Avascular Necrosis of the Femoral Head
AVN of the femoral head is a result of impaired blood supply, a common complication of many disorders of the hip from infancy to adulthood. In the United States, 10,000 to 20,000 new cases present annually.35 AVN occurs most often in men between 40 and 50 years of age and is bilateral in 40% to 80% of patients.36 The chief blood supply to the head comes from branches of the medial and lateral circumflex arteries that enter the capsule distally and pass along the posterior surface of the head. The infarction of the femoral head may be total or incomplete. If incomplete, it is limited to one segment of the femoral head, and the radiographic appearance will be spotty.37
Any condition that disrupts the blood supply to the femoral head can cause this disorder (Table 18–1). Trauma to the major blood vessels is the most common cause. Femoral neck fractures that disrupt the retinacular vessels causes AVN. The incidence of AVN after femoral neck fractures is 20% to 30%. AVN is more likely to develop with proximal fractures and those fractures that are improperly reduced, thus permitting greater shearing stresses to occur at the fracture site.
TABLE 18–1Conditions Associated with Avascular Necrosis of the Femoral Head ||Download (.pdf) TABLE 18–1 Conditions Associated with Avascular Necrosis of the Femoral Head
Femoral neck fracture
AVN is also commonly seen after hip dislocation at a rate of up to 40%.38 The pathogenesis is thought to be an ischemic insult to the head while it remains dislocated. Reduction results in reperfusion, stressing the importance of early detection and treatment of this condition. In the setting of dislocation, AVN usually becomes clinically apparent within 2 years.38
Atraumatic conditions associated with AVN are numerous. Steroid use and alcohol ingestion are associated in as many as 90% of atraumatic cases.35 Corticosteroid-induced AVN may be either from exogenous administration (common) or Cushing disease (rare).39 AVN can complicate sickle cell disease due to the impaired circulation of the small vessels that supply the femoral head.36,40 Collagen vascular disorders, such as systemic lupus erythematosus and small vessel vasculitis, may also precipitate AVN of the femoral head.41 Other associated conditions include Caisson disease, Gaucher disease, and renal osteodystrophy.35,42,43 In 10% to 20% of cases, despite thorough investigation, the cause remains idiopathic.35
The articular cartilage covering the necrotic head survives usually because it derives its nutrition from the synovial fluid. If subcondylar bone cortex collapses, the cartilage then undergoes degeneration. The added stress of weight bearing, before bony replacement is complete, can cause collapse and severe degenerative changes.
AVN can be clinically silent, but the most common complaint is pain.35,44 The pain is localized to the groin area, but may be felt in the buttock or refer to the knee. The onset may be insidious or sudden. On examination, the patient will walk with a limp. Joint motion is decreased and painful. Passive internal rotation will be severely limited. Abduction will also be limited.
The clinical picture will vary, however, depending on the underlying cause and the patient’s age. The onset of symptoms does not correlate well with the appearance on radiographs. It is not the death of bone cells that causes hip pain, but rather the collapse and fracture of subchondral bone that heralds the onset of clinical symptoms.45
In a child, spasm around the hip appears to be an early sign. A limp or a slight spasm of the hip is often the first clinical manifestation of this disorder. It is followed by pain that is present on weight bearing and often referred to the thigh or knee. A high index of suspicion is needed in the absence of radiographic findings.46
Radiographs should include AP and “frog-leg” (flexed and externally rotated) lateral views. Multiple systems have been developed for the radiographic classification of AVN of the femoral head. The most widely used is the Arlet–Ficat staging system that organizes the radiographic appearance into four stages (Fig. 18–18).35
Avascular necrosis (AVN). A. Schematic representation demonstrating subchondral bone collapse, the crescent sign (arrows). B. Radiograph demonstrating subchondral sclerosis with bone collapse (Stage III). C. Further joint space narrowing and collapse of the head, heralding stage IV AVN.
|Stage ||Radiographic Appearance |
|I ||Normal plain radiographs |
|II ||Density change in femoral head, subchondral |
sclerosis and cysts
|III ||Crescent sign |
|IV ||Joint space narrowing, osteophyte formation, |
The crescent sign is a curvilinear radiolucent subchondral line along the anterolateral aspect of the proximal femoral head. It is most commonly present on the frog-leg lateral view, but may be detected on CT scan.47
Early diagnosis of stage I disease can only be established by MRI or bone scan.19,48,49 Bone scan may show an area of low-uptake representative of the necrotic bone surrounded by an area of increased uptake that corresponds to rapid bone turnover. MRI is highly sensitive for the diagnosis (88%–100% sensitive) and is considered the imaging study of choice for early detection.35
The emergency physician should keep the patient from bearing weight as pressure may cause the necrotic head to collapse.
The definitive treatment for this condition depends on which stage the AVN has reached. In stage I and early stage II, core decompression is the recommended procedure.35,44 This involves removing an 8- to 10-mm core of bone from the anterolateral segment of the femoral head through a lateral trochanteric approach. This procedure is highly effective in relieving pain, prevents further changes in the femoral head, and delays the need for total hip arthroplasty.
In the later stages, when collapse and deformation of the femoral head have occurred, reconstruction is necessary. Stage III and IV disease requires a total hip arthroplasty.35,50 In young patients, some authors have placed a vascularized fibular graft in the subchondral region of the femoral head that delays the need for hip replacement.51,52
Septic arthritis of the hip occurs within the native joint or following hip arthroplasty. When the native joint is affected, 70% of cases occur in patients 4 years of age or younger.53 The younger the child affected by septic arthritis of the hip, the worse the prognosis.
In children, the infection usually reaches the hip joint from a focus of osteomyelitis within the joint capsule. The osteomyelitis is usually of hematogenous origin and arises in the metaphysis by way of nutrient vessels. From there it may spread outward and develop as a subperiosteal abscess. The articular cartilage is damaged by the increased intra-articular pressures resulting from the pus produced by the infection. It can withstand these forces for approximately 4 to 5 days before destructive changes occur.54
Infection of the native joint is rare in adult patients. In one study of 4 hospitals, only 10 cases occurred over a 10-year period.55 The majority of cases occur in immunocompromised patients, in an already diseased hip, following instrumentation, or from contiguous spread of infection.56–62 Nonetheless, native joint septic hip arthritis can occur in the absence of these risk factors.63 In adult patients who undergo total hip arthroplasty, however, the risk of infection is approximately 1%.64 The increasing number of elderly patients undergoing this procedure since its introduction in the early 1960s makes it likely that the emergency physician will encounter such a patient.
Staphylococcus aureus (S. aureus) is the most prevalent organism in septic arthritis of the native hip.65 Methicillin-resistant S. aureus (MRSA) is common.66 Adult cases involving prosthetic replacement are caused by gram-positive bacteria in 75% of cases, with the most common bacterium being Staphylococcus epidermidis (30%) and S. aureus (20%). Of gram-negative organisms, Pseudomonas aeruginosa is the most common pathogen. Anaerobes, fungi, and mycobacterium may also be involved.64
Characteristically, the patient presents to the emergency department (ED) with a fever and severe pain in the affected hip. The onset of symptoms is usually acute, although in patients with underlying rheumatoid arthritis, the onset can be insidious, frequently without fever. In these patients, the diagnosis may be difficult and the patients may be thought to have an arthritic flare rather than septic arthritis.67
On examination, the patient has tenderness anteriorly in the groin and over the hip joint accompanied by grossly restricted motion in all directions and muscle spasm. The patient walks with a limp or does not walk at all. These patients usually do not want any pressure placed on the lower extremity and avoid any movement due to severe pain.
In children with a native joint, the diagnosis can be made if any four of the following five are noted: (1) temperature >38.3°C; (2) pain localized to the hip that is worse with gentle passive motion; (3) swelling of the involved joint; (4) systemic symptoms of lethargy, irritability, or toxicity with no other demonstrable pathologic process; or (5) if a satisfactory response is noted to antibiotic therapy. The hip may be held in the flexed, externally rotated, and abducted position.53 Unlike transient synovitis in which the patient generally appears well with a mild febrile illness, patients with septic arthritis appear toxic. See Chapter 6 for a further discussion of septic arthritis of the hip in children and how it is differentiated from transient synovitis.
Patients who present after total hip arthroplasty will present in one of three stages, depending on the amount of time that has elapsed since their procedure.64 In stage I infection, purulent drainage is present at the wound site in the days following the procedure. Stage II infections are indolent and present 6 months to 2 years postoperatively. Finally, patients who present later than 2 years after replacement are considered to have stage III infections, which are thought to be due to infection from a hematogenous source.
If septic arthritis is suspected, a complete blood count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) are recommended. The ESR and CRP are sensitive, but lack specificity. The ESR is elevated in almost all patients with septic arthritis.65
Plain radiographs are usually normal initially. Abnormal subluxation of the hip with widening of the joint space is most common. Osteomyelitis of the proximal femur is noted in some.
An ultrasound that demonstrates fluid in the joint suggests septic arthritis. With the patient supine, the knee is slightly flexed and the hip is held in slight internal rotation. The probe is placed below the inguinal ligament and lateral to the neurovascular bundle. It is angled superomedially toward the umbilicus. The acetabulum, femoral head, and femoral neck are easily visualized approximately 3 to 5 cm below the skin. Synovial fluid cannot readily be seen in the normal hip, but if an effusion is present, a hypoechoic area appears, most prominently just anterior to the femoral neck. A comparison view of the other hip may be useful. In some settings, ultrasound-guided arthrocentesis may be accomplished in the ED.68 In other cases, the procedure may be performed by a radiologist or orthopedic surgeon. Using sterile technique, an 18-gauge spinal needle is introduced in the long axis of the ultrasound probe from the inferior position.
In septic hip arthritis, the synovial white blood cell (WBC) count averages 57,000/mL; however, it can be as low as 10,000/mL or as high as 250,000/mL.69,70 Blood cultures are positive in >50% of the cases.53,54
CT scan may also demonstrate an effusion. MRI has demonstrated little usefulness in making this diagnosis and may be difficult to obtain from the ED.71 However, a gadolinium-enhanced MRI shows a decreased perfusion of the femoral epiphysis and may be useful in making the diagnosis in difficult cases.72,73
In adults with a prosthetic replacement, an indium-labeled autologous WBC study is recommended in patients with stage I and II infections.64 A positive result will be followed by aspiration and arthrography. Radiographs of a patient with stage II disease will reveal a radiolucent line at the bone–cement interface indicative of a loosening prosthesis.
Perhaps the most important point for the emergency physician to be aware of is that a delay in diagnosis and treatment is the most important factor affecting the prognosis. The initiation of treatment beyond 3 weeks has been shown to predict the need for hip replacement in adult patients.74
In native joint infection, the goals of treatment are to clean the joint to avoid articular cartilage destruction and adhesion formation, as well as to decompress the joint to avoid vascular embarrassment of the epiphysis.75 Antibiotic coverage should be broad-spectrum until Gram stain and culture results are available.
Definitive therapy includes arthrotomy and early irrigation. More recently, several authors have recommended arthroscopic drainage of the joint.76–78 Although arthrotomy is considered the standard of care, it may be complicated by AVN or postoperative hip instability. Thus, three-dimensional arthroscopic surgery with large volumes of irrigation fluid is effective and less invasive.78 Successful treatment requires early and good surgical drainage.79
Patients with infected prosthetic hips generally require removal of all the prosthetic components, surgical debridement, and intravenous antibiotics.64 A one-stage surgical approach in which the hip is reconstructed and antibiotic-infused polymethylmethacrylate beads are implanted locally has been successful in eradicating the infection.
Degenerative Joint Disease
This condition is discussed because it is so commonly encountered. For further information on osteoarthritis, the reader is referred to Chapter 3.
Degenerative arthritis or osteoarthritis of the hip takes place with advancing age. Among Whites, where osteoarthritis is most common, the prevalence is 3% to 6%.80 In Asian, Black, and East Indian populations, the prevalence is low.81 It is accelerated by any incongruity of the articular surface causing abnormal friction. A secondary form occurs after conditions such as AVN, trauma, joint infection, slipped capital femoral epiphysis, congenital hip disease, and rheumatoid arthritis. The primary form is most common, however, and there appears to be a genetic predisposition. Other contributory factors include obesity and occupations that require high physical demands.80,82–84
The patient usually complains of an insidious onset of stiffness about the hip. At first, there are repeated attacks of slight pain lasting only a day or two. The pain is exacerbated by prolonged periods of weight bearing. There is often a protective limp due to muscle spasm accompanied by pain and a sense of stiffness that progressively worsens. The pain may be anterior, lateral, or posterior, depending on the site of inflammation. Referral is typically to the anterior and medial aspects of the thigh and the inner aspect of the knee. Characteristically, the pain is worsened with prolonged weight bearing and movement, particularly with abduction, internal rotation, and extension. Patients often complain of worsening pain in cold weather and relief with heat and salicylates.
During an acute exacerbation of osteoarthritis of the hip, there is tenderness over the site of capsular inflammation accompanied by muscle spasm, primarily involving the adductors. The Fabere test (Flexed, Abducted, Externally Rotated) is usually positive. This test is performed by having the patient place the heel of the affected extremity on the dorsum of the normal foot. The patient then “slides” the heel up the leg until the knee is reached. If pain is elicited, the test is considered positive. This test is not specific for acute exacerbations of degenerative hip disease, but it will be positive in any inflammatory process involving the hip.
In the early stages of this disorder, plain radiographs will be negative. Later, however, one will note an irregular subchondral sclerosis that gradually evolves into joint space narrowing. Additional findings include flattening of the head of the femur at the superior pole, accompanied by cystic changes in this area (Fig. 18–19).
Severe degenerative joint disease of the left hip marked by obliteration of the joint space, periarticular sclerotic and cystic changes, and acetabular osteophyte formation.
Conservative treatment is indicated for acute exacerbations that present to the ED. This includes abstinence from weight bearing, heat, and massage. Nonsteroidal anti-inflammatory medications are an important adjunct in relieving the inflammatory process.
There is no clear consensus regarding the decision to undergo total hip arthroplasty. Many variables are considered, including age, pain severity, functional limitations, bone quality, and surgical risk.85,86 A survey of orthopedic surgeons found that most surgeons required at least severe daily pain, rest pain several days per week, and destruction of most of the joint space on radiographs before considering surgery.85 In patients with significant functional limitations, the procedure not only improves quality of life, but is cost-effective over long-term–assisted living.87
Many bursae surround the hip, but only four are clinically important: the deep trochanteric, superficial trochanteric, iliopsoas (iliopectineal), and the ischiogluteal bursa (Fig. 18–20).
The deep trochanteric bursa is located between the tendinous insertion of the gluteus maximus muscle and the posterolateral prominence of the greater trochanter.88,89 The superficial trochanteric bursa is located between the greater trochanter and the skin. The iliopsoas bursa is the largest of all the hip bursae.90 It lies between the iliopsoas muscle anteriorly and the iliopectineal eminence posteriorly along the anterior surface of the hip joint capsule. The ischiogluteal bursa is superficial to the tuberosity of the ischium. The obturator internus bursa has recently been described as a cause of bursitis in some patients.91
The usual causes of bursitis include reactive inflammation secondary to overuse or excessive pressure and trauma. Other causes of bursitis are infectious and metabolic conditions, such as gout.
Deep trochanteric bursitis characteristically presents with pain and tenderness localized to the posterior aspect of the greater trochanter, which is increased by flexion of the hip and internal rotation. Abduction and external rotation of the hip relaxes the gluteus maximus and relieves the pressure on the bursa. Trendelenburg sign is present in three-fourths of patients.92 This sign is elicited when the patient is asked to stand on the affected leg and the pelvis drops to the unaffected side; indicating inhibition of the gluteus muscles. The pain may radiate down the back of the thigh and any motion may cause discomfort.
Deep trochanteric bursitis is associated with repetitive microtrauma caused by active use of the muscles inserting on the greater trochanter. It is most common between the fourth and sixth decades of life.93 Degenerative diseases have been associated with this condition, as well as inflammatory arthritis of the hip, obesity, and iliotibial band syndrome.
Calcification around the greater trochanter is evident in many patients with trochanteric bursitis, suggesting concomitant pathology of the gluteus medius muscle (tears) and tendons (tendonitis). Pathologic involvement of several soft-tissue structures has caused some authors to refer to this condition as greater trochanteric pain syndrome.92
Superficial trochanteric bursitis presents with tenderness and swelling over the inflamed bursa with accentuation on extreme adduction of the thigh.
Iliopsoas bursitis presents with pain and tenderness over the lateral aspect of the femoral triangle (area bound by the inguinal ligament, sartorius, and adductor longus) (Fig. 18–21). Irritation of the adjacent femoral nerve causes pain to be referred along the anterior thigh. This condition is common in sports such as soccer, ballet, or hurling that require extensive use of the hip flexors.94 The patient usually holds the hip in a position of flexion and abduction with external rotation. Pain is increased by extension, adduction, or internal rotation of the hip. This condition must be differentiated from a femoral hernia, psoas abscess, synovitis, or infection of the joint.
Area for palpating the iliopsoas muscle and bursa.
Ischiogluteal bursitis is common in patients with occupations requiring prolonged sitting on hard surfaces. Tenderness is elicited over the ischial tuberosity. Pain radiates down the back of the thigh and along the course of the hamstrings, mimicking a herniated disk.
The treatment of bursitis is bed rest, heat application, and anti-inflammatory agents. In ischiogluteal bursitis, a cushion or pillow helps relieve the discomfort and prevents recurrence. Sixty percent of the patients with greater trochanteric bursitis treated by injection demonstrated total relief of symptoms from a single injection at 6 months.93 A rare complication of steroid injection is femoral head necrosis, which has been described due to injection into the joint rather than the bursa.95 In the event that symptoms are refractory, arthroscopic bursectomy has been successfully employed.96
Septic bursitis in one of the bursae about the hip is rare. However, if suspected, this presents a true emergency and must be diagnosed early by the emergency physician. Parenteral antibiotics are indicated. Patients who fail to respond to intravenous antibiotics and percutaneous aspiration of the bursa may require surgical drainage or bursectomy.97
This condition is comparable to calcific tendinopathy in the shoulder. Amorphous calcium deposits in the tendons of the gluteus medius, lateral to the greater trochanter and superior to the capsule.98 It is associated with deep trochanteric bursitis, as previously described, and is frequently referred to as greater trochanteric pain syndrome. Long-distance runners develop tendonitis secondary to the insertion of the iliopsoas tendon on the lesser trochanter.99
The patient usually presents with severe pain in the hip. The hip is held in a position of flexion, abduction, and external rotation to relax the involved gluteus medius muscle. Muscle spasm limits motion in all directions. The examiner elicits tenderness over the site of inflammation. If the patient is able to ambulate, a Trendelenburg gait will be noted, in which the pelvis drops to the unaffected side when the patient steps onto the leg of the affected side.
The radiograph will often reveal a cloudy opacity in the soft tissues overlying the hip joint.
Heat application, rest, and anti-inflammatory agents are usually effective. The calcium depositions are more readily absorbed when broken up by a needling of the involved tendons under local anesthesia.100 Endoscopic treatment of this condition is also being used.101
Coxa saltans or snapping hip syndrome is now regarded as a common cause of hip pain in runners and is typically caused by sudden maneuvers in the course of running.102 Pain is present in less than one-third of patients.94 The condition affects young athletes and is slightly more common in women. Snapping hip syndrome is especially common in ballet dancers.103 This syndrome should be differentiated from a painless, deep “pop” that occurs with normal hip motion and holds no clinical importance. The pain is characterized by a sharp and burning discomfort exacerbated by activity.102
There are several causes of snapping hip syndrome. They are classified as external or internal based on their etiology.
External coxa saltans occurs when the iliotibial band or the gluteus maximus tendon snaps over the greater trochanter (Fig. 18–22).102 This is the most common cause of snapping hip syndrome. Affected patients state that they feel a snapping sensation over the lateral aspect of their hip.104 Snapping of the tendon over the greater trochanter is frequently demonstrated while walking or upon hip flexion. Passive internal and external rotation of the abducted limb usually demonstrates the snapping.105 Pain, if present, is mild unless a bursitis of the greater trochanteric bursa develops. External snapping hip caused by the iliotibial band is common in ballet dancers and is also a complication of total hip replacement.
In the snapping hip syndrome, the iliotibial band courses over the greater trochanter.
An internal cause of snapping hip syndrome is less common, but can occur when the iliopsoas tendon snaps over the pelvic brim as it proceeds to its insertion on the lesser tuberosity (Fig. 18–23). Another proposed mechanism is a sudden “flipping” of the iliopsoas tendon over the iliac muscle.106
Internal snapping hip syndrome occurs when the iliopsoas tendon snaps over the iliopectineal eminence of the pelvic brim as it proceeds to its insertion on the lesser tuberosity.
Patients complain of snapping during extension of the flexed hip. It is decreased by internal and increased by external rotation of the hip. Tenderness and pain occur at the anterosuperior spine and medial to the sartorius muscle.
Snapping hip syndrome can also be caused by injuries to intra-articular structures that obstruct the motion of the iliopsoas tendon. Injury to the acetabular labrum, a cartilaginous structure that encircles the acetabulum, or a loose body from an osteochondral injury are two examples. The painful pop or snap is most often anterior but may be posterior and is often accompanied by a sudden weakness of the leg.
Plain films of the hip are usually normal in cases of external coxa saltans. Ultrasound has been used to establish the diagnosis, but clinical findings are usually sufficient.107 If internal causes are suspected, plain radiographs will establish a diagnosis in one-third of patients. If the diagnosis remains unresolved, ultrasound and CT will establish the cause in approximately 90% of patients. MRI is 100% sensitive.108 MRI demonstrates thickening of the iliotibial band or thickening of the anterior edge of the fascia around the gluteus maximus muscle.107,109–111
Most patients with snapping hip are treated conservatively. The main principle of management is stretching exercises to promote the lengthening of the iliotibial band.112 Steroid injection is beneficial for eliminating external coxa saltans. If this condition becomes resistant to conservative treatment, surgical lengthening of the band can be performed.113,114 This procedure, called a “Z-plasty,” has been reported to be highly successful, but is rarely necessary.94,115 Z-plasty lengthens the tight iliotibial tract and also brings the thickened band anteriorly so that it no longer flicks over the greater trochanter during hip flexion.105 Endoscopic release of the iliotibial band has also been successful in treating this syndrome.116,117 Surgery is also indicated for loose bodies.94 Labral tears are treated with conservative management (nonweight-bearing) or arthroscopic debridement.
Hip dislocations constitute 5% of all traumatic joint dislocations and may occur in an anterior or posterior direction.118,119 Posterior dislocations are more common, accounting for 90% to 95% of all hip dislocations.1,38,120 Inferior dislocations (luxatio erecta of the hip) have also been reported, but are extremely rare.121
Posterior Hip Dislocation
The classification of posterior hip dislocations is based on the system developed by Stewart and Milford.122 In this classification, posterior hip dislocations are graded on the basis of the presence and type of associated fractures.
|Grade I ||A simple dislocation, without fracture (Fig. 18–24) |
|Grade II ||Dislocation associated with a large |
acetabular rim fracture that is stabilized
|Grade III ||Dislocation associated with an unstable or |
|Grade IV ||Dislocation associated with a femoral head |
and neck fracture
Posterior dislocation of the hip.
Posterior dislocations occur after a blow to the knee while the hip and knee are flexed. In over 50% of patients, this injury occurs following a high-energy trauma such as automobile accidents where the knee of an unrestrained driver strikes the dashboard (Fig. 18–25).38,118,119 Fortunately, with the increased use of lap belts, the frequency of these injuries is decreasing. Other high-energy mechanisms include motorcycle collisions, pedestrians struck by automobiles, and sporting events such as downhill skiing.123
Low-energy dislocations are common in children and adults with prosthetic hips. Children younger than 6 years old are especially prone to dislocation after minimal trauma due to general laxity of the surrounding ligamentous structures and the largely cartilaginous acetabulum.124 Spontaneous dislocations occur in up to 10% of patients after total hip replacement.125
Posterior dislocations present with limb shortening, hip adduction, and internal rotation of the involved extremity (Fig. 18–26). The femoral head may be palpable within the muscle of the buttock. The patient should be carefully evaluated for sciatic nerve injury that may manifest as sensory and motor deficits.126 Distal pulses must also be assessed; however, vascular injury is uncommon following a posterior hip dislocation.
Clinical picture of a posterior dislocation of the hip.
A single routine AP view of the pelvis is usually adequate in demonstrating these injuries (Figs. 18–27 and 18–28).38 The femoral head is no longer congruent with the roof of the acetabulum. On a true AP film, the femoral head will appear smaller than the contralateral side due to its posterior displacement. Shenton’s line should be evaluated whenever a hip injury is suspected (Fig. 18–3). Additional radiographs of the ipsilateral extremity may be indicated on the basis of the physical examination.
Posterior dislocation of the right hip.
Posterior dislocation of a prosthetic hip.
Although the dislocation is usually obvious, the radiograph must also be closely inspected for associated fractures. Associated fractures of the femoral head, neck, and acetabulum are frequently present after these dislocations. An attempt at closed reduction of a posterior hip dislocation with an associated subtle femoral neck fracture is contraindicated, as it may displace the fracture and increase the likelihood of AVN of the femoral head.
A CT scan of the hip with thin, 2-mm cuts should be obtained in several situations.1,38
Before reduction, if there is suspicion of a femoral neck fracture on plain films. Closed reduction, when a femoral neck fracture is present, will increase the risk of AVN.
After unsuccessful attempts at reduction, to evaluate for the presence of loose bodies within the joint.
Following reduction, to evaluate the acetabulum.
Hip dislocations of a native hip joint may be associated with other significant injuries. In one study, 95% of patients had an associated injury (head, abdomen, chest) severe enough to require hospital admission.127
Acetabular fractures. In adults, these fractures are seen in 75% of patients.124
AVN of the femoral head. This injury is seen in approximately 10% of uncomplicated dislocations.120 The incidence is 4.8% if the hip is reduced in <6 hours, but increases to 50% if reduced after 6 hours.128 Hip dislocations with Stewart and Milford classification grades III and IV were more likely to undergo AVN compared to grades I and II.128 All hip dislocations must be regarded as true emergencies and reduced promptly in order to minimize the incidence of AVN of the femoral head.129
Femoral head fractures. These fractures occur in up to 16% of posterior hip dislocations.16 Osteochondral fractures due to impaction of the femoral head can cause locking of the dislocated joint.130
Femoral shaft fractures. These fractures occur in 4% of patients with hip dislocation.122 Rotation of the shaft after fracture may alter the position of the extremity and confuse the diagnosis.38
Sciatic nerve injury. A deficit of the sciatic nerve is present in 10% to 13% of posterior hip dislocations.1,122
Ipsilateral knee injuries. Knee injuries were present in up to 25% of patients in one series.122 These injuries vary from ligamentous damage, to fractures of the patella, or femoral/tibial condyles.
Arterial injuries (rare).
Posterior hip dislocations are best managed with immobilization and emergent reduction within 6 hours.128 Delay in reduction increases the rate of AVN of the femoral head and the potential for sciatic nerve injury.126 If emergent referral is not available and there is no evidence of a femoral neck, head, or shaft fracture on radiographs, closed reduction should be attempted.1,38
Many closed reduction maneuvers have been described.123,125,131–133 In all maneuvers, in-line traction of the thigh is exerted with countertraction frequently provided by an assistant. Traction should be applied in a steady manner, as forceful jerky motions will not be successful and may result in femoral neck fractures. If closed reduction is unsuccessful after two to three attempts, the dislocation should be considered irreducible and operative management is indicated. 38
Closed reduction should begin by placing the patient on a backboard and administering procedural sedation, as outlined in Chapter 2.
This method was developed in 1893 by Allis (Fig. 18–29).125
A. The Allis maneuver. B. A second assistant applying lateral traction to the thigh may aid in the reduction. (Modified with permission from Reichman EF, Simon RR. Emergency Medicine Procedures. New York, NY: McGraw-Hill; 2004.)
The patient should be lowered to the floor while on the backboard, or the physician can stand on the stretcher.
An assistant immobilizes the pelvis by holding the iliac crests down.
The physician then applies traction in-line with the deformity along with gentle flexion of the hip to 90 degrees.
As traction is maintained, external rotation, abduction, and extension of the hip is performed.
A second assistant can apply lateral traction to the thigh.
Stimson’s method of reducing posterior hip dislocations is also safe and effective (Fig. 18–30).
A. The Stimson maneuver. B. Alternatively, the clinician’s knee can be used to reduce the dislocation. (Reprinted with permission from Reichman EF, Simon RR. Emergency Medicine Procedures. New York, NY: McGraw-Hill; 2004.)
The patient is prone with the hip flexed over the edge of the stretcher.
Traction is applied to the hip by placing pressure over the posterior aspect of the knee by either the physician’s hand or knee.
External and internal rotation is provided by the opposite hand.
An assistant aids in the reduction by directly manipulating the femoral head into the reduced position.
Variations of this technique have been described by multiple authors (Fig. 18–31).123,125,132
The physician stands on the side of the dislocation and places his/her arm under the knee of the affected leg and onto the unaffected knee.
The physician’s opposite hand is placed on the anterior aspect of the ankle.
The arm under the patient’s knee is elevated and traction is applied to the thigh. The palm of the hand on the unaffected knee creates countertraction.
The hand on the patient’s ankle is used to provide slight internal and external rotation of the hip while also flexing the knee.
This technique was developed in Fresno and published in 2011 (Figs. 18–32 and Video 18–1).133
Video 18-1: The Hendey technique to reduce a posterior hip dislocation.
(Courtesy of Greg Hendey. All rights reserved.)
The Captain Morgan technique. A. The patient is placed supine on a gurney, and the pelvis is fixed to a backboard with a strap. The patient’s hip and knee are flexed to 90 degrees. The physician places one foot on the board, with a knee behind the patient’s knee. The physician holds the patient’s knee in flexion by holding the ankle down and applies an upward force to the hip by lifting with his or her calf and then gently rotates lower leg. B. Captain Morgan. Used with permission from Diageo PLC.
The stretcher is lowered as much as possible and the patient’s pelvis is secured to a backboard by a strap.
The patient’s hip and knee are flexed to 90 degrees.
The physician stands on the side of the dislocation and places his/her foot on the bed with their knee under the patient’s knee.
The physician’s hands are used to apply a gentle downward force at the patient’s ankle and upward force at the patient’s knee. The major force, however, is created by the physician’s leg, which applies an upward force by ankle plantarflexion to push off from the bed.
Whatever technique is applied, it is mandatory to evaluate the arterial pulses before and after reduction. If unsuccessful, reduction should be performed under general anesthesia. After successful reduction many patients are admitted with strict nonweight-bearing and observation. However, some may be discharged with home assistance and good follow-up, particularly those with a recurrent prosthetic hip dislocation. There is no benefit from skeletal traction after reduction.128
Operative intervention is necessary in (1) reduced, but unstable dislocations, (2) irreducible dislocations, and (3) dislocations associated with proximal femur fractures. In those dislocations complicated by an acetabular fracture, an attempt at closed reduction is indicated. If the reduction is unstable, operative fixation is needed. Closed reduction is unsuccessful in up to 15% of posterior hip dislocations.38
Hip dislocations are associated with several significant complications, including AVN of the femoral head, sciatic nerve injury, and traumatic arthritis.118,134
In one study, which followed patients with traumatic posterior dislocations of the hip for an average of 12.5 years, it was found that even with simple dislocations, 24% of the patients had poor results and up to 70% of the patients had fair-to-poor results.118 It is clear that even with simple posterior dislocations of the hip treated properly, late osteoarthritis may develop in as many as 20% of cases. Thus, posterior dislocations of the hip have a very guarded prognosis.
Anterior dislocations are less common than posterior dislocations and are classified as follows (Fig. 18–33):
Anterior dislocations of the hip. Three types are demonstrated: obturator, pubic, and iliac.
Obturator dislocation (most common)
Anterior dislocations are the result of forced abduction resulting in impingement of the femoral neck or trochanter against the superior dome of the acetabulum and a levering of the femoral head through a tear in the anterior capsule.
Obturator dislocations occur when the hip is in flexion at the time of the injury. This type of anterior dislocation results in a limb fixed in up to 60 degrees of abduction, external rotation, and some flexion.
Injuries to a hip held in extension produces a pubic or iliac dislocation. Pubic dislocations reveal a limb in marked external rotation, full extension, and some abduction.120 A pubic dislocation can also be the result of severe hyperextension with external rotation, thus forcing the head of the femur anteriorly. Anterior dislocations may be associated with a shear fracture of the femoral head.135
Anterior obturator dislocations usually present with abduction, external rotation, and flexion of the involved extremity. Anterior iliac or pubic dislocations present with the hip in the position of extension, slight abduction, and external rotation. The femoral head is palpable near the anterosuperior iliac spine with iliac dislocations and near the pubis after a pubic dislocation. The neurovascular status of the extremity must be documented in all patients with hip dislocations.
Routine hip and pelvic views are usually adequate in demonstrating these injuries. The femoral head will appear larger on the affected side because of its anterior location. Shenton’s line should be evaluated whenever a hip injury is suspected (Fig. 18–3). Additional radiographs of the ipsilateral extremity may be indicated on the basis of the physical examination.
Hip dislocations may be associated with several significant injuries. The associated injuries are similar to a posterior dislocation; however, vascular injury is more common in an anterior dislocation, while sciatic nerve injury is more common after a posterior dislocation.
Although the above reduction methods may be attempted in some cases, many require reduction in the operating room. Open reduction is indicated if attempts at closed reduction fail.
Long-term complications of anterior hip dislocations are similar to posterior dislocations and include AVN of the femoral head and traumatic arthritis.
Muscle Strain and Tendinopathy
This is an uncommon injury occurring primarily in dancers and gymnasts. Strain of the iliopsoas may occur at its attachment to the lesser trochanter or at the musculotendinous junction. The usual mechanism of injury is excessive stretch placed on the iliopsoas. On examination, the patient characteristically holds the thigh in a flexed adducted and externally rotated position. Extension and internal rotation of the thigh accentuate pain.
Ice packs and bed rest are the mainstays of management in this injury. The tendon is usually not repaired surgically even if it is completely avulsed or has an incorporated bone fragment.
This is more commonly seen in young athletes; however, even in this group it is an uncommon injury. Strain of the gluteus medius usually occurs as a result of overexertion of the gluteus medius. Pain is noted on abduction against resistance and is accentuated by having the patient rotate the thigh medially against resistance. The treatment of this injury is the same for any other muscle strain, and includes rest, moist heat application, and analgesics.
In young patients with chronic buttocks pain, one should consider gluteus medius tendon tear or even rupture as the cause. In one study, 46% of patients with chronic buttocks pain had this as the etiology. The diagnosis is best made by doing the Trendelenburg test, which is most sensitive for this condition.136,137
External Rotator Tendinopathy
This condition can be acute or chronic, and commonly involves the external rotators. The external rotators of the thigh include the piriformis, gemellus superior and inferior, obturator internus and externus, quadratus femoris, and gluteus maximus. Tendinopathy of these muscles is characterized by pain and tenderness on active external rotation. Treatment for the condition includes local moist heat application, anti-inflammatory agents, and analgesics. In younger patients with overuse syndromes of the external rotators, treat with cold packs for 20 minutes several times a day as well as ultrasound and ionophoresis.137