ageing rapidly around the world. [7]
The incidence rates themselves are rising in some regions, and any further improvements in life
expectancy will compound the problem. [7]
A substantial portion of the population is at risk of hip fracture by virtue of low bone mass and frequent
falls. [7]
Due to the sheer size of the affected population, control programs for osteoporosis are likely to be
expensive, but effective and efficient prevention efforts have great potential promise Risk factors other
than low bone mineral density (BMD), defined by the National Osteoporosis Foundation (National
Osteoporosis Foundation, 1998) are personal history of fracture as an adult, history of fracture in a first
degree relative, low body weight, and current cigarette smoking.[14]
Another risk factor that is frequently discussed for the last years is the proximal femoral geometry. It is
suggested as an important marker for the hip fracture risks.[14]
Fractures can be classified radiographically into intracapsular and extracapsular fractures (figure2).
These can be further subdivided, depending on the level of the fracture and the presence or absence of
displacement and comminution. [14]
About 3% of hip fractures are related to localized bone weakness at the fracture site. Secondary to
tumor, followed by bone cysts, or Paget’s disease. More than half of the remaining patients have
osteoporosis, and nearly all are osteopenia. [15]
Characteristics/Clinical Presentation
Specific features for patients with hip fracture include:[10][11]

Dull ache in the groin and/or hip region [12] (level of evidence B)
Inability to put weight on the injured leg causing immobility right after the fall [13] (level of evidence
A1)
If the femur bone is completely broken the injured leg might be shorter compared to the other leg
Severe pain
The patient tends to keep the injured hip as still as possible, positioning it in external rotation [13]
A swelling might occur
Patients may not be able to achieve the same level of functional recovery as their cognitively intact
counterparts do
Intertrochanteric Fractures, subcapital fractures, subtrochanteric fractures, cervical fractures, fracture of

the acetabulum, posterior fracture (femoral neck fracture / fracture of superior or inferior ramus of
pubis) + hip dislocation
The most frequent fractures are the subcapital fractures (especially by decreasing bone density in
osteoporosis) and intertrochanteric fractures.
There are two types of fractures: intra- and extra capsular fractures.
Intra capsular = femoral neck / cervical
Extra capsular = intertrochanteric / pertrochanteric / subtrochanteric
Signs and symptoms of a hip fracture include:
Inability to move immediately after a fall [4]
Severe pain in your hip or groin [4]
Inability to put weight on your leg on the side of your injured hip [4]
Stiffness, bruising and swelling in and around your hip area [4]
Shorter leg on the side of your injured hip [4]
Turning outward of your leg on the side of your injured hip [4]
During the physical examination, displaced fractures present with external rotation and abduction, and
the leg will appear shortened. [5] (level of evidence C2)
Patients with hip fractures have pain in the groin and are unable to bear weight on the affected
extremity [5]
During the physical examination, displaced fractures present with external rotation and abduction, and
the leg will appear shortened [5]
Differential Diagnosis
A hip fracture diagnosis usually is established based on patient history, physical examination, and plain
radiography. A patient with hip fracture typically presents with pain and is unable to walk after a fall.
[16]
On physical examination, the injured leg is shortened, externally rotated, and abducted in the supine
position. Plain radiographs of the hip (a posteroanterior view of the pelvis and a lateral view of the
femur) usually confirm the diagnosis. [16]
However, when clinical suspicion for hip fracture is high and plain radiographs are normal, occult
fracture should be ruled out with magneticresonanceimaging (MRI). [16]If MRI is contraindicated, a
bone scan may be useful in diagnosing fracture, but results may be normal for up to 72 hours after
the injury. [16]
In the scientific research that we use as source, the researchers emphasized different types of hip
fractures. [17]
The mean age of the tests subjects (201 in the beginning, 27 patients were lost to follow-up and 32
patients died) is 81,3 years old with a SD of 8,7 years. [17]
If we look at the different types of hip fractures we can conclude that there are 6 different
categories. The fracture pattern is shown in figure 3. [17]
The majority of hip fractures are traumatic. Only 1.5% are metastatic fractures. [17]
About 37% of the hip fractures are intracapsular, 58% of the fractures are located in the
trochanteric region and less than 5% are subtrochanteric. [17]
Diagnostic Procedures
The diagnosis of a hip fracture is established based on patient history, physical examination and
radiography.[13]
A patient with hip fracture typically presents with pain and is unable to walk after a fall.Hip
fractures encompass a wide range of variety of types and imaging techniques. The most common
types of hip fractures include stress fractures and occult fractures (not detectable via radiograph).
[3][18][19]
Initially, radiographs are usually taken if fracture is suspected due to ease of use and immediate
results. However, radiographs have a poor reliability of picking up fractures in early stages. MRI is
considered the gold standard due to high sensitivity in detecting hip fractures. [3][18][19]
The majority of hip fractures are found by plain radiography, the initial imaging modality used in
the diagnosis of hip fracture, which has a sensitivity ranging from 90%-95%. Standard x-ray
examination of the hip includes an anteroposterior (AP) view of the pelvis and an AP and cross-
table lateral view of the involved hip. Plain x-rays without evidence of fracture do not exclude the
diagnosis of hip fracture. [3][18][19]
Magnetic resonance imaging (MRI) has become the imaging modality of choice for diagnosing
occult hip fractures not detected by radiography. [3][18][19]
MRI has been shown to have 100% sensitivity and 100% specificity in diagnosing occult hip
fractures. Another advantage of MRI is its ability to identify other causes of hip pain involving soft
tissue injuries and non-femoral pelvic fractures, thus allowing for appropriate, cost-effective
treatment. [3][18][19]
Berger et al demonstrated that radiographs had a sensitivity of 15-35% on initial examination of

stress fractures, increasing to 30-70% on follow-up visits. The same study also indicated MRI
having a specificity of 86%, sensitivity of 100%, accuracy of 95%, positive predictive value of 93%,
and negative predictive value of 100%.[3][18][19]
It is suggested that the best method of detecting occult fractures is a combination of a T1 and T2
weighted MRI. This allows the differentiation of fractures versus soft tissue injuries, and is
important as it will significantly alter the course of intervention.[3][18][19]
On a MRI one can see that a proximal hip fracture consists many kinds:
Subcapital neck fracture: right below the femoral head
Femoral neck fracture (intracapsular fracture)[20] (level of evidence B)
Intertrochanteric fracture: between the greater and the small trochanter (extracapsular fracture)
[20][11]
Subtrochanteric fracture: 2 ½ inch below the small trochanter (extracapsular fracture)[11]

Fracture of the greater trochanter
Fracture of the small trochanter
intracapsular fracture
Extracapsular fracture (femur fracture and implant failure)
To determine surgery, partial or complete hip replacement: take into account different criteria: age,
sports, bone density / bone osteoporosis
Outcome Measures
Locomotion (ability to walk and to climb stairs) can be measured with a subscale of the FIM
(Functional Independence Measure). It is a predictor for locomotion This test rates the patient's
independence in traveling 45 m (150 ft) walking or in a wheelchair and in going up and down 12 to
14 stairs. A higher score on the test represents a better locomotion.
Age and prefracture residence at a nursing home were significant predictors of locomotion (P = .02
for both).[20] (Level of evidence A2)
International Hip Outcome Tool (iHOT) The test consists of 33 questions that relate to Symptoms
and Functional Limitations, Sports and Recreational Activities, Job-Related Concerns, Social,
Emotional, and Lifestyle Concerns.
iHOT is one of the most carefully and comprehensively validated outcome measures in orthopaedic
surgery. Each question has a Visual Analoge Scale (VAS) line where the patient has to put on a
marker. The total score is a calculation of the mean of all VAS scores measured in millimeters.
Cumulated Ambulation Score (CAS) is a valid tool to evaluate the basic mobility from patients with
hip fracture. The test is highly recommended after hip fractures to test the basic mobility. Certainly
recommended for hospital treatments.
Timed Up and Go Test (TUGT) is used to test the functional mobility level.
The test consists in rising from a chair, walk 3 meters on a straight line, turn around and go back to
the chair and sit down. When the time is less than 10 seconds, it indicates a normal mobility.
Between 11-20 seconds are normal limits for frail elderly and disabled patients but for others it’s an
indication for examination and has a higher fall risk. Greater than 20 seconds, there is need to
further examination and intervention.
http://www.physio-pedia.com/Timed_Up_and_Go_Test_(TUG)
Chair Stand- Test The amount of time it takes to rise and sit back from a chair or the number of
times someone can rise from a chair in 30 seconds.
The test was performed with the person sitting on a chair (height 45 cm) without arms, but a chair
with arms was used if the patient was unable to stand without the use of the armrests. The patient
was instructed to stand and sit from a seated position as many times as possible within 30 seconds.
Early surgery was not associated with improved function and increased mortality. Though it was
associated with reduced pain and length of stay. Early surgery also resulted in fewer complications.
These conclusions were obtained by comparing patients having surgery within 24 hours with those
having surgery after 24 hours on the following outcomes: [21] (Level of Evidence A2)
Mean pain scores over the first 5 hospital days;
Number of days of severe and very severe pain over hospital days 1 to 5 (assessed by asking
patients if they were experiencing no pain, or mild, moderate, or severe pain);
Major postoperative complications;
LOS;
mortality through 6 months;
FIM locomotion (a 2-item subscale focusing on walking and climbing stairs) score at 6 months;
FIM self-care (a 6-item scale of self-care activities including bathing and dressing); and
FIM transferring (a 3-item scale focusing on transfers from the bed, toilet, and tub).[21] (Level of
Evidence A2)
In the study of Diamond TH et al. are the main outcome measures Prognostic factors (such as pre-
existing illness and osteoporotic risk factors) and outcome data (such as fracture-related
complications, mortality, and level of function as measured by the Barthel index of activities of daily
living at six and 12 months postfracture).
The results of these outcome measures are that fracture-related complications affected similar
proportions of men and women (30% v. 32%), and mean length of hospital stay was similar.
Fourteen per cent of men died in hospital compared with only 6% of women (P = 0.06). Men had
more risk factors for osteoporosis (P < 0.01). [22] (Level of evidence C)
Physical functioning (measured by the Barthel index) deteriorated significantly in men from 14.9 at
baseline to 13.4 at six months (P < 0.05) and 12.4 at 12 months (P < 0.05) after fracture.[22] (Level
of evidence C)
Jay Magaziner et al. investigated eight areas of function after hip fracture. This eight areas of
function (i.e., upper and lower extremity physical and instrumental activities of daily living; gait and
balance; social, cognitive, and affective function) were measured by personal interview and direct
observation during hospitalization at 2, 6, 12, 18, and 24 months.
Levels of recovery are described in each area, and time to reach maximal recovery was estimated
using Generalized Estimating Equations and longitudinal data.
Most areas of functioning showed progressive lessening of dependence over the first postfracture
year, with different levels of recovery and time to maximum levels observed for each area. New
dependency in physical and instrumental tasks for those not requiring equipment or human
assistance prefracture ranged from as low as 20.3% for putting on pants to as high as 89.9% for
climbing five stairs.
Recuperation times were specific to area of function, ranging from approximately 4 months for
depressive symptoms (3.9 months), upper extremity function (4.3 months), and cognition (4.4
months) to almost a year for lower extremity function (11.2 months) [23]
(Level of evidence C)
position. There is little to no external bruising at the fracture site.[3] Plain radiographs of the hip
usually confirm the diagnosis. [13]
Examination
position. There is little to no external bruising at the fracture site.[3] Plain radiographs of the hip
usually confirm the diagnosis. [13]
Radiographic evaluation: standard trauma radiographics withstand an anteroposterior view of the

chest, a lateral view of the cervical spine, an anteroposterior view of the abdomen and an
anteroposterior view of the pelvis.
Anteroposterior radiograph of the pelvis:

anterior lesions
iliac fractures
L5 transverse process fractures
Obturator and iliac oblique views:
• May be used for (suspected) acetabular fractures
Inlet radiograph:
• Taken in the suspine position. Useful for determining anterior or posterior displacement of the
sacroiliac joint, sacrum or iliac wing. And may also determine internal rotation deformities of the
ilium and sacral impaction injuries.
Outlet radiograph:
• Taken in de supine position. Useful for determination of vertical displacement of the hemipelvis.
• Computed tomography
• Magnetic resonance imaging
• Stress view
www.physio-pedia.com/Hip_Examination
Medical Management
The principal goals of management are a return to a pre-event functional level and the prevention of
recurrent fractures, 50% of survivors fail to regain their former levels of autonomy and mobility.
There are many different kinds of operations and treatments if we talk about hip fracture. The sort
of operation or treatment that is used is based on the sort of fracture and personal factors. [16]
In the previously used source (16) almost 80% of the subcapital fractures were treated with a
cemented bipolar hemiarthroplasty. All but one of the undisplaced subcapital fractures were treated
with screw fixation. [16]
Half of the hip fractures were treated with a dynamic hip screw. This represents 87.2% of the
fractures in the trochanteric region. Intramedullary nailing was used in less than 4% of the cases.
[16]
Cemented bipolar hemiarthroplasties with diaphy- seal support were implanted in six patients with
complex inter- or subtrochanteric fractures. [16]
Only one primary total hip arthroplasty was performed for a hip fracture associated with
osteoarthritis of the hip.
One stable undisplaced subcapital fracture was treated conservatively. (2)
In figure 4 you can find an overview of different type of treatment performed for a hip fracture.[16]
The recommended treatment of pelvic fractures depends from institution to institution:
General treatment options:
• External fixation – An external frame design is a rectangular construct mounted on two to three
pins, 1cm distance from each other along the anterior iliac crest.
Postoperative plan for immobilization:
Lateral compression: external fixation for 3 to 6 weeks is advised. With mobilization depending on
the comorbid injuries
Anteroposterior compression: external fixation for 8-12 weeks, depending on the principle of the
posterior sacroiliac ligaments.
Vertical shear: external fixation for 12 weeks with mobilization leaded by radiographic evidence of
healing. This may require combination with open reduction and internal fixation for adequate
stabilization.
•Internal fixation – this significantly rises the forces resisted by the pelvic ring when compared to
external fixation. Biomechanical studies suggest the following treatments:
Iliac wing fractures: open reduction and internal fixation
Diastasis of the pubic symphysis: plate fixation if undergoing laparotomy
Sacral fractures: transiliac bar fixation, but may cause compressive neurologic injury
Unilateral sacroiliac dislocation: internal fixation with cancellous screws fixation can be indicated
Bilateral posterior unstable disruptions: fixation of the displaced part of the pelvis to the sacral
body may be accomplished by posterior screw fixation.
• Open fractures: priority should be given to the evaluation of the anus, rectum, vagina and
genitourinary system.
• Postoperative plan: Generally, early mobilization is desired

Intracapsular Fractures:
Surgical management is the treatment of choice for the majority of femoral neck fractures, but
treatment for nondisplaced femoral neck fractures can be non-operative. [3]
Non operative treatment involves protected weight bearing with crutches for 6 weeks. Non
operative repair is usually reserved for patients who present late after a fracture or who have
significant comorbidities and a high operative risk. [3]
The treatment of displaced femoral neck fractures is more complex, and surgical repair is usually
the treatment of choice. These fractures are not amenable to non-operative management, which
should be reserved for patients with extremely high surgical risk or non-ambulatory elderly
patients with dementia and very limited life expectancies. [3]
Intracapsular fractures are further classified as nondisplaced or displaced based on radiographic

findings. This classification is called: Garden classification (figure 5). [3]
Type 1: un-displaced and incomplete fracture
Type 2: un-displaced complete fracture
Type 3: complete fracture but incompletely displaced
Type 4: complete fracture and completely displaced
Extracapsular Fractures:
Surgical stabilization is standard treatment, and non-operative measures are only considered for
patients who are deemed at very high surgical risk or who have a limited life expectancy.
The goal of surgery is to achieve a stable fracture reduction and fixation, allowing early weight
bearing and mobilization of the patient.
Non-operative management is only considered for non-ambulatory patients with minimal pain and
for medically unstable patients with major un-correctable comorbid disease or terminal illness [3].
Delirium may be the most common medical complication after hip fracture. Delirium may interfere
with recovery and rehabilitation, increase duration of hospitalization, and increase mortality after
one year. [16]
Common precipitating factors include electrolyte and metabolic abnormalities, inadequate pain
control, infection, and psychoactive medications.
Physicians can help prevent delirium by avoiding polypharmacy, minimizing the use of
anticholinergic and psychoactive medications, removing urinary catheters and intravenous lines as
soon as possible, and minimizing sleep interruptions.
If delirium occurs, a thorough evaluation and treatment of the underlying cause is needed. Patients
who do not respond to conservative measures may benefit from low-dose tranquilizers (e.g.,
haloperidol [Haldol]) or atypical antipsychotics (e.g., risperidone [Risperdal], olanzapine
[Zyprexa]).
These agents should be discontinued as soon as possible after the delirium is resolved [16].
Prolonged bed rest can increase the risk of pressure sores, atelectasis, pneumonia, deconditioning,
and thromboembolic complications. Weight bearing immediately after hip fracture surgery is safe in
most patients.[16]
Doing your physical therapy “homework” after a hip fracture can save your life. Within two years of
a hip fracture, more than half of men and 40% of women are either dead or living in a long-term
care facility.
The sooner you return to daily physical tasks after surgery or being injured, the healthier you’ll be .
“Complications following hip surgery involve blood clots, pneumonia, wound infections, and more,
all of which can be reduced with activity,” Dr. Salamon says. [27]
There are some important rules postoperative:
internal rotation from hip flexion is very stressful for the joint
impact activities should be avoided for six weeks postoperative
depending on the surgical procedure is unloaded or partially loaded mobilize postoperatively

crucial to the joint
Avoid straight leg raise for 4 weeks postoperatively to not provoke irritation of the nerve
Cardiovascular training is important

Prolonged bed rust can increase the risk of pressure sores and deconditioning. Therefore it’s
important to start rehabilitation on the first post-operative day (on patients with a total hip
replacement). This includes quadriceps strengthening exercises, isometric exercises, and flexion
and extension mobilizations in the hip joint …[13]
On the second and third post-operative day the patient can start with walking between parallel
bars, and later on they can walk with a walker or a cane. This walking is supervised.
The physiotherapist will begin with range of motion exercises for the hip, knee and ankle because
mobility is decreased following immobilization. Mobilization is a very important treatment in the
recovery process.
The patient can also begin strengthening exercises based on the surgeon's orders (typically six
weeks post-op). Patients should also undergo balance and proprioceptive rehab and these abilities
are quickly lost with inactivity.[28]
Weight-bearing exercises are very important for mobility, balance, activities of daily living and
quality of life[5](level of evidence B), examples:
Stepping in different directions
Standing up and sitting down
Tapping the foot and stepping onto and off a block.
It is ordinarily suggested that patients who underwent a prosthetic replacement have to avoid for
approximately 12 weeks:[24] (level of evidence 5)
Hip flexion greater than 70–90°
External rotation of the leg
Adduction of the leg past midline
Should not bend forward from the waist more than 90

The patient training begins the day after surgery from a sitting position, with abducted hip during
transfer from bed to chair.[24]
Progressive weight-bearing as tolerated till full weight-bearing should start soon after surgery
according to general physical status.[24]
When internal fixation is performed, partial weight-bearing is recommended for a period of 8–10
weeks (according to the radiological evaluation of fracture healing), and after 3 months full weight-
bearing should be allowed.[24]
A warming up on a stationary bicycle for 10 to 15 minutes is recommended.[25]
Among patients who had completed standard rehabilitation after hip fracture, the use of a home-
based functionally oriented exercise program resulted in modest improvement in physical function
at 6 months after randomization.[26] (level of evidence B1)
Program components [26]:
Hip extension (theraband and manual exercise)
Heel raises onto toes (theraband and manual exercise)
Resisted rowing (double arm lifting) (theraband and manual exercise)
Standing diagonal reach (theraband and manual exercise)
Modified get up and go (theraband and manual exercise)
Overhead arm extensions (theraband and manual exercise)
Repeated chair stands (vest and manual exercise)
Lunges - forward and back (vest and manual exercise)
Stepping up and down step (vest, manual exercise and plyometric step)
Calf raises - both legs and one leg (manual exercise)
Twelve weeks of progressive strength training once a week, as a follow-up to a more intensive
training period after hip fracture has no measureable effect upon the BBS (Berg Balance Scale)
score, but may improve strength, endurance, self-reported NEADL (The Nottingham Extended
Activities of Daily Living score), and self-perceived health.
Home-dwelling hip fracture patients seem to constitute a group that needs prolonged follow-up to
achieve the improvements that are important for independent functioning.[25]
Prevention is also a part of the rehabilitation process to prevent fractures. Prevention of hip
fractures should focus on preventing falls and osteoporosis.
Several strategies could help reduce the loss of bone density that underlies hip fracture. Among
these, a substantial body of evidence indicates that physical activity is the most important, and it is
a method of prevention that can be enjoyable and sociable.
Regular exercise would reduce the risk of hip fracture by at least half.
Stopping smoking is also important, and a woman who stops smoking before the menopause will
reduce her risk by about a quarter. [29]
Both these policies can be adopted by both sexes and continued into old age. Postmenopausal
oestrogen replacement more than halves the risk of hip fracture, but the loss of this protection
within a few years of stopping treatment limits its utility.
Oestrogen replacement would need to be continued almost indefinitely if it were to do more than
reduce the incidence of hip fracture in younger age groups, in whom hip fracture is uncommon and
recovery generally uncomplicated. General calcium supplementation is not justified as the likely
benefit is too small.[29]
Interventions to reduce the risk of falls should target identified risk factors (e.g., muscle weakness;
history of falls; use of four or more prescription medications; use of an assistive device; arthritis;
depression; age older than 80 years; impairments in gait, balance, cognition, vision, or activities of
daily living).(26)
Luxation of the hip is a dislocation of the hip. Which means that the head of the femur comes out of
the acetabulum. Most of the times this causes damage at the tissues around the hip.
The hip anatomy exist of the acetabulum and the caput femoris. The acetabulum has the shape of a
cup and the caput femoris has the shape of a ball. These caput femoris placed in the acetabulum
creates the hip joint which is an ball-and-socket or articulatio spheroidea. So The femoral head has
to ‘roll’ in the acetabulum. 6
The hip is a bearing ball joint with as main function support. The stability of the hip joint is
provided mainly by the capsule and by the muscles and ligaments who are located there. They
stabilize the femoral head in the acetabulum and ensure that the hip joint can make all the
necessary movements.
Characteristics of patients with an increased risk of developing a luxation: female gender, alcohol
abuse, various preoperative disorders and older age because decreased muscle mass reduces the
stress on the hip prosthesis and decreases the natural protection against hip dislocation.
Older people often have balance disorders, making them often have fall and this increases the risk of
dislocation. Moreover, they often have neuromuscular dysfunction. In particular, neuropathy causes
an increased luxation risk. Even with a (pre) cerebrovascular accident (CVA) is the risk high.
Cognitive impairment is also associated with more dislocations.
The biggest risk factors for hip luxation are great dexterity, poor follow instructions and increased
tendency to fall 10.
There are two main causes for a luxation of the hip :
- Congenital hip dislocation
- Acquired hip dislocation
Hip dislocation after an accident (posterior / anterior) or hip dislocation after hip replacement
surgery.
Congenital hip dislocation (CHD)
This condition has recently been renamed developmental dysplasia of the hip or DDH. All newborn
babies have their hips checked for DDH within a few days of birth and at six weeks by doctors, so
that treatment can be started early if necessary, long before damage occurs14. CHD occurs with an
incidence that vary between 1.5 and 20 per 1.000 births and 8 times more commonly in girls than in
boys 1,2 . This is explained by the greater mobility of the hip by women 3.
Acquired hip dislocation
The traumatic luxation of the hip, mostly caused by car accidents, is always the result of an external
force with high intensity. This means that this is rarely the only injury being suffered. In the
direction of the force, we distinguish 2 main types of hip dislocations: luxatio posterior, where the
caput femoris is pushed out of the acetabulum (by far the most common, 85% - 90% 4) and the
luxatio anterior, whereby the femoral head is moved forward. By posterior dislocation the hip is in a
fixed position, bent and twisted in toward the middle of the body. By the anterior dislocation, the
femur has slip out of its socket in a forward direction where the hip will be bent only slightly and
the leg will twist out and away from the middle of the body.
Dislocation after hip replacement surgery has the highest incidence rate immediately after the
surgery or in the first three months. The incidence of hip dislocation following hip replacement
surgery greatly depends on patient, surgical and hip implant factors. In general, the larger the head
of the femur post surgery, the less likely a patient is to experience dislocation.
Pain
Severe pain is the most common symptom. Because the femur is separated, muscles and tendons
can be damaged as well. The knee can also hurt.
Swelling
There can be a swelling at the site of the injury. The surrounding skin is puffy.
Hip or leg deformity
In most of the cases is the affected leg shortened. The hip joint appears deformed
Hip immobility
Patients can experience difficulty moving the affected hip and so the inability to walk because of the
pain and swelling.
Hip luxation occurs from a lower-energy forward fall on the ﬂexed knee and hip. These patients
present with painful and limited ROM.7 But these symptoms are not only the symptoms of a hip
luxation but also of a hip dysplasia.9 The term hip dysplasia means an abnormality of shape or size
of the acetabulum or femoral head, or of their proportions or alignment one to the other. 13 There is
still a difference, in the case of a luxation, the patient isn’t able to walk and a patient with a hip
dysplasia can still walk but he has muscle pain in his upper leg. 9 In both cases there can be
radiating pain to the knee and the range of motion will be reduced. Actually, in the most cases, a hip
luxation is a result of a hip dysplasia. Patients with more chronic hip instability may be able to
voluntarily sublux or dislocate their hip.7 Because when the femoral head or the acetabulum is
abnormal, the femoral head can easy go out of the cup and in that case you have a luxation of the
hip. When they think about a luxation of the hip, they must take a x-ray photo for the security. The x-
ray photo is also necessary for to know sure that the luxation doesn’t have a fracture also. When
they definitely want to know that there is nothing wrong with the spine, a CT-scan is an option.12
add text here related to medical diagnostic procedures
Outcome Measures
add links to outcome measures here (also see Outcome Measures Database)
Examination
add text here related to physical examination and assessment
Medical Management
In the recognition and treatment of patients with hip dislocation, the following points are
important:
Radiographic examination before and after you put the hip in the right place to determine the type
of dislocation and potential fractures.
There should be a radiographic examination of the pelvis with patients who have a severe injury at
their thigh (fracture of the femur).
A dislocated hip should be placed in position as soon as possible. Otherwise, the risk of Avascular
necrosis, nerve damage, and second luxation increases.
Repositioning of the hip without surgery is done by a traction performed in the opposite direction
of the dislocation, with 90° flexion in the hip. This should preferably be done under general or
regional anesthesia and muscle relaxation; this to prevent greater damage to cartilage and soft
tissue5.
After the repositioning, the stability of the hip should be tested very carefully.
If the repositioning fails, with instability or there are fractures of acetabulum or femoral head,
operation must take place.
In surgery, the joint must be cleaned of any loose bone fragments or soft tissue that would prevent
proper articulation. The purpose of the operation is to let the femoral head make the same
movements like before. They have to take attention for the emergence of a osteonecrosis from the
femoral head.11
Hip arthroscopy can be used to remove intra-articular fragments, evaluate intra-articular fractures
and chondral injuries.
More than 80% of clinically unstable hips noted at birth have been shown to resolve
spontaneously5. In newborn babies, flexion / abduction maneuvers can be sufficient. Another way
to treat DDH is to holding the hip flexed and abducted (with the leg pulled up and turned out) for
one or two months by the use of a brace, splint or harness. This keeps the top of the femur in the
right position while the ligaments and bones grow and strengthen around it. If all this fails, surgical
management is indicated. A study 7 suggests that the surgeon release the adductor longus, lengthen
the psoas tendon, and insert a Kirschner wire. This simple and safe surgical procedure results in
marked improvement in hip function and prevents complications later.
Traction treatment is very common and important part of the therapy treatment.
Hip flexion can help increase strength and muscular support in the hip. Hip flexion can help
increase strength and muscular support in the hip. We do hip flexion passive ! Hip extension is a
very good way to work on the range of motion of the hip, especially for person with a Hip dysplasia.
If a person has a luxation of the hip, there is always also a hip dysplasia. If you have a hip dysplasia
however, it is not always the case that you have a luxation.
Stretching and joint mobilization is a notable way necessary for the rehabilitation. Step by step the
patients learn to use the hip to its full extent.
Slipped Capital Femoral Ephysis, the most common hip disorder affecting adolescents, (SCFE) is a
disorder of the immature hip in which anatomic disruption occurs through the proximal femoral
physis. The physis, also known as the growth plate, is the part of the bone which is responsible for
lenghtening (see figure). SCFE is associated with a highly variable degree of posterior translation of
the epiphysis and simultaneous anterior displacement of the metaphysis. In SCFE, there is a
spectrum of each of the following elements: temporal acuity physical stability of the slipping physis
degree of displacement between the proximal femoral neck and the epiphysis and the amount of
deformity that the protruding anterior metaphyseal prominence presents to the anterior acetabular
rim with hip flexion.
Fortunately, SCFE can be treated and the complications averted or minimized if diagnosed early. In
most of the cases surgery is necessary to stabilize the hip and prevent the situation from getting
worse. [1] (L.O.E.2A)
The hip joint, a ball and socket synovial joint at the juncture of the leg (femur) and pelvis (os coxa)
is one of the most flexible joints in the human body. In addition to being flexible, the hip joint must
be able to support half of the body’s weight along with any other forces acting upon the body [2]
(L.O.E 5) During running and jumping, for example, the force the forces that are created by the
body’s movements multiplies the force on the hip joint to many times the force exerted by the
body’s weight. The hip joint must be able to accommodate these extreme forces repeatedly during
intense physical activities. In the femur of a growing child, the femoral growth plates are placed
between the epiphysis and metaphysis[3] (L.O.E.5). As we grow, the growth plate builds bone on
top of the end of the metaphysis, which assures bone lengthening.
The strength of the cartilage epiphyseal plate itself is inferior to those of its surrounding bone parts.
Subsequently, increased force on the hip at a time when the femoral head is not fully ready to
support these forces makes the femoral head fail at the weakest point, through the epiphyseal plate.
In addition, the capital femoral epiphysis is a special one. It is one of the only epiphyses in the body
that is inside its joint capsule. The blood vessels that go to the epiphysis run along the side of the
femoral neck and are in real danger of being torn or pinched off if something happens to the growth
plate. When this happens, it can result in a loss of the blood supply to the epiphysis which leads to
an avascular necrosis and chondolysis. [4] (L.O.E.5)
Epidemiology / Etiology
SCFE presents bilaterally in 18 to 50 percent of patients[5] (L.O.E. 2A). The prevalence is more
common in boys than girls and varies widely among etnic groups (higher prevalence rate in blacks,
Hispanics, Polynesians, and Native Americans ), geographic locations (higher rates in the north and
western parts of the United States), and different seasons (late summer and fall).
However pathogenesis is most likely multifactorial, mechanical factors (mainly obesity and growth
surges/abnormal morphology of the proximal femur and acetabulum) seem to play a determinant
role. Other factors that either reduce the resistance to shear or that increase the stresses across the
proximal femoral physis are, for example endocrine disorders, (hypothyroidism, growth hormone
supplementation, hypogonadism, panhypopituitarism,…) less commonly.
There are several factors that can contribute to developing a SCFE:
Those who cannot ambulate with crutches or other assistive devices are deemed unstable.
Antropometric risk factors can be a long, small person, but the most widely recognized factor is
obesity[6]. It is hypothesized that as weight increases, shearing forces across the physis are also
increased, causing it to weaken[7]. Other mechanical contributors to this condition are retroversion
of the femur and increased physeal obliquity.
Changes in hormone levels (spikes in testosterone) during growth spurts can having a weakening
effect on the physis.
There is some association with endocrine disorders, such as Hypothyroidism, Hypopituitarism,

hupogonadisme and metabolic disorders resulting from the English disease or treatment of
chemotherapy or radiation. These situations lead to weakening of the growth plate[6]. However,
this is not a prevalent finding[7][8].
There are several classification systems to determine the severity of a SCFE:
Acute, acute-on-chronic, and chronic

Acute signifies the SCFE occurred with trauma and results in immediate pain and decreased hip
ROM (abduction and internal rotation).
Acute-on chronic describes a patient having symptoms for months and then has an increased slip
due to trauma.
Chronic is identified as the most common presentation, and the child has had symptoms for several
months[8]
The preferred classification system is stable/unstable, which is based on the stability of the physis
[9](L.O.E.2A).
A classification of stable is given to those who can bear weight with/without an assistive device on
the affected leg.
Those who cannot are deemed unstable.[7]
Characteristics / Clinical Presentation
Typical presentation is a child between the ages of 10 - 20 years. There are some differences found
between the literature about the exact age. This has to do with the maturity of the growth plate
(epiphysial line). There is an increased prevalence during the period of rapid growth, shortly after
puberty. The disorder is more prevalent in male than females (2:1 ratio).
The child usually presents with some combination of hip, knee, thigh, and groin pain. The leg is
typically externally rotated and an antalgic gait is noted. The majority of patients will be able to
bear weight and will present with a limp[7][8]. When testing hip range of motion, internal rotation,
flexion, and abduction are limited. External rotation and adduction are often increased and
movement in all directions are painful. Typically, the involved hip will fall into external rotation
when the hip is passively flexed beyond 90 degrees[7][8].
Other conditions to rule out[7]:
Femoral fractures
Avascular necrosis of the femoral head
Legg-Calve-Perthes Disease
Osteomyelitis
Septic Arthritis
Groin pull
* A groin pull, or groin strain, results from putting too much stress on muscles in your groin and
thigh. If these muscles are tensed too forcefully or too suddenly, a tear or rupture to any one of the
adductor muscles is common and ressults in inner thigh pain. Groin pulls are common in people
who play sports that require a lot of running and jumping. In particular, suddenly jumping or
changing direction is a likely cause. [10] (L.O.E. 2B)
For a correct and reliable medical diagnosis, medical imaging is necessary, for example radiographs.
With radiographs, even a slight displacement of the epiphysis is recognizable. With antero-posterior
films, you can examine for SCFE. Lateral radiographs are essential to see when the epiphysis is tilted
over towards the back of the femoral neck[11]. Radiographs in both the Anterior/Posterior view
and the "frog" postion (or Lauenstein-projection) of each hip is required[7][8].
The Wilson classification system utilizes the radiographs to classify a mild slip (less than 1/3
displacement), moderate slip (between 1/3 - 1/2 displacement), and severe slip (greater than 1/2
displacment)[7].
Outcome Measures
Diagnostic Imaging
Radiographs[7][8][6]:
Anterior/posterior view
Lauenstein-projection
Wilson classification system
Bonescan (MRI, CT)[6]:
Epifysiolyse
MRI[6]:
Epiphyseal avascular necrosis

Functional outcome measures
Functional Gait Assessment
International Hip Outcome Tool (iHOT)
Lower Extremity Functional Scale (LEFS)
Examination
With passive movement, there will typically be a restriction with internal rotation, and a
remarkably large hip external rotation[12] (L.O.E. 5).Presentation may include limp or vague pain
in the hip, thigh orknee. It is vital to remember that the complaint of knee pain may be present
because of referred pain from pathology at the hip. Every child presenting with a complaint of hip,
thigh or knee pain must undergo a hip examination. Likewise, a "groin pull" is exceedingly rare in
children and must be a diagnosis of exclusion [13](L.O.E 5).
On physical examination, the patient may be unable to bear weight with a severe slip. Limited
internal rotation of the hip is the most telling sign in the diagnosis of SCFE. Obligatory external
rotation is noted in the involved hip of patients with SCFE when the hip is passively flexed to 90
degrees. Sometimes also restricted abduction. Unless the patient has bilateral SCFE, it is helpful to
compare range of motion with the uninvolved hip [14](L.O.E. 2A).
Patients usually present with limping and poorly localized pain in the hip, groin, thigh, or knee.
Diagnosis is confirmed by bilateral hip radiography, which needs to include anteroposterior and
frog-leg lateral views in patients with stable slipped capital femoral epiphysis, and anteroposterior
and cross-table lateral views in patients with the unstable form[15] (L.O.E. 5).
Medical Management
Once the diagnosis of SCFE is made, , the patient should be placed on non–weight-bearing crutches
or in a wheelchair and quickly referred to an orthopedic surgeon familiar with the treatment of
SCFE. The initial goals of treatment are to prevent slip progression and avoid complications.[16]
(L.O.E 2B)
Prophylactic treatment of the contralateral hip in patients with SCFE is controversial, but it is not
recommended in most patients. Prophylactic pinning may be indicated in patients at high risk of
subsequent slips, such as patients with obesity or an endocrine disorder, or those who have a low
likelihood of follow-up. [17](L.O.E 2B)
Stable SCFE[18](L.O.E 2B)
The standard treatment of stable SCFE is in situ fixation with a single screw. Case series and animal
model studies have shown this to be a simple technique with low rates of recurrence and
complications. After closure of the growth plate, progression of athletic activities may be allowed,
including running and, eventually, participating in contact sports. Most patients with mild to
moderate SCFE who are treated with in situ fixation have well to excellent long-term outcomes.
Unstable SCFE[19](L.O.E 2B)
Unstable SCFE is a much more severe injury than stable SCFE. The rate of osteonecrosis is as high as
20 to 50 percent in patients with the unstable form. Treatment goals are similar to those of stable
SCFE with in situ fixation, but there is controversy as to the specifics of treatment, including timing
of surgery, value of reduction, and whether traction should be used.
Once the patient is diagnosed with SCFE, the patient should stop to bear weight on this leg. The first
goal of treatment is to prevent the further slipping and avoid complications. [20] (L.O.E. 2A) [21]
(L.O.E 2B)
If you don’t want to be treated surgically but by the conservative way the therapist can use Spica
Casting and the therapist can perform easy ROM-exercises and hydrotherpeutic exercises. This
method consists of a period of immobilization that is much longer than when you use surgical
treatment. A long immobilization phase is associated with a lot of complications like atrophy and
strength loss of the muscles, reduced bone mineral density and it is unfavorable to prevent
chondrlysis. However “Pinheiro et al” [22] (L.O.E 2B) suggest that whatever treatment you use the
chances for chondrolysis are 7%. As soon as the risk of femoral head slippage is reduced the
therapist can use partitial weight bearing whit help of crutches and an exercise program. In this
exercise program he will have to do strenght exercises toe regain power in all the muscles of his leg
an he will also have proprioception and coordination exercises to regain full control and stability of
the hip.
When a pinning-in-situ operation is performed the first goals is to is decrease the pain that comes
with the surgery, modalities as ice, ultrasound ans electrical current may be used. “zilkens et al” [23]
(L.O.E 2B) recommends continuous passive motion of the hip to maintain range of motion. The
patient can also bear up to 20kg but should always be assisted by the therapist. Cryotherapy can be
used to relief the pain. When the when the surgery is properly healed the therapist can use an
exercise program to improve range of motion of the hip, augment muscle strength and coordination.
Up to 3 weeks the patient has to limit himself to the 20kg of weight bearing. After this, if the patient
is pain free, full range of motion is achieved and six weeks have passed, the patient can fully bear his
weight. If not partial weight bearing must go on.
linically Relevant Anatomy
The hip labrum is a dense fibrocartilagenous structure, mostly composed of type 1 collagen that is
typically between 2-3mm thick that outlines the acetabular socket and attaches to the bony rim of
the acetabulum. The labrum has an irregular shape as it is wider and thinner in the anterior region
of the acetabulum and thicker in the posterior region[1][2]. Hip labral disorders are pathologies of
this structure; in most cases this is caused by a tear in the labrum but it can also be caused by a
dislocation, misalignment from bony structures ore a not optimal angle of the caput femoris.
As for the blood supply, it is thought that the majority of the labrum is avascular with only the
outer third being supplied by the obturator, superior gluteal, and inferior gluteal arteries. There is
controversy as to whether there is a potential for healing with the limited blood supply and this is
an important clinical consideration. The superior and inferior portions are believed to be
innervated and contain free nerve endings and nerve sensory end organs (giving the senses of pain,
pressure, and deep sensation)[1][2].
The labrum functions as a shock absorber, joint lubricator, and pressure distributor. It resists
lateral and vertical motion within the acetabulum along with aiding in stability by deepening the
joint by 21%. The labrum also increases the surface area of the joint by 28% allowing a wider area
of force distribution and is accomplished by creating a sealing mechanism to keep the synovial fluid
within the articular cartilage[1].
Acetabular Labrum copyright and courtesy of Primal Pictures Ltd.
Acetabular Labrum copyright and courtesy of Primal Pictures Ltd.

Labral tears can be classified by their location (anterior, posterior, or superior/lateral),
morphology (radial flap, radial fibrillated, longitudinal peripheral, and unstable), or etiology[1]. It is
generally accepted that most labral tears occur in the anterior, anterior-superior, and superior
regions of this acetabulum.
Epidemiology/Etiology
The labrum is susceptible to traumatic injury from shearing forces that occur with twisting, pivoting
and falling. The most common mechanism is an external rotation force in a hyperextended position.
In some cases pain develops over time. It is believed the microtraumata are responsible of the labral
lasions in these cases.
Hip dysplasia is an important risk factor. Hip dysplasia is a general term used to describe certain
abnormalities of the femur or the acetabulum, or both that result in inadequate containment of the
femoral head within the acetabulum. A shallow acetabulum, a femoral or acetabular anteversion,
and a decreased head offset or perpendicular distance from the center of the femoral head to the
axis of the femoral shaft are a few of those bony abnormalities.
With the advent of arthroscopic surgery as an accurate means of diagnosis (magnetic resonance
arthrography), hip labral injuries have become of growing interest to the medical profession. Direct
trauma, including motor vehicle accidents and slipping or falling with or without hip dislocation,
are known causes of acetabular labral tears[2]. Additional causes of labral tears may include
acetabular impingement, joint degeneration, and childhood disorders such as Legg-Calve-Perthes
disease, congenital hip dysplasia, and slipped capital femoral epiphysis[3][4][5][6]. While most
tears occur in the anteriosuperior quadrant, a higher than normal incidence of posterosuperior
tears appear in the Asian population due to a higher tendency toward hyperflexion or squatting
motions[3].
According to a systematic review by Leiboid et al,
Hip labral tears commonly occur between 8 to 72 years of age and on average during the fourth
decade of life.
Women are more likely to suffer than Men.

22-55% of patients that present with symptoms of hip or groin pain are found to have an
acetabulular labral tear[1].
Up to 74.1% of hip labral tears cannot be attributed to a specific event or cause[1].
In patients who identified a specific mechanism of injury, hyperabduction, twisting, falling, or direct
blow from a car accident were common mechanisms of injury [7]. Women, runners, professional
athletes, participants in sports that require frequent external rotation and/or hyperextension,
Those attending the gym 3 times a week all have an increased risk of developing a hip labral tear[7].
Mechanism of Injury
There are five common mechanisms of labral tears that are widley recognized:
Femoroacetabular impingement (FAI)
Trauma
Capsular Laxity
Dysplasia
Degeneration.
FAI has been categorized into two types: CAM and Pincer. Cam type impingment exists with a large
femoral head with resulting abdnormal junction between the femoral head and neck. This causes
impingement between the femur and acetabular rim, particularly during hip flexion and internal
rotation.Pincer impingement occurs with an acetabular overcoverage, causing abutment of the
femoral head into the acetabulum.Cam impingement is the proposed etiology of atererosuperior
labral tears, and pincer type is thought to be on eof the causes posterioinferior chondral lesions.
Traumatic injury to the hip labum is thought to occur with a shearing force associated with twisting
and falling. This can lead to joint instabililty resulitng in abnormal movment patterns with eventual
degenerative changes and labral fraying.
Capsular laxity with resulting labral pathology is thought to occur in one of two ways; cartilage
disorders (ie. Ehlers-Danlos syndrome) or rotational laxity resulting from excessive external
rotation. These forces are often seen in certain sports including ballet, hockey and gymnastics.Hip
dysplasia occurs with development of a shallow acetabular socket resulting in decreased coverage
of the femoral head. This places increased stress into the anterior portion of the hip joint resulting
in impingement and possible tears over time.
Patients with pain deep in the groin, instability of the hip, a "clicking" or "locking" feeling and
stiffness of the hip might be suffering from an acetabular labral tear. These symptoms can increase
when the patient's bearing weight or performing twisting movements of the hip. Pain may also
occur while climbing stairs. Most patients (90%)[8] diagnosed with acetabular labral tears have
had complaints of pain in the anterior hip or groin. This can be an indication for an anterior labral
tear, whereas buttock pain is more consistent with posterior tears and less common. [8]
Labral tears have been classified into 4 types:
Radial flap: most common, disruption of free margin of the labrum
Radial fibrillated: fraying of the free margin, associated with degenerative joint disease
Longitudinal peripheral: least common
Abnormally mobile: can result from a detached labrum
There is some variation in the presentation of hip labral tears. Frequently patients present with
anterior hip and groin pain, although some do present with GT, buttock, and/or medial knee pain.
Mechanical symptoms associated with a tear are clicking, popping,giving way,catching,and stiffness.
Patients offent describe a dull ache which increases with activities such as running or brisk walking.
Some special tests performed are: FABER test,scour test, resisted SLR, and anterior hip
impingement test.
Due to difficulties in identifying specific mechanisms of injury for hip labral tears, generalizing
typical signs and symptoms proves to be challenging. Ninety percent of patients with a hip labral
tear have complaints of anterior hip and/or groin pain[1][2]. Less common areas of pain include
anterior thigh pain, lateral thigh pain, buttock pain, and radiating knee pain[7][1]. Pain patterns and
additional symptoms reported in studies include insidious onset of pain, pain that worsens with
activity, night pain, clicking, catching, or locking of the hip during movement [2][1]. Functional
limitations may include prolonged sitting, walking, climbing stairs, running, and twisting/pivoting
[2][7][1].
According to a 2008 study by Martin et al, symptoms of groin pain, catching, pinching pain with
sitting, FABERs test, flexion-internal rotation, adduction impingement test, and trochanteric
tenderness were found to have low sensitivities (.6-.78) and low specificities (.10-.56) in identifying
patients with intra-articular pain[9].
A variety of pathologies have to be taken into account when facing hip pain. As stated above, in 90%
of cases this pain is situated in the anterior hip or goin region as well as some patients complaining
of pain in the lateral region or deep in the posterior buttocks.
Schmerl and colleagues provide a thorough list for differential diagnosis of labral injury causing hip
pain[3][10]:
Contusion (especially over bony prominences)
Strains Athletic pubalgia
Osteitis pubis
Inflammatory arthridites
Piriformis syndrome
Snapping hip syndrome Bursitis (trochanteric, ischiogluteal, iliopsoas)
Osteoarthritis of femoral head
Avascular necrosis of femoral head
Septic arthritis
Fracture or dislocation
Tumors (malignant and benign)
Hernia (inguinal or femoral)
Slipped capital femoral epiphysis
Legg-Calve-Perthes disease
Referred pain from lumbosacral structures and the sacroiliac joint
Imaging from plain radiographs, computed tomography (CT) and magnetic resonance imaging
(MRI) are ineffective when identifying labral tears due to how they take images of the body and the
chemical composition of the labrum. For these reasons magnetic resonance arthrography (MRa) is
the method of imaging which is most effective[8]. MRa uses a dye injection into the hip capsule
before imaging several planes with an MRa. Although an MRa can give some indications for labral
tears, studies have indicated that the sensitivity and specificity of the test varies. In a systematic
review, Burgess et al, reported that the majority of studies (11/12) found the sensitivity of MRA to
be .63 - .1. Diagnosis should be based on the combination of MRa, physical examination and
arthroscopy. Arthroscopy is considered the golden standard and can be used for diagnostic as well
as therapeutic means. There has been favorable results reported utilizing MRA, however studies
have reported wide ranges of sensitivity from 60%- 100% and specificity from 44% - 100%. [8]
Examination
As mentioned diagnosed should be aided though physical examination. In some cases the first signs
can be spotted while observing the patient; during a brief walk, the ipsilateral knee may be used to
absorb the shocks created in ground reaction forces thus presenting with a flexed knee gait.
Additionally related to gait, the step length of the affected leg may also be shortened, again to
reduce the nociceptive input caused by walking. Aside from simple observation there are a number
of provocative tests that can be performed. Because each test stresses a particular part of the
acetabular labrum, they can also give an indication of where the tear is located[8].
McCarthy test, both hips have to be in a flexed position. The affected hip needs to be brought into
extension. If this movement reproduces a painful click, the patient is suffering from a labral tear.[11]
FABER Test, flexion-abduction-external rotation test test elicates 88% of the patient with an
articular pathology. However this test is non-specific and should be considered a general test for hip
articular surfaces[10].
Anterior labral tear, the patient's leg has to be brought into full flexion, lateral rotation and full
abduction. Then the leg has to be extended with medial rotation and adduction. Patients with an
anterior labral tear will experience sharp catching pain and in some cases there might be a
"clicking" of the hip[12].
Posterior Labral tear, is identified by bringing the patient's leg into extension, abduction and lateral
rotation followed by an extension with medial rotation and adduction of the leg. Sharp catching pain
with or without a "click" will be an indication for a posterior labral tear.
Impingement Test (Flexion-Adduction-Internal Rotation Test), the patient is placed in supine and
the examiner passively flexes the hip to 90 degrees while performing adduction and internal
rotation. Similar to the FABER test, this should be considered a generalised test aditionally, test
positions and definitions of a positive test vary in literature. The Impingement test (Flexion-
Adduction-Internal Rotation Test) has a sensitivity of .75. [4]
Fitzgerald Test. The Fitzgerald test utilizes 2 different test positions to determine if the patient has
an anterior or posterior labral tear. To test for a anterior labral tear, the patient lies supine while the
physical therapist (PT) performs flexion, external rotation, and full abduction of the hip, followed by
extending the hip, internal rotation, and adduction. To test for a posterior labral tear, the PT
performs passive extension, abduction, external rotation, from the position of full hip flexion,
internal rotation, and adduction while the patient is supine. Tests are considered to be positive with
pain reproduction with or without an audible click[7][2]. The Fitzgerald test has a sensitivity of .
98[7][4].
Other tests
Other tests found to have high specificities but lacking high-quality study designs and supportive
literature include the Flexion-Adduction-Axial Compression test and palpation to the greater
trochanter. Flexion-Internal Rotation-Axial Compression test, Thomas test, Maximum Flexion-
External Rotation Test, and Maximum Flexion-Internal Rotation Tests were found to have poor
diagnostic measures[7].
Medical Management
The most commen treatment and usually the first step on the treatment ladder is conservative
treatment and medication; anti-inflammatory drugs (NSAIDs). When conservative treatment does
not resolve symptoms, surgical intervention is often appropriate.
The most common procedure is an excision or debridement of the torn tissue by joint arthroscopy.
However, studies have demonstrated mixed post-surgical results. Fargo et al, found a significant
correlation between outcomes and presence of arthritis on radiography. Only 21% of patients with
detectable arthritis had good results from surgery, compared with 75% of patients without
arthritis. Arthroscopic detection of chondromalacia was an even stronger indicator of poor long-
term prognosis[2].
For a simple tear the surgery involves a bioabsorbeble suture anchor being placed over the tear to
stabilize the fibrocartilaginous tissue back onto the rim of the acetabulum when the labrum has
detached from the bone.
If the pathology is caused due to a malalignment, such as perthes or hip dysplaysia, then femoral or
pelvic osteotomies are considered. A femoral osteotomy is a surgical treatment where the femur is
cut and angled differently in an attempt to improve the mechanics of the leg.
Surgical treatment has been shown to have short-term improvements, however the long-term
outcomes remain unknown. [2]
The goal during PT management of an acetabular labral tear is to optimize the alignment of the hip
joint and the precision of joint motion [2]. This can be done by
Reducing anteriorly directed forces on the hip[2]
Addressing abnormal patterns of recruitment of muscles that control the hip [2].
Instructing patients to avoid pivoting motions, especially under load, since the acetabulum rotates
on a loaded femur, thus increasing force across the labrum [1].
So far there has been no research on the efficacy of hip mobilization or manipulation in the
treatment of labral disorders. Although it is suggested that the therapy should focus on optimizing
the alignment of the hip joint and the precision of joint motion, avoiding pivoting motions and
correcting gait patterns. [10][12]
As these patients have abnormal recruitment patterns of the hip muscles due to the biomenchanics
of the pathology, treatment should optimize control of these muscles, specifically the hip adductors,
deep external rotators, gluteus maximus, and iliopsoas muscles [2][13]. Additionally, if quadriceps
femoris and hamstring muscles dominate, this should be corrected, as decreased force contribution
from the iliopsoas during hip flexion and from the gluteal muscles during active hip extension
results in greater anterior hip forces [14].
Through gait and foot motion analysis, any abnormalities such as knee hyperextension causing hip
hyperextension, walking with an externally rotated hip, or stiffness in the subtalar joint can be
analysed and can be corrected through taping, orthotics or strengthening [2]. Gait analysis may also
uncover decreased hip abduction during both the stance and swing phase, as well as decreased hip
extension during swing phase -- characteristics that may be part of a hip joint stabilization strategy
used by patients to compensate for deficient hip musculature functionality[15].
Additionally, patients need to be educated regarding modification of functional activities to avoid
any positions that cause pain, such as sitting with knees lower than hips or with legs crossed,
getting up from a chair by rotating the pelvis on a loaded femur, hyperextending the hip while
walking on a treadmill, etc.After addressing abnormal movement patterns, focused muscle
strengthening work and recovery of normal range of motion, patients eventually need to be
progressed to advanced sensory-motor training and functional exercises, sport specific if applicable
[13].
If surgery is performed, usually the first 6 weeks post-surgery are NWB or TTWB. Active and active
assisted exercises are appropriate in gravity-minimized positions to maintain motion of the hip.
Stationary bike, not recumbent bicycle, is appropriate; end range hip flexion should be done
passively rather than actively. Rehabilitation protocols are currently based on surgeon and PT
experience and can follow either labral debridement or repair guidelines, depending on the
procedure performed, and move through 4 basic phases. The four basic phases follow the general
progression of initial exercises, intermediate exercises, advanced exercises and sports specific
training
Clinically Relevant Anatomy:
© Primal Pictures
© Primal Pictures
The hip (acetabulofemoral joint) is a synovial joint formed by articulation between the femur and
acetabulum of the pelvis. The head of the femur is cover by type II collagen (Hyaline cartilage) and
proteoglycan. The acetabulum is the concaved portion of the ball and socket joint. The acetabulum
has a ring of fibrocartilage called the labrum that deepens the acetabulum and improves stability of
the hip joint. The hip joint is very stable because of the congruence of the femoral head and
acetabular labrum as well as the five ligaments that surround the joint. The three extracapsular
ligaments are the iliofemoral, ischiofemoral, and pubofemoral ligament attached to the bones of the
pelvis. The ligamentum teres (intracapsular ligament) is attached to the acetabular notch and the
femoral head.
There are a variety of pathoanatomical lesions that may be the cause of hip and groin pain in
athletes. Recently femoroacetabular impingement has been recognizes as a possible cause of hip
pain. Femoroacetabular impingement can be subdivided into a CAM or pincer impingement,
although both typically occur together. CAM impingement is characterized by morphological
abnormality of the superior-anterior aspect of the femoral head-neck junction. This increase in
bone results in impingement of the superior-anterior aspect of the femur with the superior-anterior
aspect of the acetabulum. Pincher impingement is characterized by excessive bone growth of the
superior-anterior aspect of the acetabulum which results in impingement in the same area as the
CAM lesion. Both CAM and pincher impingement typically result in cartilage delamination and
labral lesions. Either Cam or pincher impingement can cause significant disability with athletic
activities and/or ADL’s.
Mechanism of Injury / Pathological Process
Pathological Process CAM Type FAI
Abnormal morphology of the anterior femoral head–neck junction.
Prominence of the femoral head-neck junction in the anterior/anterosuperior portion of the

proximal femur is known as the “pistol grip deformity"
Younger males.
Prominence femoral head-neck junctions produces intermittent and consistent stress (the cam
effect) on the associated articular cartilage.
The shear forces cause damage to both the acetabular labrum and the articular cartilage of the
femoral head and acetabulum.
Pathological Process PINCER Type FAI
Abnormal acetabulum contacting a normal femur.
Usually presents in elderly women.
This can be due to increased acetabular anteversion or coxa profunda.
Acquired causes can be acetabular protrusio or postsurgical prominent anterosuperior acetabulum.
Acetabular retroversion: may be seen as a result of trauma or as part of acetabular dysplasia (either
in isolation or part of a complex).
The acetabular labrum is the first structure to be effected.
The repetitive impact results in degeneration of the labrum with intrasubstance ganglion formation
or ossification of the acetabular rim.
Ossification can lead to further deepening of the acetabulum and therefore more overcoverage of
the femoral head by the acetabulum.
When cartilage lesions do occur with pincer impingement they are typically focal and involve small
areas of the acetabular rim Clinical Findings:
Estimated prevalence: 10-15%
Onset of hip pain usually in the young 20-40 y/o, usually unilateral
CAM type: Male:Female 14:1 (avg age: 32).
Pincer type: Male:Female 1:3 and usually middle age women (avg age: 40)
Present with groin pain with hip rotation, in sitting position, or during/after sports
Typically aware of limited hip mobility long before sx.
Clinical exam:
Loss of internal rotation out of proportion to the loss of range of movement at other positional
extremes.
Osteoarthosis will usually produce a universal limited range of motion.
A grinding and popping sensation can be felt when the femur is externally rotated when the hip is
maximally abducted
Restricted range of motion, particularly flexion and internal rotation
Positive impingement test: for anterior femoroacetabular impingement if forced internal
rotation/adduction in 90 degreea of flexion reproduces pain.
For posterior impingement: painful forced external rotation in full extension with legs hanging off
the end of table and uninvolved leg flexed.
Drehmann’s sign: unavoidable passive external rotation while performing hip flexion.
The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement.
Using standardised MRI, the symptomatic hips of patients who have impingement have significantly
less concavity at the femoral head-neck junction than do normal hips. This test may be of value in
patients with loss of internal rotation for which a cause is not found[1].
Outcome Measures
Harris Hip Score (HHS) [2]
Non-arthritic Hip Score [2]
Management / Interventions
Surgical management for Femoroacetabular Impingment.
Acute hip pain due to tumore, infection, septic arthritis, osteomyelitis, or an inflammatory
condition, fracture, and avascular necrosis are all "red flag" conditions that should be ruled out
VASCULAR
BLOOD
Legg-Calvé-Perthes disease (LCPD) is an idiopathic juvenile avascular necrosis of the femoral head
in children. [1]
The bone death appears in the femoral head due to an interruption in blood supply. As bone death
appears, the ball develops a fracture of the supporting bone. This fracture indicates the outset of
bone reabsorption by the body. As bone is slowly absorbed, it is replaced by new tissue and bone.[2]
Other names are: ischemic necrosis of the hip, coxa plana, osteochondritis and avascular necrosis of
the femoral head. [2]
Blood supply to the femoral head: [3]

The femoral head is supplied with blood from the medial circumflex femoral and lateral circumflex
femoral arteries, which are branches of the profunda femoris artery.
The medial femoral circumflex artery:
extends posteriorly and ascends proximally deep to the quadratus femorus muscle.
At the level of the hip it joins an arterial ring at the base of the femoral neck.
The lateral femoral circumflex artery:
extends anteriorly and gives off an ascending branch,
which also joins the arterial ring at the base of the femoral neck.
This vasculare ring gives rise to a group of vessels which run in the retinacular tissue inside the
capsule to enter the femoral head at the base of the articular surface.
There is also a small contribution from a small artery in the ligamentum teres to the top of the
femoral head which is a branch of the posterior division of the obturator artery.
The origin of Perthes’ disease is unknown, there is consensus however concerning the pathology.
First, there is interrupted blood supply to the capital femoral epiphysis. After this, an infraction of
the subchondral bone occurs. Next, revascularization of the area occurs and new bone ossification
begins. This is the turning point where a percentage of patients will have normal bone growth and
development; while others will develop Legg Calve Perthes Disease. (LCPD). This disease is present
when a subchondral fracture occurs. Usually, there is no trauma to cause this scenario. LCPD is most
commonly the result of normal physical activity. Because of the subchondral fracture, changes occur
to the epiphyseal growth plate.
Classification:
Severity and prognosis of the disease is determined by using a variety of classification systems.
Two of the classification systems are listed here.
The Catteral Classification specifies four different groups to define radiographic appearance during
the period of greatest bone loss.
These four groups are reduced down to two by the Salter-Thomson Classification. The first group,
which is Group A (Catteral I,II) shows less than 50% of the ball is involved. Group B (Catteral III, IV)
shows that more than 50% of the ball is involved. If there is less than 50% involvement the
prognosis is good; if there is more than 50% there is usually a poor prognosis.
The Herring Classification is based on the integrity of the lateral pillar of the caput femoris. Group A
of this classification shows no loss of height in the lateral 1/3 of the head and little density change.
In Lateral Pillar Group B, there is less than 50% loss of lateral height and lucency is present in the
joint. In some cases, the ball is beginning to extrude the socket. In Lateral Pillar Group C, there is
more than 50% loss of lateral height.
There are four phases of Legg-Calve Perthes Disease which are as follows:
1. Increased density of femoral head possibly leading to fractures
2. Bone undergoes fragmentation and reabsorption
3. Growth of new bone
4. Reshaping of new bone
LCP disease is present in children 2-13 years of age and there is a four times greater incidence in
males compared to females. The average age of occurrence is six years.
The limp:
A psoatic limp is typically present in these children secondary to weakness of the psoas major. The
limp:[4] is worse after physical activities and improves following periods of rest. The limp becomes
more noticeable: late in the day, after prolonged walking, …
The pain: [4]
The child is often in pain during the acute [1]. The pain is usually worse late in the day and with
greater activity.[4] Night pains is frequent.[4]
ROM:
The child will show a decrease in extension and abduction active ranges of motion. There is also a
limited internal rotation in both flexion and extension in the early phase of the disease [5]
Unusual high activity level: [6]
Children with Legg-Calvé-Perthes disease are usually, physically very active, and a significant
percentage has true hyperactivity or attention deficit disorder.
Abnormal growth patterns: [7]
General pattern:
The forearms and hands are relative short compared to the upper arm. [8]
The feet are relatively short compared to the tibia. [8]
Stature low-normal
Severe delays are related to bilateral disease.
Local pattern:
There is an anteversion asymmetry, the affected hip is very often the more anteverted and
the opposite femur has an anteversion pattern different from normal.
There is usually no traumatic event to initiate symptoms
Listed are some other disorders that should be included in the differential diagnosis for LCPD:
Septic arthritis-This is an infection in the joint
Sickle cell-Osteonecrosis of the hip can be a result of this disease
Spondyloepiphyseal Dysplasia Tarda-This disease typically affects the spine and the larger more
proximal joints
Gaucher’s Disease- This is a genetic disorder that often times includes bone pathology
Transient Synovitis-This is an acute inflammatory process and is the most common cause of hip
pain in childhood
A MRI is usually obtained to confirm the diagnosis; however x-rays can also be of use to determine
femoral head positioning.
Outcome Measures
The Lower Extremity Functional Scale is one that measures how this disease is affecting the child in
a functional way. Since this questionnaire does ask about certain activities the child may not be
allowed to perform (i.e. running, hopping, etc), it may not be the outcome measure of choice. The
Harris Hip score is another questionnaire that has more to do with a lower level of functional
activities such as walking, stair climbing, donning/doffing shoes, sitting, etc. Questionnaires that
test the patient on a functional level are useful to provide a baseline and monitor functional
progress in the patient’s activities.
Examination
1. The limp:
The limp is usually antalgic.[4]
It is possible that the child has a Trendelenburg gait (a positive Trendelenburg test on the affected
side) which is marked by a pelvic drop on the unloaded side during single stance. [9]
The child can also have a Duchenne gait, which is marked by a trunk lean toward the stance limb
with the pelvis level or elevated on the unloaded side. [9]
2. Range of motion: [4]
The restriction of hip motion is variable in the early stages of the disease;
Many patients, may only have a minimal loss of motion at the extremes of internal rotation and
abduction.
At this stage there usually is no flexion contracture.
Loss of hip ROM in patients with early Perthes’ disease without intra-articular incongruity is due to
pain and muscle spasm. [10]
This is why, if the child is examined for instance after a night of bed rest, the range will be much
better then later in the day.
Further into the disease process;
Children with mild disease may maintain a minimal loss of motion at the extremes only and
thereafter regain full mobility.
Those with more severe disease will progressively lose motion, in particular abduction and internal
rotation.
Late cases may have adduction contractures and very limited rotation, but the range of flexion and
extension is only seldom compromised.
3. Pain: [4]
Pain occurs during the acute disease.[1] The pain may be located in the groin, anterior hip area, or
around the greater trochanter. Referral of pain to the knee is common.
4. Atrophy: [4]
In most cases there is atrophy of the gluteus, quadriceps[11] and hamstring muscles, depending
upon the severity and duration of the disorder.
Medical Management
Medications include nonsteroidal anti-inflammatory medication (NSAIDs) for pain and/or

inflammation.
There is no consensus concerning the possible benefits of physiotherapy in LCP disease, or in which
phase of the development of the health problem it should be used.
Some studies mention physiotherapy as a pre- and/or postoperative intervention, while others
consider it a form of conservative treatment associated with other treatments, such as skeletal
traction, orthesis, and plaster cast.
In studies comparing different treatments[12], physiotherapy was applied in children with a mild
course of the disease. The characteristics of the patients were:
Children with less than 50% femoral head necrosis (Catterall groups 1 or 2) [12]
Children with more than 50% femoral head necrosis, under six years, whose femoral head cover is
good (>80%)[12]
Herring type A or B[13]
Salter Thompson type A[13]
For patients with a mild course, physiotherapy can produce improvement in articular range of
motion, muscular strength and articular dysfunction(meaning?....)[13]. The physiotherapeutic
treatment included:
Passive mobilisations for musculature stretching of the involved hip.
Straight leg raise exercises, to strengthen the musculature of the hip involved for the flexion,
extension, abduction, and adduction of muscles of the hip.
They started with isometric exercises and after eight session, isometric exercises.
A balance training initially on stable terrain, and later on unstable terrain.
For children over 6years at diagnosis with more than 50% of femoral head necrosis, proximal
femoral varus osteomy gave a significantly better outcome than orthosis and physiotherapy[12].
Key Research
add links and reviews of high quality evidence here (case studies should be added on new pages
using the case study template)
According to a research article in the Journal of Bone and Joint Surgery, Legg Calve Perthes is best
treated with surgery if the child is eight years old or older at the time of onset; and second if the
child falls into a category B or B/C border group of the laterall pillar system (herring).
In other studies, good prognosis of a child with this disease under the age of eight has been shown
to be up to 80%. This is with minimal treatment given to the patient. In this study, children between
the ages of 4 and 5 and 11 months had a less favorable chance of a good outcome.
infection of the hip
Septic arthritis is also commonly referred as bacterial or infectious arthritis. Septic arthritis is an
intensely painful infection in a joint.[1] Bacteria, viruses and fungi may infect the joint which will
invade and cause inflammation of the synovial membrane.[2] With the onset of inflammation,
cytokines and proteases are released thus, resulting in cartilage destruction.[3] The infection is
located in the synovial or periarticular tissues and is most commonly bacteria.[4] Bacteria can
spread from other infected areas in your body to a joint.[1] Sometimes bacteria will only infect one
joint, leaving other areas of your body unharmed. Septic arthritis is common at any age. It most
commonly occurs in children under the age of three. [4] The sites that are most common for
developing septic arthritis include the hip and the knee.[5]
Prevalence
In the United States, there are approximately 20,000 cases of septic arthritis reported each year.
Europe reports a similar incidence.[6] Most common is the staphyloccoccus aureus which is found
in 60% of positive cultured joint aspirations. Bactermia is not as common as staphylococcus but it
can lead to polyarticular involvement in 15% of the cases with septic arthitits.[7]
Septic arthritis can present with acute symptoms of joint pain, swelling, tenderness and loss of
motion.[4] The symptoms usually come on quick and a fever may be present. The patient may be
unable to weight bear through the joint.[3]
Symptoms in Newborns/Infants[5]
Cries when infected joint is moved
Fever
Unable to move the limb
Irritability
Symptoms in Children and Adults[5]
Unable to move the limb
Intense joint pain
Joint swelling
Joint redness
Low fever
Chills may occur
Possible Tachycardia
Patient who has another type of arthritis will likely be taking medication and septic arthritis pain
may be masked by that medication so being aware of the other signs and symptoms are very
important. In adults, the joints of the arms and legs are usually affected. The knees are most
commonly affected by septic arthritis. The hip is most commonly affected in children. Children will
usually hold their hip in a fixed position and try to avoid any movement. [1]
Prognosis:
The best outcome for individuals with septic arthritis is immediate treatment. Mortality ranges
from 19-25% and permanent joint disability occurs in 25-50% of the cases.[2] Fifty percent of
adults with septic arthritis have significant decreased range of motion or chronic pain after the
infection.[8] Poor outcome predictors in prognosis of septic arthritis include the following: Age
older than 60, infection of the hip or shoulder joints, underlying rheumatoid arthritis, positive
findings on synovial fluid cultures after 7 days of therapy, delay of 7 days or longer in beginning
treatment.[6]
Associated Co-morbidities[2]
• Systemic corticosteroid use
• Radiation therapy
• Preexisting arthritis
• Arthrocentesis: joint aspiration
• Human Immunodeficiency virus
• Diabetes Mellitus
• Alcohol or drug use
• Trauma
• Other infectious diseases
Medications
Needle joint aspiration is often the initial choice of treatment. Floroscopy is used at the sacroiliac
joint and hip due to the difficulty of performing needle aspiration. Following the results of the
cultures, antibiotics are chosen.[2]
[1]
www.cmaj.ca/content/176/11/1605.full.pdf+html
Common Antibiotic Used:[6]
Ceftriaxone (Rocephin)- Effective against gram-negative enteric rods
Ciprofloxacin (Cipro) - Treat N gonorrhoeae and gram-negative enteric rods.
Cefixime (Suprax) –Broad activity against gram-negative bacteria, by binding to one or more of the
penicillin-binding proteins. Arrests bacterial cell wall synthesis and inhibits bacterial growth.
Oxacillin - Oxacillin is useful against methicillin-sensitive S aureus (MSSA).
Vancomycin (Vancocin) - An anti-infective agent used against methicillin-sensitive S aureus (MSSA),

methicillin-resistant coagulase-negative S aureus (CONS), and ampicillin-resistant enterococci in
patients allergic to penicillin.
Linezolid (Zyvox) - An alternative antibiotic that is used in patients allergic to vancomycin and for
the treatment of vancomycin-resistant enterococci.
Diagnostic Tests/Lab Tests/Lab Values[9]Arthrocentesis with synovial fluid examination and

culture
Increased White blood cell count
Increased Erythrocyte sedimentation rate (ESR)
Increased Temperature
Increased C-Reactive Protein (CRP)
Imaging studies are used to rule out other conditions
[10]
www.vumc.nl/afdelingen-themas/41463/27797/2089686/2090082/1608664/8.pdf
Etiology/Causes
Septic arthritis is caused by invasion of bacteria, viruses, or fungi into the synovial membrane of a
joint. This occurs most commonly by direct inoculation, penetrating wound, or direct extension.
[3]The most common mechanism of infection is via hematogenous. [2]
www.merckmanuals.com/media/professional/pdf/Table_039-2.pdf
The most important risk factors to consider include age (children and older adults are at greatest
risk), diabetes mellitus, IV drug use, indwelling catheters, immunocompromised condition,
rheumatoid arthritis, osteoarthritis, alcohol abuse, or a recent history of joint damage. [3]An
additional risk factor is recent ACL reconstruction with a contaminated bone-tendon-bone allograft.
[3] This is not a common occurrence secondary to advances in medicine.
Risk Factors for Acquiring Septic Arthritis
Age (Neonates, children, older adult)
Alcoholism
Anemia
Arthrocentesis or joint surgery
Bacteremia
Cancer
Diabetes
Hemodialysis
Hemophilia
History of previous joint infection
Immunodeficiency
Immunosuppressive therapy
IV drug use
Joint Replacement
RA
Risk for sexually tramitted disease
Sickle cell disease
Skin infection
SLE
Any other chronic illness not listed
Systemic Involvement
Septic arthritis presents with a multitude of signs and symptoms affecting visceral systems. Joint
symptoms may present in conjunction with a skin rash, low-grade fever, chills, and
lymphadenopathy. [3]Bilateral joint involvement is common in the fingers, knees, shoulders, and
ankles. The classic signs of infection may be present including increased temperature, swelling,
redness, and loss of function. [2] Acute symptoms of an arthritic joint in the presence of fever
should alert the health care provider of potential septic arthritis and should be treated as a medical
emergency.
Medical Management (current best evidence)
Antibiotic Treatment- Septic arthritis is best treated immediately with antibiotics. There is no one
antibiotic better than another; rather it is based on the organism involved. Antibiotics will need to
be chosen based on the culture.[11]
Joint Drainage and Surgical options- Removal of infected joint material is imperative in improving a
patient’s status. One systematic review found “the results suggested that needle aspiration
appeared, in general, to be preferable to surgical treatment as an initial mode of treatment of joint
sepsis, although the results did not reach statistical significance (and there was a trend towards
higher mortality in the needle aspiration group)".[11]
Management regarding antibiotic choice, dosage, route of administration, and duration of treatment
is unknown in the treatment of septic arthritis. In addition, no evidence has shown if closed
aspiration or open arthroscopy is better at removing materials from a joint that’s infected.[11]
[12]
Physical Therapy Management (current best evidence)[6]
It is important to first immobilize the joint. This will control the patient’s pain because it is often too
painful to bear weight. Gentle mobilization of the infected joint can begin if the patient is
responding well following 5 days of gentle treatment. Patients will usually respond better to
aggressive PT to allow maximum post infection functioning. PT needs to consists of allowing the
joint to be in its functional position and positioning the joint to allow passive range of motion
activities.
Septic arthritis presents as many associated arthropathies, these must be ruled out in order for a
definitive diagnosis to be made. With the immediacy of joint destruction with septic arthritis, the
differential diagnosis must be performed with urgency to initiate proper treatment immediately.
Conditions that must be considered include: rheumatoid arthritis, osteoarthritis, HIV infection,
Lyme disease, and gout. Patients with these diagnoses often have a poor prognosis secondary to
delays in the proper diagnosis of septic arthritis. Clinicians often attribute the signs and symptoms
to the preexisting conditions. Other conditions that must be ruled out include: infective
endocarditis, reactive arthritis, and viral arthritis.[8]
Case Reports/ Case Studies
OSTEOMYELITIS
Osteomyelitis, or bone infection, is an inflammation of bone caused by an infectious organism such

as bacteria. However, fungi, parasites, or viruses can also cause osteomyelitis. Acute osteomyelitis is
the clinical term for a new infection in bone that can develop into a chronic reaction when
intervention is delayed or inadequate. Osteomyelitis can occur for a variety of reasons and can affect
all populations but is most common in infants, children, and older adults. Individuals with
compromised immune systems, a history of IV drug abuse, or alcohol abuse are more susceptible to
developing this rapidly progressing pyogenic infection. The pathophysiology of osteomyelitis is
complex and poorly understood. There are several key factors contributing to the infection
including: the virulence of the infectious organism, the individual’s immune status, any underlying
disease, and the type, location, and vascularity of the involved bone[1].
Prevalence
The prevalence of osteomyelitis has decreased throughout the years due to greater control of the
spread of infection in hospitals as well as a better understanding of osteomyelitis treatment
approaches. This enables the infection, in many cases, to be caught within 48 hours and prevented
from becoming a chronic recurrence.
The incidence of osteomyelitis in children has decreased to 47/10,000 in 1990 from 87/10,000 in
1970[2].
The incidence of vertebral osteomyelitis has been estimated at 2.4 cases per 100,000, with the risk
increasing with age (0.3/100,000 among individuals <20 years of age to 6.5/100,000 among
individuals >70 years of age)[3].
Osteomyelitis of the spine is rare, accounting for only about 2-4% of all cases[4].
Individuals presenting with osteomyelitis may have the following symptoms[5]:
Pain and/or tenderness in the infected area
Inflammation, redness, and warmth in the infected area
Fever, chills, and excessive sweating
Nausea and generalized feeling of being ill
Lower back pain (if the vertebrae are involved)
Swelling of the legs, ankles, and feet
The primary manifestations of osteomyelitis may vary between adults and children. In adults, back
pain is typically the chief complaint but once the infection becomes systemic, a low-grade fever may
be present. Children are more likely to present with acute, severe complaints, such as high fever and
intense pain, but in some cases the predominating symptoms are edema, erythema, and tenderness
in the infected area. In both cases, pain may not always be a factor early in the infectious process
due to the lack of pain fibers in cancellous bone. When the infection extends into the periosteum of
the bone, individuals may experience joint pain, decreased function, and systemic signs, such as
fever, swelling, and malaise[1].
Individuals may also present with increased pain, described as deep and constant, during weight
bearing and may exhibit an antalgic gait pattern when the infection involves the lower extremity.
Range of motion of the lumbar spine may be decreased and painful at the end range of motion with
vertebral involvement.
“Sausage toes”, a clinical sign that has been shown to have good sensitivity and specificity, can help
determine the presence of osteomyelitis affecting the phalanges of the feet in diabetic
individuals[1].
Associated Co-morbidities
The following are risk factors and/or associated co-morbidities that could increase an individuals
chance of developing osteomyelitis[6]:
Diabetes
Peripheral arterial disease (PAD)
Sickle cell disease
Systemic Lupus Erythematosus (SLE) can also be associated with developing osteomyelitis. In fact,
one fourth of all persons with Lupus develop progressive musculoskeletal damage in the form of
arthritis, osteoporosis with fracture and vertebral collapse, and osteomyelitis[7].
Medications
(Table courtesy of American Family Physician. Available at: Diagnosis and Management of
Osteomyelitis)
Diagnostic Tests/Lab Tests/Lab Values
Medical diagnosis is often difficult because of the lack of specific signs and symptoms, especially in
chronic osteomyelitis. Signs and symptoms that are usually associated with infection may be
mistaken for normal postoperative changes[1].
Radiographs
May not detect bony abnormality in infections less than 10 days in duration[1].
Lytic lesions may be demonstrable on radiographs within 2 weeks of onset of the infection[1].
Magnetic resonance imaging (MRI) and isotope bone scans are the procedures of choice to
delineate the diseases anatomic extent[1].
Flourine-18-flourodeoxyglucose positron emission tomography (FDG-PET) scans provide accurate

localization of infection and/or source of fever of undetermined origin, thereby guiding further
testing[1].
(Photo courtesy of The New England Journal of Medicine. Available at:

http://blogs.nejm.org/now/index.php/vertebral-osteomyelitis/2010/03/18/)
Etiology/Causes
Osteomyelitis can occur in a variety of bones in different areas of the body. The area affected often
depends on the causative agent, the individuals’ age, and previous medical history as certain types
of osteomyelitis can affect different populations. The bones commonly involved in children are long
bones (adjacent to growth plates) such as the femur, tibia, humerus, and radius due to the amount
of bone marrow present in long bones. Osteomyelitis in adults usually affects the vertebral column,
in particular the lumbar spine, the sacrum, and the pelvis.
Staphylococcus aureus is the usual causative agent of acute osteomyelitis. Once bound to cartilage,
the organism produces a protective glycocalyx and stimulates the release of endotoxins. Other
organisms such as group B streptococcus, pneumococcus, Pseudomonas aeruginosa, Haemophilus
influenza, and Escherichia coli are also capable of producing bone infection. In individuals
diagnosed with sickle cell anemia, Salmonella infection can be associated with osteomyelitis[1].
Surgical procedures, open fractures, and implanted orthotic devices are also causative agents of
acute osteomyelitis. A form of osteomyelitis, exogenous osteomyelitis, occurs when bone extends
out from the skin allowing a potentially infectious organism to enter from an abscess or burn, a
puncture wound, or other trauma such as an open fracture. These examples of osteomyelitis
secondary to infection are common in immunocompromised individuals and in those diagnosed
with diabetes mellitus or severe vascular insufficiency[1].
Hematogenous osteomyelitis is acquired from the spread of organisms from preexisting infections
such that occurs in impetigo; furunculosis (persistent boils); infected lesions of varicella
(chickenpox); and sinus, ear, dental, soft tissue, respiratory, and genitourinary infections.
Genitourinary infections can lead to osteomyelitis of the sacrum or iliac[1].
There are several systemic factors that affect immune surveillance, metabolism, and local
vascularity that may lead to an increased risk for developing osteomyelitis[8]:
Malnutrition
Renal or hepatic failure
Diabetes mellitus
Chronic hypoxia
Immune disease
Extremes of age
Immunosuppression
Immune deficiency
Immediate treatment is indicated for osteomyelitis, especially in the acute phase. Treatment is
usually initiated with an antibiotic, determined by the results of the bone biopsy or cultures taken,
given intravenously at a high dose. Factors such as the patients age, health status, location of
infection, and prior antimicrobial therapy are taken into consideration when determining the
antibiotic used for treatment[1]. The antibiotics are usually prescribed for 4-6 weeks followed by
>8 weeks of oral therapy[9].
Osteomyelitis may also need to be treated surgically. Options include:
Draining the infected area
Removal of necrotic bone and soft tissue
Restoring normal blood flow to the bone
Removing any foreign objects
Amputation of the infected limb[6].
Physical Therapy Management (current best evidence)

Physical therapists can play a vital role in the screening process for osteomyelitis. Individuals who
present with signs and symptoms of infection, possibly causing osteomyelitis, should be referred to
a physician for further diagnostic testing. These signs and symptoms are included in the above
section.
Prevention is another area in cases of osteomyelitis where physical therapists can play an important
role. Chronic osteomyelitis is often a result of complication of treatment with open fractures,
therefore, prevention of infection is highly important[1]. Since the role of nutrition is vital in cases
of infection, patient need to be properly educated on proper nutrition in early post-surgical
intervention due to the fact that most infections occur in the immediate post-operative period[1].
Individuals who are at risk for developing osteomyelitis should also be taught proper preventative
measures and be aware of early warning signs that infection may be present such as, excessive pus
present coming from incision line, redness, extreme tenderness, increased skin temperature near
area of injury or surgical procedure, and symptoms of nausea or vomiting.
If treated surgically for osteomyelitis, physical therapy may be indicated post-operatively to address
any impairments in strength, ROM, proprioception, etc. as well as treatment for any functional
limitations or disabilities secondary to the infection.
The following are possible conditions that could have similar signs and symptoms or relate in other
ways to osteomyelitis[10]:
Ewing Sarcoma
Osteosarcoma
Reactive bone marrow edema
Traumatic or stress fractures
Inflammatory arthritis
Gout
Benign osteoblastic tumor consisting of vascular osteoid tissue centrally and sclerotic bone
peripherally. This type of tumor is commonly found in the diaphysis of long bones such as the femur
(more than 50% of cases). This type of tumor can also occur more rarely in the bones of the hands,
feet, and posterior spine.[1][2]
Prevalence
Osteoid osteomas account for 1/8 to 1/10 of symptomatic bone tumors and 5% of all primary bone
tumors.[3]
Osteoid osteomas occur in children and young adults between the ages of 7 and 25. This type of
bone tumor also occurs two to three times more often in males than in females.[1]
This type of tumor is commonly found in the diaphysis of long bones (proximal femur), hands and
feet, and posterior elements of the spine (lamina and spinouse processes).[1]
Clinical presentation is typically pain in the area of the tumor described as a dull ache, pain that is
worse at night, increased skin temperature, sweating and tenderness to palpation of the localized
area. Pain is relieved by salicylates or aspirin. [1][2]
Ninety percent of cases occur in patients younger than 25 years so osteoid osteomas can easily be
mis-diagnosed as a musculoskeletal disorder because when someone in their twenties reports pain,
the vast majority of people assume the pain is musculoskeletal in nature.[3] The true diagnosis is so
easily overl ooked because epiphyseal lesions mimic intra-articular derangement and pain is
typically localized to the site of the lesion, so the location of pain can be anywhere, and may coincide
with common sites of musculoskeletal inflammation or strain.[4] Another reason diagnosis is easily
misled is that pain usually occurs before the lesions are visible on radiographs and in the early
stages can be easily missed on a radiograph.[5] Finally, these lesions may be associated with
proliferative synovitis due to prostaglandin secretion that decreases range of motion, creates joint
effusion, and can mimic inflammatory arthritis.[6]
Associated Comorbidities
None
Medications
Pain caused by osteoid osteomas can be relieved with aspirin and NSAIDS, which inhibit the
prostraglandins released by the tumor cells. Prostaglandins cause changes in vascular pressure,
which stimulates sensory nerve endings locally, causing pain. Inhibition of these prostaglandins
relieves pain.[1] [2]
Diagnostic Tests/Lab Tests/Lab Values
Radiograph reveals a well demarcated area of translucency (nidus) inside the bone, often times
with a central calcified dot. This is surrounded by bony sclerosis. Usually less than 1 cm in size[7]
TUMOR
HIP
An osteoid osteoma can also be detected with bone scan, or scintigraphy, which will show a focal
uptake of the radiotracer by the tumor.Scintigraphy is often used to detect an osteoid osteoma that
is not easily seen on a radiograph, such as a vertebral tumor.[1]
Osteoid osteomas can be detected on an MRI and CT scan, which are often used to identify the
location of the nidus when the tumor is intra-articular. A CT scan will reveal the nidius as a small
area of low attenuation surrounded by reactive bone formation, seen as a larger area of higher
attenuation.[1] [1][2]
Causes
An ostoid osteoma is a vascular lesion consisting of an area of immature bone surrounded by

osteoblasts and osteoclasts. The tumor starts with the nidus, or nest of vascular osteoid tissue in the
center of the tumor. The nidus then becomes surrounded by reactive bone sclerosis. After the
removal of the nidus, the secondary bone sclerosis generally disappears gradually.[2]
Systemic involvement is uncommon with an osteoid osteoma.[2]
Treatment options include medical management with NSAIDs, surgical excision (wide/enbloc
excision or curetting), or the use of CT- or MRI-guided minimally invasive procedures including core
drill excision, laser photocoagulation, or radiofrequency ablation. For many years, complete surgical
excision was the classic treatment of osteomas, usually performed in patients with pain despite
medical management.
Physical Therapy Management (current best evidence)
None
PEDIATRICS
Hip dysplasia is a general term used to describe certain abnormalities of the femur or the
acetabulum, or both that result in inadequate containment of the femoral head within the
acetabulum. A shallow acetabulum, a femoral or acetabular anteversion, and a decreased head
offset or perpendicular distance from the center of the femoral head to the axis of the femoral shaft
are a few of those bony abnormalities.
The hip exist of the acetabulum and the caput femoris. The acetabulum has the shape of a cup and
the caput femoris has the shape of a ball. These caput femoris placed in the acetabulum creates the
hip joint witch is an articulatio speroidea.
Hip dysplasia exists in two forms. You have the "developmental dysplasia of the hip" or DDH and
"congenital dislocation of the hip" or CDH. DDH is the sort of hip dysplasia witch is acquired
condition. This is often created due to swaddling infant and the use of cradle board which locks the
hip joint in an "abducted" position for extended periods. Other risk factors are firstborn and breech
born. In breech position the caput femoris tends to be pushed out of the acetabulum. A narrow
uterus also facilitates hip joint dislocation during fetal development and birth. CDH is the sort of hip
dysplasia witch is created by a genetic factor witch runs in the family ore who is increased in certain
ethnic populations(Native Americans and Sami people). Same studies suggest it has something to
do with the hormone relaxine and others suggest it has something to do with chromosone 13.
Conditions can also be bilateral or unilateral. With bilateral dysplasia botch hips are affected. With
unilateral dysplasia only one hip is affected.
Hip Dysplacia can be caused by a lot of structural abnormalities like a shallow acetabulum, a
femoral or acetabular anteversion, and a decreased head offset or perpendicular distance from the
center of the femoral head to the axis of the femoral shaft, a flat ore irregular caput femoris are a
few of those bony abnormalities.
Hip dysplasia an be recognized by legs of different length, uneven skin folds on the thigh or
asymmetric gluteus folds, Less mobility or flexibility on one side limping, toe walking, or a
waddling, duck-like gait.
In 1979 Dr. John F. Crowe et al created a classification to define the degree of malformation and
dislocation. This clasification has 4 degrees from less severe(1) to severe(4).
Class Description Dislocation
Crowe I Femur and acetabulum show minimal abnormal development. Less than 50%
dislocation
Crowe II The acetabulum shows abnormal development. 50% to 75% dislocation
Crowe III The acetabula is developed without a roof. A false acetabulum develops opposite the
dislocated femur head position. The joint is fully dislocated. 75% to 100% dislocation
Crowe IV The acetabulum is insufficiently developed. Since the femur is positioned high up on
the pelvis this class is also known as "high hip dislocation". 100% dislocation
Pain in the hip region can also be caused by hip joint contusion, strain, athlethis pubalgia, osteitis
pubis, inflammatory arthritis, osteoarthritis, septic arthritis, piriformis syndrome, snapping hip
syndrome, bursitis, femoral head avascular necrosis, fracture, dislocation, tumor, hernia, slipped
femoral capital epiphysis, Legg-Calve-Perthes disease, or referred pain from the lumbosacral and
sacroiliac areas.
Two maneuvers commonly employed for diagnosis in neonatal exams are the Ortolani test and the
Barlow test. If the patient feels a ‘click’ ore ‘cluck’ during one of those test it is possible that a hip
dysplasia is present. Also X-rays and ultrasound can be used to confirm a hip dysplasia. A
ultrasound has proven to be more useful defining the anatomy until the cartilage is ossified.
Sometimes an MRI is also used. CT scans or 3D CT scans rarely are used. Sonografic examination is a
new diagnostic procedure. Its main disadvantage is that it might lead to over diagnosis, which might
cause over treatment.
Other signs of hip dysplasia are asymmetric gluteus folds and an apparent limb-length inequality.
Outcome Measures
add links to outcome measures here (also see Outcome Measures Database)
Examination
add text here related to physical examination and assessment
Medical Management
There are a lot of possibilities when you chose for a surgery to treat hip dysplasie. Children have
two options. Soft tissue surgery and bony surgery also called osteotomies. The first option is closed
reduction. Witch this treatment they try to manipulate the bone structures to correct the joint
without surgical exposure of the fragments. The other option of soft tissue surgery is open
reduction. This is used when a closed reduction failed to correct the joint. In an open reduction, the
surgeon cuts into the hip capsule and re-positions the femoral head. Once the hip is sutured, a spica
cast is applied for 4 months or longer to stabilize the hip. Once children are older soft tissue surgery
isn’t possible anymore. Then there are the bony surgeries. Here are two options including reshaping
and redirecting. With the reshaping treatment the hip socket is reshaped to increase the hip
congruention. This is only possible witch children who have pliable bones. Redirecting is performed
on older patients who no longer have pliable bone. The surgeon repositions the socket but does not
change its shape.
When you are not a child you have the option between two surgeries. The first reshapes, redirects
or salvages bone in order to preserve the natural joint for as long as possible. The second option is a
hip replacement. Shelf and Chiari osteotomy are some of those salvage procedures. In these cases
non-articular cartilage is used to help hold the hip in place. The cartilage added in these procedures
is fibrocartilage rather than true articular cartilage. Arthroscopy is a surgical procedure often
performed on the soft tissue surrounding the joint. It's a minimally invasive procedure that can
postpone more invasive surgery. In some cases where the dysplasia is relatively non-advanced,
arthroscopy can rule out the need for further surgery altogether. Also the use of stam cells is
possible. These stam cells are used in grafting or by seeding porous arthroplasty prosthesis with
autologous fibroblasts or chondrocyte progenitor cells to assist in firmly anchoring the artificial
material in the bone bed.
Another option for the treatment are diets. Diatry suplements are often used. Oral glucosamine
comes from shellfish (although vegetarian options exist) and may help rebuild cartilage. Another
alternative treatment is an anti-inflammatory diet, which may reduce inflammation. Ginger, garlic,
green tea and Omega-3 fatty acids may have anti-inflammatory effects and can be found in fish and
fish oil supplements, as well as in flaxseed, squash, collard greens, nuts, broccoli, cauliflower and
spinach. Certain foods in the nightshade family can increase inflammation. The most common
edible nightshades are tomato, potato, eggplant and red pepper.
Also anti-inflammatory medications or NSAIDs can be used.
Doctor can also give steroid shots to reduce inflammation an pain. However some studies have
shown that repeated use of cortisone can weaken tendons and soften cartilage.
The treatment of hip dysplasia depends on the age of the child. The goal of the treatment is to
position the hip in the proper position. Once the proper position is obtained the doctor will hold the
hip in that position and that will allow the body to adapt to the new position. The younger the child,
the better capacity to adapt the hip, and the better chance of full recovery. When the child is
younger then 6 month the use of a special brace called a Pavlik harness is used. The brace holds the
hips of the baby in the correct position. Over time the joint begins normal formation. About 90% of
the newborns treated by de Pevlik harness will recover fully. Also a Frejka Pillow is used but is not
indicated in all forms of hip dysplasia. Complications mainly arise because the sheet of the iliopsoas
muscle pushes circumflex artery against the neck of the femur and decreases blood flow to the
femoral head. When the child is older then 6 months the Pevlik harness may not be successful. In
that case a surgeon will place the hip in the proper position under anesthasia. Once in this position
the child will be placed in a spica cast. The spica cast is similar to the Pevlik harness but allows less
movement. When the child is older surgery is used to position the hip in the proper position.
Surgery is needed because the body made scar tissue that prevents the hip from assuming its
proper position. After surgery a spica cast is also used. A treatment that in’t often used is traction.
Traction exists of the application of a force to stretch certain farts of the body in a certain direction.
This will soften the tissue around the caput femoris and will allow the caput femoris to move back
in the acetabulum. Traction consists of pulleys, strings, weights, and a metal frame attached over or
on the bed. Traction is most often used for approximately 10 to 14 days. The application of ice on
the painful regions helps to numb pain and reduces the inflammation.
Regular, low- or non-impact exercise such as swimming, aquatic therapy or cycling train strength
and range of motion. Strong muscles will act like shock absorbers and provide greater support for
the hip.
Weight loss for those with overweight can significantly reduce the stress on the hip and reduce pain.
Physical therapy can be used to increase strength and flexibility around the joint witch will decrease
pain. Physical therapy can also be used to teach the body to better align itself what will lead to a
decrease of tress on the joint.
MUSCULORSKLETAL
Piriformis syndrome (PS) is a painful musculoskeletal condition, characterized by a combination of

symptoms including buttock or hip pain.[1][2][3] In several articles, piriformis syndrome is defined
as a peripheral neuritis of the branches of the sciatic nerve caused by an abnormal condition of the
piriformis muscle (PM), such as an injured or irritated muscle.[4][3] There are more women
diagnosed with Piriformis syndrome than men, with a female–to–male ratio of 6:1. This ratio can be
explained by the wider quadriceps femoris muscle angle in the os coxae of women.[5][6][3] There
are two types of piriformis syndrome. The first type is called “Primary piriformis syndrome.” It is
caused by an anatomical variation, like a split piriformis muscle, a split sciatic nerve or an
anomalous sciatic nerve path. The second type is called “Secondary piriformis syndrome.” It is the
result of a precipitating cause, such as a macrotrauma, microtraumata, ischemic mass effect or local
ischemia.[6][3]
The piriformis muscle (PM) originates from the pelvic surface of the sacral segments S2-S4 in the
regions between and lateral to the anterior sacral foramina, the sacro-iliac joint (superior margin of
the greater sciatic notch), the anterior sacroiliac ligament and occasionally the anterior surface of
the sacro-tuberous ligament. It passes through the greater sciatic notch to insert onto the greater
trochanter of the femur.
The PM is functionally involved with external rotation, abduction and partial extension of the hip.[7]
[8]
The sciatic nerve generally exits the pelvis below the belly of the muscle, however many congenital
variations may exist.[8]
The relationships between the PM and sciatic nerve have been classified by Beaton and Anson using
a six category classification system (Beaton and Anson, 1938). An anomalous relationship would be
labelled between type ‘‘B’’ through type ‘‘F’’ since type ‘‘A’’ is considered to have a normal
relationship between the PM and the sciatic nerve.[9]
Variations in the relationship of the sciatic nerve to the piriformis muscle shown on the diagram
above: (A) the sciatic nerve exiting the greater sciatic foramen along the inferior surface of the
piriformis muscle; the sciatic nerve splitting as it passes through the piriformis muscle with the
tibial branch passing (B) inferiorly or (C) superiorly; (D) the entire sciatic nerve passing through
the muscle belly; (E) the sciatic nerve exiting the greater sciatic foramen along the superior surface
of the piriformis muscle. The nerve may also divide proximally, where the nerve or a division of the
nerve may pass through the belly of the muscle, through its tendons or between the part of a
congenitally bifid muscle.[3]
According to Boyajian- O’ Neill L.A. et al., who has a level of evidence of 2A, there are two types of
piriformis syndrome- primary and secondary.
Primary piriformis syndrome
Primary piriformis syndrome has an anatomical cause, with variations such as a split piriformis
muscle, split sciatic nerve, or an anomalous sciatic nerve path. Among patients with piriformis
syndrome, fewer than 15% of cases have primary causes.[3] At present, there are no accepted
values for the prevalence of the anomaly and little evidence to support whether or not the anomaly
of the sciatic nerve causes piriformis syndrome or other types of sciatica.[9] These findings suggest
that piriformis and sciatic anomalies may not be as important to the pathophysiology of piriformis
syndrome as previously thought.[9]
Secondary piriformis syndrome
Secondary piriformis syndrome occurs as a result of a precipitating cause, including macrotrauma,

microtrauma, ischemic mass effect, and local ischemia.
Piriformis syndrome is most often (50% of the cases) caused by macrotrauma to the buttocks,
leading to inflammation of soft tissue, muscle spasms, or both, with resulting nerve compression.
Muscle spasms of the PM are most often caused by direct trauma, post-surgical injury, lumbar and
sacroiliac joint pathologies or overuse.[4][5][6][10][2][3]
PS may also be caused by shortening of the muscles due to altered biomechanics of the lower limb,
low back and pelvic regions [7]. This can result in compression or irritation of the sciatic nerve. [4]
[6][10]
When there is a dysfunction of the piriformis muscle, it can cause various signs and symptoms such
as pain in the sciatic nerve distribution, including the gluteal area, posterior thigh, posterior leg and
lateral aspect of the foot.[5]Microtrauma may result from overuse of the piriformis muscle, such as
in long-distance walking or running or by direct compression. An example of this kind of direct
compression is known as “wallet neuritis”, which is a repetitive trauma caused by sitting on hard
surfaces.[3]
Etiology of the piriformis syndrome[11]
Gluteal trauma in the sacroiliac or gluteal areas predisposing anatomic variants
Myofascial trigger points Hypertrophy and spasm of the piriformis muscle
Secondary to laminectomy Abcess, hematoma, myositis
Bursitis of the piriformis muscle Neoplasms in the area of the infrapiriform foramen
Colorectal carcinoma Neurinoma of the sciatic nerve
Episacroiliac lipoma Intragluteal injection
Femoral nailing Myositis ossificans of the piriformis muscle
Klippel-Trénaunay syndrome
Other causative factors are anatomic variations of the divisions of the sciatic nerve, anatomic
variations or hypertrophy of piriformis muscle, repetitive trauma, sacro-iliac arthritis and total hip
replacement.[5][6][12][2] A Morton's Toe can also predispose the patient to developing piriformis
syndrome. A fraction of the population is at high risk, particularly skiers, truck drivers, tennis
players and long-distance bikers.[5]
Tonley JC[4] had another view about the cause of PS. He said: ”The piriformis muscle may be
functioning in an elongated position or subjected to high eccentric loads during functional activities
secondary to weak agonist muscles. For example, if the hip excessively adducts and internally
rotates during weight-bearing tasks, due to weakness of the gluteal maximus and / or the gluteus
medius, a greater eccentric load may be shifted to the piriformis muscle. Perpetual loading of the
piriformis muscle through overlengthening and eccentric demand may result in sciatic nerve
compression or irritation”.[4]
Patients with piriformis syndrome have many symptoms that typically consist of persistent and
radiating low back pain, (chronic) buttock pain, numbness, paraesthesia, difficulty with walking and
other functional activities such as pain with sitting, squatting, standing, with bowel movements and
dyspareunia in women.[4][5][1][12][3][13][14].
They can also have pressure pain on the buttock on the same side as the piriformis lesion and point
tenderness over the sciatic notch in almost all instances.[13]]
Swelling in the legs and disturbances of sexual functions have also been observed in patients with
PS.[13]
The buttock pain can radiate into the hip, the posterior aspect of the thigh and the proximal portion
of the lower leg.[4]
There may be an aggravation of pain with activity, prolonged sitting or walking, squatting, hip
adduction and internal rotation and maneuvers that increase the tension of the piriformis muscle.
[4][5][1][12]
Depending on the patient, the pain can lessens when lying down, bending the knee or when
walking. However, some patients cannot tolerate the pain in any position and can only find relief
when they’re walking.[14][13]
Piriformis syndrome is not characterized by neurological deficits typical for a radicular syndrome,
such as declined deep tendon reflexes and myotomal weakness. The patient may present with a
limp when walking or with their leg in a shortened and externally rotated position while supine[1]
[13]. This external rotation while supine can be a positive piriformis sign, also called a splayfoot. It
can be the result of a contracted piriformis muscle.[6][3]
Three speciﬁc conditions may contribute to PS:
Myofascial referred pain from trigger points in the PM

Adjacent muscles, nerve and vascular entrapment by the PM at the greater sciatic foramen
Dysfunction of the sacroiliac joint.[11]
Dysfunction, lesion and inflammation of sacroiliac joint [1]
Pseudoaneurysm in the inferior gluteal artery following gynaecologic surgery Thrombosis of the
iliac vein [2]
Painful vascular compression syndrome of the sciatic nerve, caused by gluteal varicosities
Herniated intervertebral disc [3]
Post-laminectomy syndrome or coccygodinia [4]
Posterior facet syndrome at L4-5 or L5-S1 [5]
Unrecognized pelvic fractures [6]
Lumbar osteochondrosis
Undiagnosed renal stones [15]
Lumbosacral radiculopathies
Osteoarthritis (lumbosacral spine)
Sacroiliac joint syndrome
Degenerative disc disease
Compression fractures
Intra-articular pathology in the hip joint: labral tears [9], femuro-acetabular impingement (FAI)[14]
Lumbar spinal stenosis
Tumors, cysts
Gynaecological conditions
Diseases such as appendicitis, pyelitis, hypernephroma, uterine disorders, prostate disorders and
malignancies in pelvic viscera.
Psychgenic disorders: physical fatigue, depression, frustration
Sacroiliitis [13][16][11][4]
Pathology
There are two types of piriformis syndrome - primary and secondary.
Primary piriformis syndrome has an anatomic cause, such as a split piriformis muscle, split sciatic
nerve, or an anomalous sciatic nerve path.
Secondary piriformis syndrome occurs as a result of a precipitating cause, including macrotrauma,

microtrauma, ischemic mass effect, and local ischemia.
Among patients with piriformis syndrome, fewer than 15% of cases have primary causes. Piriformis
syndrome is most often caused by macrotrauma to the buttocks, leading to inflammation of soft
tissue, muscle spasm, or both, with resulting nerve compression. Microtrauma may result from
overuse of the piriformis muscle, such as in long-distance walking or running or by direct
compression. An example of this kind of direct compression is “wallet neuritis” (ie, repetitive
trauma from sitting on hard surfaces).
Investigations
Radiographic studies have limited application to the diagnosis of piriformis syndrome. Although
standard antero-posterior radiographs of the pelvis and hips, lateral views of the hips and either CT
or MRI of the lumbar spine are recommended to rule out the possibility that the symptoms
experienced by the patients originate from the spine or the hip joint.[11]
Electromyography (EMG) may be also beneficial in differentiating piriformis syndrome from other
possible disorders, such as intervertebral disc herniation. Interspinal nerve impingement will cause
EMG abnormalities of muscles proximal to the piriformis muscle. In patients with piriformis
syndrome however, EMG results will be normal for muscles proximal to the piriformis muscle and
abnormal for muscles distal to it.
Electromyography examinations that incorporate active maneuvers, such as the FAIR test, may have
a greater specificity and sensitivity than other available tests for the diagnosis of piriformis
syndrome[3]
Outcome Measures
Roland-Morris Disability Questionnaire

Examination
A complete neurological history and physical assessment of the patient is essential for an accurate
diagnosis. The physical assessment should include the following points:
an osteopathic structural examination with special attention to the lumbar spine, pelvis and sacrum,
as well as any leg length discrepancies
diagnostic tests
deep-tendon reflex testing, strength and sensory testing
Diagnostic tests
Palpation
The patient reports sensitivity during palpation at the greater sciatic notch, in the region of
sacroiliac joint or over the piriformis muscle belly. It is possible to detect the spasm of the PM by
careful, deep palpation.[6][1][12]
With deep digital palpation in the gluteal and retro-trochanteric area, there may be tenderness and
pain with an exacerbation of tightness and leg numbness.[16]
Pace sign
Pace’s sign consists of pain and weakness by resisted abduction and external rotation of the hip in a
sitting position. A positive test is occurs in 46.5% of the patients with piriformis syndrome.[5][1][3]
[11]
Lasèque sign[11]
The patient reports buttock and leg pain during passive a straight leg raise performed by the
examiner.[16]
Freiberg sign
Involves pain and weakness on passive forced internal rotation of the hip in the supine position. The
pain is thought to be a result of passive stretching of the piriformis muscle and pressure placed on
the sciatic nerve at the sacrospinous ligament. Positive in 56,2% of the patients.[11]
FAIR[16]
Painful flexion-adduction-internal rotation
Beatty’s maneuver
An active test that involves elevation of the flexed leg on the painful side, while the patient is lying
on the asymptomatic side. The abduction causes deep buttock pain in patients with PS, but back and
leg pain in patients with lumbar disc disease.[11]
The Hughes testExternal isometric rotation of the affected lower extremity following maximal
internal rotation may also be positive in PS patients.[11]
Hip Adbuction Test
The patient lies on the side with lower leg flexed to provide support and the upper leg straight, in
line with the trunk. The practitioner stands in front of the patient at the level of the feet and
observes (no hands on) as the patient is asked to abduct the leg slowly.
Normal – Hip abduction to 45°.
Abnormal – if hip flexion occurs (indicating TFL shortness) and/or leg externally rotates (indicating
piriformis shortening) and/or ‘hiking’ of the hip occurs at the outset of the movement (indicating
quadratus overactivity and therefore, by implication, shortness)
Patients with piriformis syndrome may also present with gluteal atrophy, as well as shortening of
the limb on the affected side.
In chronic cases muscle hypotrophy is present in the affected extremity.
Trendelenburg test may also be positive.[16]
Management/Intervention
Medical management
Conservative treatment for piriformis syndrome includes pharmacological agents (non-steroidal

anti-inflammatory agents (NSAIDs), muscle relaxants and neuropathic pain medication), physical
therapy, lifestyle modifications and psychotherapy.[11]
Injections of local anaesthetics, steroids, and botulinum toxin into the PM muscle can serve both
diagnostic and therapeutic purposes. The practitioner should be familiar with variations in the
anatomy and the limitations of landmark-based techniques. An ultrasound guided injection
technique has recently been utilized. This technique has been shown to have both diagnostic and
therapeutic value in the treatment of PS.[11]
Piriformis syndrome often becomes chronic and pharmacological treatment is recommended for a
short time period.[16]
Surgical management
Surgical interventions should be considered only when nonsurgical treatment has failed and the
symptoms are becoming intractable and disabling. Classic indications for surgical treatment include
abscess, neoplasms, hematoma, and painful vascular compression of the sciatic nerve caused by
gluteal varicosities.[11]
Surgical release with tenotomy of the piriformis tendon to relieve the nerve from the pressure of the
tense muscle has resulted in immediate pain relief, as reported by several authors.
Sometimes, the obturator internus muscle should be considered as a possible cause of sciatic pain.
However, the diagnosis of the obturator internus syndrome can only be made by ruling out other
possible causes of sciatic pain, which is similar to the manner in which piriformis syndrome is
diagnosed.[16] Surgical release of the internal obturator muscle can result in both a short- and
long-term reduction in pain in patients with retro-trochanteric pain syndrome and should be
considered if conservative treatment fails.
The postoperative management consists of partial weight-bearing using crutches for 2 weeks and
unrestricted range of motion exercises. The above surgical approach has shown promising short-
term results[16]
The treatment algorithm for retro-trochanteric pain syndrome:
Although there is a paucity of recently published controlled trials in which critically examine the
effectiveness of the noninvasive management modalities[11], a number of methods exists for the
treatment of ‘Piriformis Syndrome’.
The non-invasive treatments include: physical therapy, (osteopathic) manipulative treatment[3]

and lifestyle modification[11].
According to Tonley et al., the most commonly reported physical therapy interventions include
ultrasound, soft tissue mobilization, piriformis stretching, hot packs or cold spray and various
lumbar spine treatments (evidence level 2A). In addition, its case report Tonley et al. describes an
alternative treatment approach for piriformis syndrome. The intervention focused on functional
exercises Therapy Exercises for the Hip aimed at strengthening the hip extensors, abductors and
external rotators, as well as correction of faulty movement patterns (evidence level 4). Despite
positive outcomes (level of evidence 4) full resolution of low back pain, cessation of buttock and
thigh pain) in this single case report care must be taken in establishing cause and effect based on a
single patient. Further investigation is needed[4]
To achieve a 60 – 70% improvement, the patient usually follows 2 – 3 treatments weekly for 2-3
months.[15][17] (level of evidence 2b)
First of all, the patient must be placed in contralateral decubitus and FAIR position (Flexed
Adducted Internally Rotated). Start with an ultrasound treatment: 2.0-2.5 W/cm2, for 10-14
minutes. Apply the ultrasound gel in broad strokes longitudinally along the piriformis muscle from
the conjoint tendon to the lateral edge of the greater sciatic foramen.[4][5][15][2][17][3] (level of
evidence 2b) Before stretching the piriformis muscle, treat the same location with hot packs or cold
spray for 10 minutes. The use of hot and cold before stretching is very useful to decrease pain. [4]
[5][15][17][3] After that, begin with stretching of the piriformis which can be executed in a variety
of ways. Stretch the piriformis muscle by applying manual pressure to the muscle’s inferior border.
It is important not to press downward, rather directing pressure tangentially, toward the ipsilateral
shoulder. When pressing downward, the sciatic nerve will compress against the tendinous edge of
the gemellus superior. However, when applying tangential pressure, the muscle’s grip will weaken
on the nerve and relieve the pain of the syndrome.[4][15][17][3]
Another way to stretch this muscle is in the FAIR position. The patient lies in a supine position with
the hip flexed, adducted and internally rotated. Then the patient brings his foot of the involved side
across and over the knee of the uninvolved leg. We can enhance the stretch, by letting the physical
therapist perform a muscle–energy technique. This technique involves the patient abducting his
limb against light resistance, which is provided by the therapist for 5-7 seconds, with 5-7
repetitions.[5][6][15][17]
After stretching, continue with myofascial release at the lumbosacral paraspinal muscles and
McKenzie exercises. When the patient lies in the FAIR position, the lumbosacral corset can be used.
[15][17][3]
The therapist can also give several tips to avoid an aggravation of the symptoms. This includes:
Avoid sitting for a long period
Stand and walk every 20 minutes
Make frequent stops when driving to stand and stretch
Prevent trauma to the gluteal region
Avoid further offending activities.

Daily stretching is recommended to avoid the recurrence of the piriformis syndrome.[5][6][3]
The patient can also perform several exercises and treatments at home including:
Rolling side to side with flexion and extension of the knees while lying on each side
Rotate side to side while standing with the arms relaxed for 1 minute every few hours
Take a warm bath
Lie flat on the back and raise the hips with your hands and pedal with the legs like you are riding a
bicycle
Knee bends, with as many as 6 repetitions every few hours.
Trochanteric bursitis is an inflammation of the trochanteric bursa. The fact that it’s a Bursitis,
implicates it has an inflammatory component but we have to take into account that 3 of the 4
elements of an inflammation named rubor, calor and tumor aren’t present. Only the sign of pain is
present.
Trochanteric bursitis is an element of a greater term, hip bursitis, that envelopes 4 different
types:trochanteric bursitis, Iliopsoas Bursitis, Gluteal Bursitis and Ischial Bursitis
It’s often used as a general term to describe pain around the greater trochanteric region of the hip.
Trochanteric bursitis is frequently confused with Greater Trochanter Pain Syndrome(GTPS).
Trochanteric bursitis is in fact a component of GTPS that’s also including other conditions that
cause lateral-sided hip pain.
Trochanteric bursitis most commonly results from friction of the overlying iliotibial band.
A bursa is a double membrane filles with fluid located near a joint. A bursa is filled with synovial
fluid, which lessens friction between tissues. It forms a sort of cushion between bones and muscles
and acts as a shock absorber and lubricant during the movement of muscles and joints.
For the mechanism of injury or the pathological process of bursitis: see page of Bursitis
When you have a trochanteric bursitis two bursae can ignited. The first one is the subgluteus
medius bursa. This bursa is located above the greater trochanter. It also lies underneath the
insertion of the gluteus medius. The second one is the subgluteus maximus bursa. This bursa is
situated between the greater trochanter and the insertion of the gluteus medius and gluteus
maximus muscle.
Inflammation of the bursa is a slow process, which progresses over time. This bursitis most often
occurs because of friction, overuse, trauma or too much pressure.
The etiology of a bursitis isn’t entirely known.
There are two types of bursitis. Acute bursitis occurs because of trauma or a massive overload. After
a few days’ symptoms like pain, swelling and a warm feeling when touching the affected area can be
noticed. It will also be very painful to move the joint. The second one is chronic bursitis which is
caused by overuse, too much pressure on the structures or by extreme movements. Wrong muscle
strain can also be a cause of chronic bursitis. The main symptom – which is always present – is pain.
There are many factors that may cause trochanteric bursitis:
• Sex: there are more women with problems of the bursa trochanterica than men;
• Overweight;
• Trauma: e.g. injury of the greater trochanter: this can deface the bursa.
• Overuse of the muscles around the bursa or the joint underneath the bursa.
• Incorrect position: this can cause an increase in pressure.
• Too much pressure on the bursa (caused by friction of the ITB)
• Dysfunction of the insertion of the muscle gluteus medius.
• Hip osteoarthritis
• Lumbar spondylosis
• Excessive or rapidly increased mileage
• Repetitive strain: e.g. frequent training with too much weight or training in a bad position
• Poorly cushioned shoes: results in increased pressure on the muscles, joint and bursa
• Excessive pronation/ extreme movement
• Leg length differences
• ITBS (iliotibiale band sydrome)
• Bacterial infection
• Other inflammatory diseases
• Hip prosthesis
Following characteristics may occur:
- Chronic pain and/or hip tenderness in the lateral aspect of the hip that may radiate down the
thigh.22
 More specifically while palpaiting superior and posterior of the greater trochanter.
 Maximum tenderness at the insertion of the M. Gluteus maximus
 Can also be felt over the iliotibial tract 4
- Pain limits the strength and makes the legs feel weak
- Pain in the area of the greater trochanter whilst walking or running. It can be felt over the lateral
aspect of the leg until the knee
- Stair-climbing is most painful 11
- Patient is not able to lie down on the affected side
 Development of pain-related sleep disturbance 2
- Lower back pain can be related to Trochanteric Bursitis 6
- Weakness of the hip-abductors
 Resistance test can cause tenderness - Pain and tenderness can arise while resisting external
rotation
- A snap felt in the lateral aspect of the hip 1
1 Level of Evidence: 1A
22 Level of Evidence: 5
It may be difficult to diagnose lateral hip pain because clinical presentations are variable and
sometimes inconclusive. That’s why it’s important to have a thorough history and complete physical
examination of the patient. That will be crucial to help the diagnosis of lateral hip pain and to know
of it’s a trochanteric bursitis or not.
Another difficult aspect is differentiating intrinsic pain from Referred_Pain. Trochanteric bursitis is
one of the pathologies that can cause lateral hip pain.
As already mentioned above trochanteric bursitis most commonly results from friction of the
overlying iliotibial band. There is frequently tenderness over the greater trochanter that can be
aggravate by external rotation and abduction of the hip. Also a lot of factors have been associated
with this affection, including leg-length difference, excessive foot pronation, a wide pelvis. During
the physical examination the bursal pain can be detected by palpation.2 We have to note that
trochanteric bursitis is frequently associated with gluteal tendon pathology.
Trochanteric bursitis is more present concerning women. It is frequently associated with

mechanical back strain and obesity. Furthermore, it is also common with reduced hip internal
rotation range of motion.
Other pathologies that can be involved in lateral hip pain are:
• Hip Pointer (contusion of iliac crest or avulsions or fractures of the lateral hip)
• Iliotibial_Band_Syndrome
• Snapping_Hip_Syndrome
• Gluteus Medius Tendon Dysfunction and Tears
• Meralgia Paraesthetica (entrapment of the lateral cutaneous nerve)
Diagnosing lateral hip pain is very complex. To be sure to diagnose the right affection the
examination has to follow a stepwise approach, including inspection, palpation, range of motion,
stability and strength in all planes.
An important diagnostic test for lateral hip pain, particularly for trochanteric bursitis is without a
doubt palpation. You have to palpate in and around the greater trochanter. This is the most
provocative clinical test by physical therapists.
As additional test you can also perform the Ober's_Test. It was originally conceived for abductor
muscle contracture, but we found that the pain reproduction or the reduced range of motion was
significant to diagnose trochanteric bursitis.
If you have any doubt about the diagnosis it’s favorable to make a MRI, which will give more specific
information.
Outcome Measures
• VAS-scale for pain 15
• International Hip Outcome Tool (iHot) 33
• Oswestry Disability Index 15
• Harris Hip score 32
• 6 Minute Walk Test
• Hip Disability and Osteoarthritis Outcome Score
• Copenhagen Hip and Groin Outcome Score 33
15 Level of evidence: 3A
32 Level of evidence: 3B
33 Level of evidence: 1A
Physical Examination
Physical examination is performed based upon the history of previous injuries and it is used to
confirm the source of the pain23 and establish any limitations or deficits that the patient might
have. It also assesses the underlying disorder or anatomical impairment that may cause a bursitis.
The physical examination must have a stepwise approach which includes inspection, gait, palpation,
Range of motion, muscle strength and the execution of special tests.23
The first part is the inspection. The most important aspect of inspection is the patient’s posture in a
seated and upright position. 24 The patient with an irritated hip will tend to stand with the joint
slightly flexed. In a seated position: slouching and leaning to the uninvolved slide allows the hip to
seek a slightly less flexed position. The observation is also focused on the asymmetry, the gross
atrophy, the spinal alignment or the pelvic skewness.
While observing the gait, one should look at leg length discrepancy, weakness and heel strike which
contributes to the function of the gluteus maximus. 25
Bursae pain may be detected by palpation. We perform palpation to assess sources of the hip pain.
The palpation starts with joint tenderness on the proximal and distal area of the hip. Also each part
of the body that is associated with this injury must be assessed, e.g.: the bone, muscle, ligaments,
etc. It is important to check the lumbar spine, sacroiliac joints, ischium, iliac crest, lateral aspect of
the greater trochanteric bursa, muscle bellis and the pubic symphysis. They can determine a
potential source of hip symptoms or pain. 23
The muscle strength can be assessed by resisted contraction which provokes symptoms.
The range of motion should be checked on the actual injured hip as well as on the contralateral hip.
An active hip flexion, an internal and external rotation, an abduction and adduction will reproduce
pain in the injured area. The range of motion can be identified with several tests: the faber test,
Trendelenburg test, Ober’s test, Thomas test and a test whereby the forced flexion combined with
internal rotation could be helpful in diagnosing the cause of lateral hip pain.
23 level of evidence: 1A
25 level of evidence: 4
Medical Management
There are several ways to treat trochanteric bursitis, depending on whether or not the bursitis has
an infection, and whether it is necessary to treat the lesion with or without surgery.
Nonsurgical treatment21
Aseptic trochanteric bursitis19,20
In most cases trochanteric bursitis is treated without surgery. If the pain results from overuse, it is
recommended to reduce the activities and change the way of doing them.
Furthermore, an exercise program of stretching and strengthening with a physiotherapist will help
to bring back full range of motion in the hip, sometimes in combination with anti-inflammatory
medications or heat and ice applications to calm inflammation.
Improving strength and coordination in the buttock and hip muscles also enable the femur to move
in the socket smoothly and can help reduce friction on the bursa.
If the above treatment fails to reduce the symptoms, an injection of cortisone into the swollen bursa
may be required. This anti-inflammatory injection will reduce the symptoms for months, but it will
not cure the problem itself.
Septic trochanteric bursitis19,20

Infectious trochanteric bursitis does occur, but only in exceptional cases.
Further examination of the bursa fluid in the laboratory is necessary to assess which bacteria has
caused the infection. Once this is known, an (intravenous) antibiotic therapy can be prescribed.
Surgical treatment21
Only when the nonsurgical therapy fails, and when the pain is still unbearable, it is recommended to
consider surgery. The aim of surgery is to remove the thickened bursa and bone spurs that have
arisen on the greater trochanter. Also the large tendon of the gluteus maximus is treated. Some
doctors prefer to remove a part of the tendon that rubs against the greater trochanter while others
prefer to lengthen the tendon somewhat.
21 Level of Evidence: 3A
Physical Therapy Management 30, 31
There are several treatments that can be used to reduce pain and swelling on a patient with
trochanteric bursitis. When pain is the main complaint, we can relieve the pain for other underlying
disorders so as to treat them more effectively.
Physical therapy is given to improve flexibility, muscle strengthening and joint mechanics. When
these aspects are improved, pain will decrease. To heal trochanteric bursitis it is necessary to
proceed to infiltration of the bursa with antiphlogistic medication (Corticosteroid-injections). In
case of a persistent bursitis, surgery has to be considered as well. Other physical therapy
interventions are the use of ultrasound, moist heat and educating the patient on activity
modification and correcting possible training errors.
The pain of this injury can be reduced in different phases: The first phase is to manage the pain and
the inflammation. Pain being the main reason for treatment of the trochanteric bursitis, we can use
two common treatments to decrease the pain: the use of ice and non-steroidal anti-inflammatory
drugs (NSAIDs). The bursa inflammation can be treated with ice therapy and techniques or
exercises that reduce the inflammation structures. There are also other treatments that a
physiotherapist can use, e.g.: electrotherapy, acupuncture, taping techniques, soft tissue massage
and the temporary use of a mobility aid to off-load the affected side.
The second phase is to reinforce the patient’s strength and to restore the normal ROM. The
physiotherapist will also to improve the muscle length and resting tension, the proprioception,
balance and gait.
The next phase of rehabilitation is the restoration of all functions. Many patients catch TB due to
their common daily activities like running, walking, … . The goal of the physiotherapist is to provide
a specialized program for the patient to improve the movement and to reduce the pain, so that the
patient can perform his daily activities.
The final phase is to prevent a relapse. It may be as simple as training your abdomines or
performing some foot orthotics to address any biomechanical faults in the legs or feet. The therapist
will examine your hip stability and function by addressing any deficits in the core strength and
balance. Furthermore, he will also teach the patient some self-management techniques. The
ultimate goal is to see the patient safely returning to his former sporting or leisure activities!
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An iliotibial friction syndrome is most frequently seen in military personnel, cyclists, runners or
other athletes submitted to repetitive motion of the knee.[1][2] This repetitive motion is
responsible for excessive friction between the lateral epicondyle and the iliotibial tract. It is
considered as an overuse injury and is often concomitant with underlying weakness of hip abductor
muscles.[3] Pain appears in the region of the lateral femur epicondyle or a bit inferior to it.[1]
During a physical examination we see an important tenderness of the lateral aspect of the knee.
This tenderness is found superior to the joint line and inferior to the lateral femoral epicondyle.[1]
Iliotibial band friction syndrome (ITBFS) is the most common injury of the lateral knee in runners
and has an incidence between 1.6 and 12%.[1][4] It has even been reported that ITFBS is
responsible for 22% of all lower extremity injuries.[1]
The iliotibial tract has its origin on the lateral border of the iliac crest. It is composed of dense
fibrous connective tissue that appears from the m. tensor fasciae latae, the gluteal fascia and m.
gluteus maximus. It descends vertically at the lateral aspect of the thigh, between the layers of the
superficial fascia, and inserts on Gerdy’s tubercle and the lateral proximal aspect of the fibular head.
[5][3]Moreover the ilitibial tract becomes denser in its distal portion and gives an expansion to the
lateral border of the patella. In this distal portion, the iliotibial tract covers the lateral femoral
epicondyle, The iliotibial tract is stretched by m.gluteus maximus and m.tensor fasciae latae, both
inserting on the proximal part of the tract.[5]
When the knee is positioned in extension the iliotibial band lies anterior to the lateral femoral
epicondyle ; but when the knee is in 30° flexion the band will lie behind the lateral femoral
epicondyle. Friction at the level of the knee takes place at the instant near footstrike, mainly in the
foot contact phase at or slightly below 30° flexion. The exact location of the friction is, between the
posterior edge of the iliotibial band and the underlying lateral femoral epicondyle. Because of the
mobility of the knee, activities with many repetitive flexions and extensions of the knee can cause
the iliotibial band to rub the lateral femoral epicondyle. This can produce irritation and eventually
an inflammatory reaction of the iliotibial band.
Other proposed etiologies for IT band syndrome include compression of the fat and connective
tissue that is deep the the IT band, as well as chronic inflammation of the IT band bursa.[6]
In many instances the anamnesis will already provide an excellent basis for suspicion of this
syndrome. As mentioned above, repetitive activities involving knee flexion-extension are usually
reported, as is a burning pain at the level of (or just underneath) the lateral femoral epicondyle. The
diagnosis in patients with this syndrome is based on different symptoms.[7] Among the
characteristics, we find an exercise-related tenderness over the lateral femoral epycondyle.[7] The
patients experience, on regular basis, an acute, burning pain when pressure is applied on the
epycondyle with the knee in flexion and in extension.[2] Sign of inflammation due to the friction
between tract and the lateral epicondyle during extension and flexion of the knee can also be found.
[1][7] There is pain on the lateral aspect of the knee during running, increasing in intensity while
running down hill. Pain is also exacerbated when running a long distance.[8] This overuse condition
is often seen in runner, cyclists, and military recruits.[6]
Biceps femoris tendinopathy, degenerative joint disease, lateral collateral ligament sprain, lateral
meniscus repair, myofascial pain, patellofemoral stress syndrome, popliteal tendinopathy, referred
pain from lumbar spine, stress fractures, and superior tibiofibular joint sprain.[9]
There are different provocative tests:
Renne test
Noble’s test
Ober’s test
Outcome Measures
Lower Extremity Functional Scale (LEFS)
Examination
Force of hip abduction:
The force of hip abductors can be decreased. These muscles should thus be tested.[7]
Noble compression test:
This test starts in supine posture and a knee flexion of 90 degrees. As the patient extends the knee
the assessor applies pressure to the lateral femoral epicondyle. If this induces pain over the lateral
femoral epicondyle near 30 degrees of flexion, the test is considered positive.[2]
Ober test:
The patient is lying on his side with the injured extremity facing upwards. The knee is flexed at 90
degrees and the hip in abduction and extension, the thigh is maintained in line with the trunk. The
patient is invited to adduct the thigh as far as possible. The test is positive if the patient cannot
adduct farther than the examination table. A positive Ober test indicates a short / tense ilio-tibial
band or tensor fasciae latae, which is frequently related to the friction syndrome.[1][10] [11]
Both the Noble compression test and the Ober test can be use to examine a patient with a suspicion
of Iliotibial friction syndrome. The result will be more obvious when we combine the two into one
special test. For this, the position of the Ober test is adopted and compression is applied on the
lateral epicondyle during passive knee extension and flexion. Moving the knee can produce more
strain on the injured structures and can help to reproduce the symptoms of the patient if the
combination does not. Medial patellar glide can also increase the symptoms (by tending the patellar
expansion of the iliotibial band) and can reveal the precise localization while lateral glides reduces
them. An internal rotation of the tibia when the knee is moved from flexion to extension can also
produce the symptoms. A combination of the Nobel and Ober tests with an unloaded knee or in a
weight bearing position can also be done the reproduce the symptoms.[2]
Medical Management
http://guideline.gov/content.aspx?id=36632&search=band+syndrome+and+knee+disorders
The treatment of ITBFS is usually non-operative, but in some cases in which conservative treatment
and physical therapy remain uneffective, it might be necessary to apply surgery.
During surgery, a small piece of the posterior part of the iliotibial band that covers the lateral
femoral epicondyle will be resected.[12]
There are also a number of case series[1] reporting resolution of ITBFS from the surgical excision of
a bursa, cyst, or portion of a lateral synovial recess.
The accepted treatment of ITBFS follows the outline common to the treatment for many connective
tissue injuries, beginning with treatment of the acute inflammatory response using medication, rest,
ice, heat or alternative techniques, progressing through a physical therapy treatment phase and
finally surgical intervention, in case the common treatments would not be effective.
1. Treatment of the acute inflammatory response
Research has confirmed that oral nonsteroidal anti-inflammatory drugs (NSAIDs) and/or
corticosteroid injections in the bursae or trigger points can be used to reduce the acute
inflammatory response and pain. However, NSAIDs alone have not been found to be effective in
providing symptom relief. Yet, in conjunction with other nonsurgical modalities and modification of
activities, they can be beneficial in the short term for the therapy management.[6][12][13]
Other care in the acute phase should focus on activity limitation or modification, and measures to
relieve pain such as ice (cryotherapy) or heat.[1][12] Some authors[14][15] suggest complete rest
from athletic activities for at least 3 weeks; other authors[16][17] suggest that it is best to rest a
period from 1 week to 2 months, but this rest period depends on the severity of the condition and
the reproduction of pain during clinical examination. But it is not necessary to stop the athletic
activities in the initial stages (grades 1 and 2). It is sufficient to lower the intensity of the trainings,
especially the activities that cause pain such as running.
In the more advanced cases (grades 3 and 4) it is requested that the patient does not perform any
athletic activity in first 3 to 4 weeks. But it is suggested that the athlete performs other physical
training activities, such as e.g. swimming, so that they can keep their functional abilities and also
keep in shape.
If no improvement of symptoms occurs and inflammation persists, the following other treatment
techniques might be considered:
• ultrasound therapy[12], providing thermal or non-thermal treatment of the injured tissue at a

frequency range of 0.75 to 3 MHz (depending on the depth of the soft tissue to be treated)[18]
• muscle stimulation[12]
• iontophoresis or phonophoresis[12], techniques in which medication is administered into the

injured tissue through ion distribution driven by an electric field or passed through the skin using
ultrasound waves, respectively.
2. Physical therapy treatment
Once the acute inflammation and pain have subsided, physical therapy can be applied on the ITBFS
in the subacute phase. The physiotherapist will determine the best approach suited for each person
on an individual basis. The following consecutive phases in physical therapy are important:
• Exercises to stretch the iliotibial band and related structures.
The best exercises to start the physical treatment of ITBFS are passive or static stretching exercises.
[19] This will lengthen the iliotibial band and will reduce friction with the lateral epicondyl of the
femur. However, not only the iliotibial band needs stretching, but also the glutea. If the lateral gluteal
muscles are found to be weak or functioning improperly, this will result in other muscles - including
the iliotibial band - to have to compensate, which will cause contraction of the iliotibial band.[13]
Furthermore, if the glutea is too short, it will also provoke a rotation of the leg and this will again
create an abnormal stress on the iliotibial band, resulting in ITBFS.[20]
The following exercices will stretch and lengthen the iliotibial band, tensor fascia latae, the gluteus
medius and the related structures. Fredericson et al. compared the relative effectiveness of 3
common standing stretches for the iliotibial band. This study found that a particular stretch B –
with the athlete standing, placing the affected foot adducted and behind the other, and laterally
flexing away from the affected side with the arms stretched overhead – created the greatest
lengthening of the band.[21]
• Myofacial treatment.
A next step in the physical therapy is to address myofacial restrictions. Frequently, soft tissue
treatment through massage and triggerpoint therapy of the affected area by the physiotherapist
decreases the pain and definitively treats the condition. The use of a foam roller on the tight
muscles could also be beneficial.[13]
The patient can also perform exercises using a foam roller at home to create deep transversal
friction, self myofascial release (massage) and stretching of the muscles. A possible exercise is to lie
on the side with the foam roller positioned perpendicular to the bottom leg, just below the hipbone.
The upper leg should be positioned in front for balance. Using the hands for support, roll from the
top of the outer thigh down to just above the knee, straightening the front leg during the movement.
Pause over any spots where the tissue feels especially tight or knotted, and hold for at least 10
seconds. Reverse the motion, rolling from the knee back up to the hip.
• Exercises to strengthen the abductor muscles and stabilize the hip.
A next important phase in the physical treatment of the ITBFS is to perform exercises to strengthen
the muscles in the affected area. Since ITBFS is often associated with hip abductor weakness,
strengthening and stabilizing of the hip will be beneficial in the treatment of ITBFS.[4]
Some examples of useful exercises: Hip hikes to strengthen the gluteus medius help stabilize the
hip. Stand on the edge of a step with the majority of the body weight on the unaffected side. Lower
the hip of the involved hip and bring it back to neutral. Repeat the exercise: first 2 sets of 10 repeats,
lateron 3 sets of 15 repeats.[22] Another example is the side-lying hip abduction exercise with the
back against a wall and the leg held at approximately 30° of hip abduction with slight hip external
rotation and neutral hip extension. This exercise can be made more stenuous by placing a 1-metre-
long band between the ankles.[4]
• Hip/knee coördination and running/cycling style modification through the increase of

neuromuscular control of gait.[1][13]
Going to the next phase of physical therapy, the physiotherapists will give training and instructions
on multidimensional movement patterns, eccentric muscle contractions and integrated movement
patterns. The main goal is to work with combinations of running, jumping, agility and balance
exercises and that all with a clear emphasis on using the proper technique.
Cyclist are also at risk for ITBFS if they tencto pedal with their toes turned in, which can cause
abnormal stretching of the iliotibial band at the knee, so being aware of correct pedaling technique
may minimize the risk of developing symptoms.[13]
These sorts of exercises need a strictly defined position so that they can be performed correctly.
Follow the clear instructions and advice from a physiotherapist. The exercises should be performed
slowly until that the patient feels the sensation of stretching. But the prolonged stretching that may
causes pain, will decrease the possibility of longer maintenance of the stretching, it also increases
the possibility of the muscle contraction that is triggered by a reflex, and it may eventually cause
damage to these muscles.
On the other hand, keeping the stretching at the “initial” point will enable a complete relaxation of
these muscles and the maintenance of the position for a longer period of time. The patient should
keep the stretching at the point of the initial stretching for 15s , and then should he increase the
time gradually to a maximum of 25saintenance and prevention
When returning to regular activity, it is important to keep performing maintenance and prevention
exercises, in order to prevent reoccurrence of the ITBFS.
The first way of preventing reoccurrence is by stretching of the iliotibial band and related structures
on a regular basis. Performing the same exercises as described in the section 'Physical therapy
treatment' can be useful to prevent shortening of the iliotibial band after starting to sport again, e.g.
the various kinds of standing stretches.
The second way to prevent ITBFS from reoccurring is to continuously strengthen the abductor
muscles of the lower extremities, since patients with ITBFS were often noted to have weakened
abductors of the affected leg compared to the other leg, or in comparison with a control group who
did not suffer from ITBFS.[1][13][23][24] The focus should be mainly on the M. tensor fascia latae
and the glutea.[23][24][20][4] This strengthening of abductors and glutea can be achieved in
various ways. Some exercises are already described in the section 'Physical therapy treatment'. This
can be expanded with the following exercises: one leg squat, steps-up, frontal plane lunges and side
lunges.[13][25]
It is also important to slowly build up the training intensity in order to prevent reoccurrence of
ITBFS.[23] Avoid training factors such as a rapid increase in weekly mileage and excessive running
in the same direction on a track.[13]
Using the right material is crucial in the prevention of ITBFS.
For runners it is important to use the correct running shoes.[26] In case of doubt, seek specialist
advice. Running shoes should also be replaced regularly. Worn shoes absorb less shock which may
lead to an increased incidence of iliotibial band pain. In case of daily running, it could also be
considered alternating between two pairs of shoes to allow 24 hours for the shoe's shock absorbing
cushion to return to its optimal form before running in them again.
Cyclists should make sure to use bicycles of proper fit. It is also suggested to lower the seat beyond
the typical height, as this will reduce the stretching of the gluteus maximus and iliotibial band and
thus allowing for less knee extension and stress on the iliotibial band. Adjustment of the cleat
position could also be beneficial.[13]
The use of orthotics could be considered, especially when runners experience unwarranted
calcaneal eversion and tibia internal rotation or in case of an anatomical leg length deficiency. For
cyclists, orthotics could be useful to prevent excessive tibial rotation and foot hyperpronation.[13]
Furthermore, also the surface on which athletes exercise plays an important role in the prevention
of ITBFS. The probability to develop ITBFS will increase when repeatedly running downhill. This
will result in the iliotibial band coming in the impingment zone because it will increase friction
between the iliotibial band and the lateral femoral epicondyle due to decreased knee flexion at foot
strike.[13][23] Also banked surfaces should be avoided.[12]
Athletes should perform selfmonitoring. Runners and cyclists should monitor themselves for
reoccurence of symptoms during training. While doing so, they can gradually increase distance and
frequency if no adverse symptoms occur.[13]
Finally, athletes should be educated about ITBFS in order to increase awareness of the syndrome, so
that they can recognize possible symptoms in a very early stage and improve their sporting
experiences.
avascular necrosis
Mechanism of injury / pathological process
Avascular necrosis of the femoral head, also known as osteonecrosis, although this term isn’t used
that much anymore, is characterized by variable areas of dead trabecular bone and bone marrow,
extending to and including the subchondral plate. Most of the time it is the anterolateral region of
the femoral head that is affected but no area is necessarily spared. This disease is often seen in
patients in the third, fourth and fifth decade. The older the patients, the less the chance of
revascularization. We can also state that most radiographically evident lesions progress until the
femoral head collapses [1].
The earliest sign of this mechanical failure is the crescent sign, which represents separation of the
subchondral plate from the underlying necrotic concellous bone. After the femoral head has
collapsed, most patients have clinical progression resulting in the need for a total hip replacement
[1].
The pathophysiology of avascular necrosis of the femoral head has not been completely accounted
for. In some patients there has clearly been a direct cause (trauma, radiation,..), while in others the
pathophysiology is still uncertain. Avascular necrosis of the femoral head has often been described
as a multfactorial disease. It is associated in some cases with a genetic predilection as well as an
exposure to certain risk factors. The most common risk factors are: corticosteroid intake, alcohol
use, smoking and various chronic diseases [2]. Patients with human immunodeficiency virus are
also at higher risk for the development of avascular necrosis of the femoral head[2]. It has to be
noted too, that osteonecrosis is a (rare) complication of pregnancy[2]. Many of these cases are
initially misdiagnosed as transient osteoporosis of the hip.
Diagnostic procedures
It is very important that avascular necrosis is diagnosed early in the disease process since the
success of the treatment is related to the stage at which the treatment starts.
There are several possible diagnostic modalities:

History and Physical Examination
Patients are often seen because of pain in the groin, but symptoms can also radiate to the knee or
buttocks. On examination, there is usually a painful range on motion, especially on forced internal
rotation[1]. It is also important to track any risk factors before the start of the examination.
Investigators need to be wary of avascular necrosis in any patient who has pain in the hip, negative
radiographic findings and any of the risk factors, described above. The other hip must also be
evaluated.
Radiographic Evaluation
When standard anteroposterior and frog-leg lateral radiographs show obvious avascular necrosis of
the femoral head, it is not necessary to perform an MRI.
Magnetic Resonance Imaging
This is the best method for cases that are radiographically occult or not obvious on radiographs. It
has been found to be 99%sensitive and 98% specific for this disease[2].
Management / interventions
1. Non-operative Treatment
a. Observation or Protected Weight-Bearing
This method is believed to slow the progression of avascular necrosis so that the femoral head
wouldn’t collapse. However more than 80% of affected hips do progress to femoral head collapse
and arthritis by four years after the diagnosis[2]. There are various methods to reduce weight-
bearing. The concept of this method is to reduce the forces on the hip joint. This (interventional)
treatment has various modalities, such as a cane, crutch, walker or two crutches.
Most studies have shown though that non-operative treatment yields poor results. The only
condition for which protected weight-bearing might be effective is a type-A lesion[1].
b. Pharmacological Treatment
c. Electrical stimulation
Electrical stimulation has been shown experimentally to enhance osteogenesis and

neovascularization as well as to alter osseus turnover.[1]
Three different methods can be described:
Non-invasive pulsed electromagnetic-field stimulation
Direct-current stimulation of the necrotic area through insertion of an electrode at the time of a
core decompression
Non-invasive direct-current stimulation by capacitive coupling after a core decompression
Electrical stimulation remains experimental for the treatment of avascular necrosis of the femoral
head. Additional study is needed to define the optimum dosage, application, and timing of
treatment. [1]
2. Operative Treatment
There are several possible ways to treat avascular necrosis of the hip: core decompression, Core
decompression with electrical stimulation, Osteotomy, Non-vascularized bone-grafting and
Vascularized grafts.
Recommendations for treatment

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Hip conditions

Image 1. Diagram of pelvis and sacrum with bony landmarks identified

A1: avulsion fractures

A3: transverse sacral or coccyx fractures

B1: open-book injuries

B3: bilateral type B injuries

C1: unilateral injury

C3: bilateral injury in which both sides are type C injuries

Physical Therapy Management

Clinically Relevant Anatomy

So a hip luxation will less likely take place. [2]

 stabilize the femoral head in the acetabulum

 accelerate the standing position

 strong hip extensors

 provide postural stability while walking or standing

 most powerful hip flexors

Etiology: Risk factors for hip fractures[6][9]:

Medical problems: Endocrine disorders can cause fragility of the bones

Trauma or laesion in the femur ( around 10% )

Fall ( Most of the hip fractures are caused by falls)

Hip fractures without injuries ( < 5% )

Causes of Acute fracture:

After extreme muscle contraction-> avulsion fracture

After extreme sports -> stress fracture due

Osteoporosis or hip osteoarthritis often cause complaints in older people.

Causes of Stress fracture:

As a result of fatigue fracture:

As a result of fatigue fracture of the bone because of repeated stress

Athletes have an increased vulnerability due to high training load

In endurance runners/ athletes the pelvic region is frequently

By decrease in bone density.

Specific features for patients with hip fracture include:[10][11]

A swelling might occur

Intertrochanteric Fractures, subcapital fractures, subtrochanteric fractures, cervical fractures, fracture of

Intra capsular = femoral neck / cervical

Extra capsular = intertrochanteric / pertrochanteric / subtrochanteric

Signs and symptoms of a hip fracture include:

Inability to move immediately after a fall [4]

Severe pain in your hip or groin [4]

Shorter leg on the side of your injured hip [4]

Berger et al demonstrated that radiographs had a sensitivity of 15-35% on initial examination of

Subcapital neck fracture: right below the femoral head

Femoral neck fracture (intracapsular fracture)[20] (level of evidence B)

Subtrochanteric fracture: 2 ½ inch below the small trochanter (extracapsular fracture)[11]

Fracture of the small trochanter

Extracapsular fracture (femur fracture and implant failure)

Mean pain scores over the first 5 hospital days;

Major postoperative complications;

mortality through 6 months;

Radiographic evaluation: standard trauma radiographics withstand an anteroposterior view of the

Anteroposterior radiograph of the pelvis:

L5 transverse process fractures

Obturator and iliac oblique views:

• May be used for (suspected) acetabular fractures

• Magnetic resonance imaging

One stable undisplaced subcapital fracture was treated conservatively. (2)

The recommended treatment of pelvic fractures depends from institution to institution:

General treatment options:

Postoperative plan for immobilization: