Hip pain is a common complaint, and commonly misunderstood. Although the pain can be associated with a broad spectrum of conditions, the presentation is often vague and nonspecific.

Thus, hip pain and injury are frequently attributed, often incorrectly, to a “hip pointer”—a contusion of soft tissues against the iliac crest. It’s not unusual for patients who receive this diagnosis to be treated conservatively for prolonged periods, leading some previously active individuals to abandon their favorite sport or self-impose limits on the activities they engage in.¹

But it doesn’t have to be this way.

Minimally invasive hip arthroscopy and advances in imaging, instrumentation, and devices have made it easier to identify and address underlying pathology associated with hip pain, helping patients return to their previous level of activity more rapidly.^2,3 And, while many conditions associated with hip pain can be treated conservatively, family physicians—whom patients often go to first—should not hesitate to provide a referral when more aggressive treatment or diagnostic confirmation is needed.

We created this guide with family physicians in mind. Our focus here is primarily on anterior hip pain—the most common presentation—in active, or athletic, patients.

When did the pain begin? Where does it hurt?

Before performing a physical examination, find out as much as possible about the onset of pain and when and under what circumstances it occurs. (A review of hip anatomy is provided here.) Did it begin suddenly, after an acute injury or a particular physical maneuver? Or is the pain insidious, as was the case with one of our patients?

Hip anatomy: A brief review

Osseous morphology of the hip includes the anterior superior iliac spine, the origin of the sartorius muscle and the ilioinguinal ligament. The anterior inferior iliac spine attaches to the rectus femoris, a major hip flexor and knee extender. The adductors of the hip originate in the anterior pelvic region.

The inguinal canal contains the ilioinguinal nerve, which is responsible for radiation of pain to the anterior hip. The hip joint itself is a spheroid comprising the femoral head and acetabulum, with most of the articular hip innervated by the femoral or obturator nerves.

Most intra-articular conditions radiate to the anterior groin or hip, although there are cases in which the pain is referred to either the lateral aspect of the hip or the buttocks. The iliopsoas muscle is the major hip flexor, and crosses under the ilioinguinal ligament to insert on the lesser tuberosity after crossing over the anterior capsule of the hip. A large bursa surrounds it, helping the tendon glide smoothly over the hip.

CASE Mack Q, a 27-year-old man with an 8-month history of right hip pain, sought care at our medical center for an achy pain in his right groin; he also described an occasional “clicking and popping sensation” in his groin but denied any trauma. The pain worsened with prolonged sitting and certain activities, such as squatting, twisting, and putting on shoes and socks. Our patient had stopped playing soccer because it hurt too much. He had tried physical therapy, oral anti-inflammatories, and a corticosteroid injection, with little relief.

Start with a gait assessment
The physical examination should begin with a gait assessment. Consider the patient’s ability to bear weight and his or her foot angle.

An individual with a stress fracture will have difficulty bearing weight on the affected side, resulting in a limp, or antalgic gait. A patient with femoral acetabular impingement (FAI) will often exhibit greater external rotation of the foot on the affected side compared with the other foot. And a patient with weakened abductor muscles, typically because of severe osteoarthritis, will exhibit the Trendelenburg sign—a pelvic tilt when the weight is shifted to the affected extremity.

Although most individuals with hip pain will not have an obvious gait abnormality, any patient who walks with a limp or needs crutches requires an immediate referral to an orthopedic surgeon.

Include these elements in the physical exam
Examine the hip with the patient sitting on the side of the exam table. Assess range of motion (ROM), comparing the range of flexion, extension, and internal/external rotation on the affected and unaffected sides. Include the following maneuvers:

Impingement testing. In patients with FAI and osteoarthritis, impingement testing—encompassing Flexion, ADDuction, and Internal Rotation (FADDIR)—will elicit pain. The maneuver can be tested starting at 45° of hip flexion, increasing to approximately 120°. Pain with <45° of hip flexion indicates that the impingement is severe.

Such testing can also reveal labral tears, which may be caused by FAI or other structural abnormalities. In a patient with anterior labral tears, FADDIR will produce groin pain; posterior labral tears will produce pain when the patient is sitting with legs hanging off the exam table and the contralateral leg is brought to the chest and the affected limb fully extended.

In patients with hip pain and bursitis, applying downward pressure will elicit a snapping sound as the iliopsoas snaps over the iliopectineal eminence or femoral head. Flexion, ABduction, and External Rotation (FABER) can also be used to diagnose iliopsoas tendonitis: The test is positive if it elicits pain in the affected extremity or in the sacroiliac joint on the opposite side.

Log roll. A painful response to this test, which involves internally and externally rotating the affected hip while it is relaxed and the knee fully extended, is an indication of synovitis of the hip caused by intra-articular pathology. To test hip stability, externally rotate the leg while it is extended. If the hip is stable, the leg will return to a neutral position; microinstability of the hip is likely if the leg remains in the rotated position.

Muscular strength testing. To assess for tendinopathy in the hip area, the patient should be in a seated position and contract the internal and external rotators and the adductor muscles while you apply resistance. To test abductor strength, have the patient assume a lateral position and hold and abduct the leg on the affected side while you apply resistance.

Hip flexion strength should be tested with the patient in both supine and seated positions. A patient with quadriceps tendonitis will have much greater pain with resisted hip flexion in the supine position vs the seated position; the opposite is true for a patient with iliopsoas tendonitis. (See “Did you know…? Hip pain facts and findings” on for additional diagnostic tips.)

Perform a neurologic evaluation to rule out a back condition that might radiate pain into the anterior hip; ask the patient to do a sit-up while you apply resistance to test for abdominal wall pathology, as well.

Hip palpation. This aspect of the physical exam is important regardless of the cause of the pain but especially crucial for pediatric and adolescent patients, whose anterior hip pain may be related to apophyseal injury. Palpate the superior iliac spine (and over the inferior iliac spine in thin patients) to determine if the sartorius or rectus femoris has been injured. The area just lateral to the symphysis will be tender to palpation in patients with osteitis pubis.

Refer or treat? Here’s what to consider

While the history and physical should provide ample information for a differential diagnosis, imaging studies are generally required for confirmation. Clinical assessment— including physical exam, imaging, and intra-articular injection—of patients with hip pain is up to 98% accurate in identifying hip abnormalities, with arthroscopy as the gold standard.⁴

CASE On physical examination, Mr. Q had right hip extension to 0°, flexion to 110°, external rotation to 50°, and internal rotation to neutral; he also had positive impingement and subspine impingement tests, a painful arc of motion from 12 to 4 o’clock, tenderness over the hip adductor, and pain with resisted hip adduction. He did not walk with a limp.

Diagnostic studies included plain radiographs, which demonstrated that the joint space was well preserved. We identified subtle anatomical abnormalities on the femoral head-neck junction, known as a cam deformity. Magnetic resonance imaging (MRI) revealed an anterior superior labral tear with cartilage delamination.

Stress fractures affect runners, military recruits
In addition to long-distance runners who have recently increased the frequency, duration, or intensity of training,^5,6 military recruits have a higher incidence of stress fractures due to the rapid onset of intensive training. Stress fractures can also occur in patients who do not have a history of intense activity but have metabolically weakened bone, in some cases as a result of an eating disorder.⁷

Patients with femoral neck stress fractures typically present with activity-related anterior groin pain that is relieved by rest; initially, they may be only mildly affected, but the condition worsens in those who continue to “work through the pain.” By the time such individuals seek treatment, they almost always have pain with weight bearing and an antalgic gait.

Symptoms consistent with a femoral neck stress fracture can be further evaluated with plain radiographs. However, x-rays are often negative for up to 4 weeks after the onset of pain.⁸ In cases in which radiographs are negative but the physical exam is suggestive of a stress fracture, MRI—which can detect an abnormality within a day or 2 of injury^8,9—should be used to confirm the diagnosis (FIGURE 1).

FIGURE 1
MRI reveals a femoral neck stress fracture

Treatment. A complete femoral neck fracture portends impending displacement and requires emergent evaluation by an orthopedist, and superior neck changes, also known as tension-sided stress fractures, require urgent treatment with percutaneous screw fixation.⁹ However, compression-sided, or inferior, stress fractures can be treated with restricted weight bearing and activity modification. Gradual resumption of activity is allowed only after the patient has been asymptomatic for 6 weeks; recurrent pain indicates residual stress reaction, and signals that activities should be abated.

Osteonecrosis has many causes

Necrosis of the femoral head is a debilitating and progressive condition primarily affecting patients between the ages of 20 and 50 years.¹⁰ It has multiple (and diverse) causes, including trauma, steroids, alcohol, smoking, lupus, sickle cell anemia, and coagulopathies, as well as scuba diving. But about 20% of cases have no apparent cause.^11,12

Patients with osteonecrosis of the hip typically present with groin pain, often described as a deep, intermittent ache that interferes with activities of daily living. Exam findings depend on the stage of presentation. Early on, pain will occur only with extreme ROM; in advanced cases, ROM is restricted and pain occurs even with limited motion.

Femoral head collapse due to loss of the structural integrity of the subchondral bone—which occurs in 80% of cases¹²—is thought to be caused by decreased blood flow. Plain radiography can confirm a diagnosis of osteonecrosis in patients with advanced disease, but MRI is useful for evaluating patients with earlier clinical presentations.

Treatment of osteonecrosis is dictated by the stage of the disease, but remains controversial because no intervention has been shown to prevent progression in all cases.¹² All patients should be referred to a specialist. Those without collapse or cartilage damage can be treated surgically with core decompression, possibly with additional vascularized bone grafting,^13,14 while those with more advanced disease typically require a total hip replacement at a relatively young age. Results for total hip replacement in patients with osteonecrosis are thought to be inferior to hip replacement in patients with osteoarthritis, although comparison is difficult because of the differences in age and activity levels in these 2 groups.^15,16

Femoral acetabular impingement can occur on the cam or pincer side
FAI pathology can exist on either the femoral (cam) or acetabular (pincer) side,¹⁷ or both.¹⁸ In pure cam impingement, the anterior femoral neck loses its normal concave anatomy and develops a “bump,” which impinges on the anterosuperior labrum during hip flexion, causing labral tears and delamination of the adjacent cartilage.

Pure pincer impingement arises from a prominent acetabular rim, causing overcoverage of the femoral head. Acetabular labral tears result from the repetitive impaction with flexion and internal rotation.

Patients report an insidious onset of groin pain that is exacerbated by flexion-type sports, such as hockey, football, and golf,¹⁹ as well as activities of daily living. In patients with cartilage damage, even walking can be painful. Physical examination of patients with FAI reveals findings that are similar to those of patients with acetabular labral tears. Abnormally large cam lesions or acetabular overcoverage will result in restriction of hip ROM, especially internal rotation and flexion due to a mechanical block.

Radiographs (FIGURE 2) are essential to diagnose FAI and to distinguish this condition from an isolated labral tear.²⁰ Cam impingement will be best demonstrated on a cross-table lateral radiograph, which shows an asphericity of the femoral head/neck junction anteriorly, while pincer impingement will show overcoverage of the femoral head on an AP radiograph. MRI or magnetic resonance arthrography (MRA) is frequently obtained to see whether any cartilage deterioration has occurred. Computed tomography, which can provide a 3-dimensional reproduction of the hip morphology, is often used for preoperative planning when surgical intervention is required.

FIGURE 2
Femoral acetabular impingement with a prominent pincer lesion

Treatment. Surgical intervention is often needed to correct or remove the abnormal anatomy, and both arthroscopic and open surgery are recommended.²⁰ Both methods include osteoplasty at the femoral head/neck junction and/or the acetabular rim to allow the proximal femur to articulate with the acetabulum without injury to the labrum with flexion and internal rotation.²¹

Results of both open and arthroscopic osteoplasty of the femur and acetabulum are still preliminary, with only a few studies reporting mid-term results. Open surgery typically has longer recovery and rehabilitation, but advocates emphasize the improved ability to contour the femur or acetabulum. Both open and arthroscopic procedures have about an 8% to 13% rate of revision in short-term follow-up.¹⁷

Labral tears occur with trauma and certain sports

In addition to FAI, causes of labral tears include dysplasia, instability, trauma, and degeneration, as well as sports that require repetitive hip flexion and/or pivoting, such as hockey, soccer, and football.^22,23

Patients with labral tears typically present with anterior hip pain radiating to the groin, worsening with twisting motions, running, walking, and sitting for prolonged periods. Clicking or catching may occur, as well. Patients may exhibit what one researcher called the “c-sign”—so named for the shape patients make with their hand as they grip their hip just above the greater trochanter to indicate where it hurts.⁴ The work-up for labral tears includes radiographs and, often, MRA, which is nearly 100% specific.²⁴

Treatment. Conservative treatment, which may include activity modification or rest and ice, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy, is often effective for labral tears; when such measures fail, surgical intervention is indicated. A systematic review found a 67% satisfaction rate after 3.5 years in patients who had undergone labral debridement, and complete resolution of mechanical symptoms in nearly 50%.²⁵ Another study showed similar results for hip arthroscopy, with symptom relief continuing for 4.8 years after surgery, on average, and 84% of patients able to return to their previous level of activity.²⁶

The long-term results of labral debridement are unknown, however, and the possibility of an association between this procedure and the development of arthritis remains. Most specialists prefer anatomic repair to restore normal hip kinematics and, potentially, long-term hip function,^27,28 but structural abnormalities must also be addressed to prevent failure of the repair or recurrent tears.

Iliopsoas tendonitis: You know the snap
Often referred to as internal snapping of the hip or internal coxa saltans, iliopsoas tendonitis/bursitis can be a recalcitrant cause of anterior hip pain. Snapping of the iliopsoas leading to bursitis or tendonitis can occur at the iliopectineal eminence, the femoral head, or the lesser trochanter.²⁹ Runners and ballet dancers are often affected.^30,31

Snapping in itself is not an indication of pathology, but chronicity of symptoms is. Patients with relatively acute symptoms typically have only bursitis, while a longer duration of symptoms leads to tendonitis or tendinopathy.³²

Treatment. First-line therapy is nonoperative, and includes activity modification, rest, ice, NSAIDs, and physical therapy. Advise patients to refrain from activities causing pain, and to apply ice to the affected every 20 minutes (with a 20- to 30-minute off period) for one to 2 hours. Physical therapy focuses on stretching the iliopsoas and rectus femoris muscles and strengthening the hamstring muscles to relieve the stress on the anterior pelvis. If such treatment is unsuccessful, ultrasound can be used to guide a therapeutic injection of cortisone.³³ If this fails to bring relief, fractional lengthening of the iliopsoas tendon can be performed to eliminate snapping and relieve pain.³⁴

Muscular strains/avulsion fractures: Sports and age play a role
Although strains can affect any of the anterior muscles around the hip, in active individuals the adductors are most commonly affected. Skeletally immature patients are an exception: apophyseal fractures at the origin of the sartorius and rectus femoris muscles are more common than muscular strains in this patient population.

Athletes who experience adductor strains often play sports in which kicking or frequent changes in direction are required—eg, football, hockey, and soccer³⁵—and generally are able to tell you exactly what they were doing when the injury occurred. Physical examination can reveal focal findings, with swelling and tenderness confined to the anteromedial aspect of the hip along the adductor muscle group. MRI can help differentiate the site of true pathology.³⁶

Treatment of adductor strains is nonoperative, with rest, ice, and activity modification until the tendon heals. In the rare case in which complete tendon avulsion is found, surgical reattachment is needed.

Apophyseal fracture in skeletally immature patients typically occurs during participation in a sport that requires rapid acceleration and deceleration with the hip in an extended position. In such patients, stretching the affected muscle should reproduce the pain. Radiographs are diagnostic and will often show minimal displacement of the apophysis. Treatment is almost always nonoperative. Surgical intervention is rarely needed, and only indicated with displacement >2 cm.³⁷

Athletic pubalgia: A challenging Dx
Also referred to as sports hernia, athletic pubalgia is an enigmatic cause of anterior hip pain in athletes. Diagnosis can be especially challenging, and patients may have lingering symptoms for years before the cause is discovered.³⁸ A sports hernia, unlike other hernias, does not involve a bulge of tissue protruding through one body part into another. In contrast, a sports hernia occurs when the oblique abdominal muscles strain or completely tear away from the pubis. A recent systematic review found that the underlying etiology involves posterior inguinal wall weakening, which can be a result of poorly balanced hip adductor and abdominal muscle activation.³⁹

Patients with sports hernia will often present with anterior hip and/or groin pain, especially with hip extension, twisting, and turning. In addition, patients can have pain in the lower abdomen and, in males, in the testicles. Physical examination will usually show pubic point tenderness, which is exacerbated by resisted hip adduction.⁴⁰ MRI and ultrasound are extremely helpful in diagnosing and forming a treatment plan.³⁹

The initial treatment of choice for sports hernias is nonoperative, and the first step is always activity modification or temporary avoidance of symptom-producing activities. Additional modalities include NSAIDs, ice, and physical therapy to strengthen the surrounding muscles. Surgical intervention, if needed, may be done laparoscopically or via an open approach with direct repair.^40,41

Less common causes to consider
While the conditions detailed here account for most anterior hip etiologies, there are other less common causes to consider. One such cause is osteitis pubis, an umbrella term for conditions that affect the area surrounding the symphysis pubis. Patients with osteitis pubis present with pain over the anterior aspect of the pelvis that is worse with sit-ups, rising from a chair, or any activity where contraction of the rectus muscles occurs.²⁹ Tenderness is found directly over and just lateral to the pubic symphysis. Radiographs are frequently negative, but occasionally chronic degenerative changes at the symphysis are present in addition to symphyseal narrowing. Additional imaging is often necessary for diagnosis.

Neuropathies. When history, physical examination, and imaging studies have ruled out other causes, neuropathies (ilioinguinal, genitofemoral, and obturator) should be considered, particularly in patients with vague, radiating anterior hip and/or groin pain.⁴² In pediatric patients, Legg-Calve-Perthes disease and slipped capital femoral epiphysis are possibilities, as well.

Getting patients back on track

Rehabilitation after hip injury resulting in anterior hip pain will be determined by the site, type, and mechanism of injury, as well as the severity. Restrictions in weight bearing and the use of an assistive device may be needed to prevent excessive stress on bone and supporting soft-tissue structures in the early stages of healing. Physical therapy, as needed, should initially focus on early controlled ROM of the hip joint to prevent both intra- and extra-articular adhesions and excessive scar tissue formation.²

For patients who undergo surgery, much of the focus will be on strengthening the supporting musculature—the hip abductor group, anterior and posterior thigh musculature, and core stabilizing muscles. Neuromuscular training may be needed to promote normal biomechanics and minimize compensatory movement patterns. For athletes, cardiovascular training and a return-to-play program should be implemented, as well.^2,43,44

CASE Mr. Q was diagnosed with right hip pain due to a labral tear secondary to a cam femoral acetabular impingement. Given that he had failed nonoperative treatment and had long-standing pain, we recommended surgery for this patient. He underwent right hip arthroscopic labral repair, acetabular rim trimming, acetabular microfracture, femoral osteochondroplasty with capsular plication. At 12-month follow-up, he was doing well, with resolution of the presurgical pain and return to all athletic activities.

CORRESPONDENCE Rachel M. Frank, MD, Department of Orthopedic Surgery, Rush University Medical Center, 1611 West Harrison Street, Suite 300, Chicago, IL 60612; [email protected]

Hip pain is a common complaint, and commonly misunderstood. Although the pain can be associated with a broad spectrum of conditions, the presentation is often vague and nonspecific.

Thus, hip pain and injury are frequently attributed, often incorrectly, to a “hip pointer”—a contusion of soft tissues against the iliac crest. It’s not unusual for patients who receive this diagnosis to be treated conservatively for prolonged periods, leading some previously active individuals to abandon their favorite sport or self-impose limits on the activities they engage in.¹

But it doesn’t have to be this way.

Minimally invasive hip arthroscopy and advances in imaging, instrumentation, and devices have made it easier to identify and address underlying pathology associated with hip pain, helping patients return to their previous level of activity more rapidly.^2,3 And, while many conditions associated with hip pain can be treated conservatively, family physicians—whom patients often go to first—should not hesitate to provide a referral when more aggressive treatment or diagnostic confirmation is needed.

We created this guide with family physicians in mind. Our focus here is primarily on anterior hip pain—the most common presentation—in active, or athletic, patients.

When did the pain begin? Where does it hurt?

Before performing a physical examination, find out as much as possible about the onset of pain and when and under what circumstances it occurs. (A review of hip anatomy is provided here.) Did it begin suddenly, after an acute injury or a particular physical maneuver? Or is the pain insidious, as was the case with one of our patients?

Hip anatomy: A brief review

Osseous morphology of the hip includes the anterior superior iliac spine, the origin of the sartorius muscle and the ilioinguinal ligament. The anterior inferior iliac spine attaches to the rectus femoris, a major hip flexor and knee extender. The adductors of the hip originate in the anterior pelvic region.

The inguinal canal contains the ilioinguinal nerve, which is responsible for radiation of pain to the anterior hip. The hip joint itself is a spheroid comprising the femoral head and acetabulum, with most of the articular hip innervated by the femoral or obturator nerves.

Most intra-articular conditions radiate to the anterior groin or hip, although there are cases in which the pain is referred to either the lateral aspect of the hip or the buttocks. The iliopsoas muscle is the major hip flexor, and crosses under the ilioinguinal ligament to insert on the lesser tuberosity after crossing over the anterior capsule of the hip. A large bursa surrounds it, helping the tendon glide smoothly over the hip.

CASE Mack Q, a 27-year-old man with an 8-month history of right hip pain, sought care at our medical center for an achy pain in his right groin; he also described an occasional “clicking and popping sensation” in his groin but denied any trauma. The pain worsened with prolonged sitting and certain activities, such as squatting, twisting, and putting on shoes and socks. Our patient had stopped playing soccer because it hurt too much. He had tried physical therapy, oral anti-inflammatories, and a corticosteroid injection, with little relief.

Start with a gait assessment
The physical examination should begin with a gait assessment. Consider the patient’s ability to bear weight and his or her foot angle.

An individual with a stress fracture will have difficulty bearing weight on the affected side, resulting in a limp, or antalgic gait. A patient with femoral acetabular impingement (FAI) will often exhibit greater external rotation of the foot on the affected side compared with the other foot. And a patient with weakened abductor muscles, typically because of severe osteoarthritis, will exhibit the Trendelenburg sign—a pelvic tilt when the weight is shifted to the affected extremity.

Although most individuals with hip pain will not have an obvious gait abnormality, any patient who walks with a limp or needs crutches requires an immediate referral to an orthopedic surgeon.

Include these elements in the physical exam
Examine the hip with the patient sitting on the side of the exam table. Assess range of motion (ROM), comparing the range of flexion, extension, and internal/external rotation on the affected and unaffected sides. Include the following maneuvers:

Impingement testing. In patients with FAI and osteoarthritis, impingement testing—encompassing Flexion, ADDuction, and Internal Rotation (FADDIR)—will elicit pain. The maneuver can be tested starting at 45° of hip flexion, increasing to approximately 120°. Pain with <45° of hip flexion indicates that the impingement is severe.

Such testing can also reveal labral tears, which may be caused by FAI or other structural abnormalities. In a patient with anterior labral tears, FADDIR will produce groin pain; posterior labral tears will produce pain when the patient is sitting with legs hanging off the exam table and the contralateral leg is brought to the chest and the affected limb fully extended.

In patients with hip pain and bursitis, applying downward pressure will elicit a snapping sound as the iliopsoas snaps over the iliopectineal eminence or femoral head. Flexion, ABduction, and External Rotation (FABER) can also be used to diagnose iliopsoas tendonitis: The test is positive if it elicits pain in the affected extremity or in the sacroiliac joint on the opposite side.

Log roll. A painful response to this test, which involves internally and externally rotating the affected hip while it is relaxed and the knee fully extended, is an indication of synovitis of the hip caused by intra-articular pathology. To test hip stability, externally rotate the leg while it is extended. If the hip is stable, the leg will return to a neutral position; microinstability of the hip is likely if the leg remains in the rotated position.

Muscular strength testing. To assess for tendinopathy in the hip area, the patient should be in a seated position and contract the internal and external rotators and the adductor muscles while you apply resistance. To test abductor strength, have the patient assume a lateral position and hold and abduct the leg on the affected side while you apply resistance.

Hip flexion strength should be tested with the patient in both supine and seated positions. A patient with quadriceps tendonitis will have much greater pain with resisted hip flexion in the supine position vs the seated position; the opposite is true for a patient with iliopsoas tendonitis. (See “Did you know…? Hip pain facts and findings” on for additional diagnostic tips.)

Perform a neurologic evaluation to rule out a back condition that might radiate pain into the anterior hip; ask the patient to do a sit-up while you apply resistance to test for abdominal wall pathology, as well.

Hip palpation. This aspect of the physical exam is important regardless of the cause of the pain but especially crucial for pediatric and adolescent patients, whose anterior hip pain may be related to apophyseal injury. Palpate the superior iliac spine (and over the inferior iliac spine in thin patients) to determine if the sartorius or rectus femoris has been injured. The area just lateral to the symphysis will be tender to palpation in patients with osteitis pubis.

Refer or treat? Here’s what to consider

While the history and physical should provide ample information for a differential diagnosis, imaging studies are generally required for confirmation. Clinical assessment— including physical exam, imaging, and intra-articular injection—of patients with hip pain is up to 98% accurate in identifying hip abnormalities, with arthroscopy as the gold standard.⁴

CASE On physical examination, Mr. Q had right hip extension to 0°, flexion to 110°, external rotation to 50°, and internal rotation to neutral; he also had positive impingement and subspine impingement tests, a painful arc of motion from 12 to 4 o’clock, tenderness over the hip adductor, and pain with resisted hip adduction. He did not walk with a limp.

Diagnostic studies included plain radiographs, which demonstrated that the joint space was well preserved. We identified subtle anatomical abnormalities on the femoral head-neck junction, known as a cam deformity. Magnetic resonance imaging (MRI) revealed an anterior superior labral tear with cartilage delamination.

Stress fractures affect runners, military recruits
In addition to long-distance runners who have recently increased the frequency, duration, or intensity of training,^5,6 military recruits have a higher incidence of stress fractures due to the rapid onset of intensive training. Stress fractures can also occur in patients who do not have a history of intense activity but have metabolically weakened bone, in some cases as a result of an eating disorder.⁷

Patients with femoral neck stress fractures typically present with activity-related anterior groin pain that is relieved by rest; initially, they may be only mildly affected, but the condition worsens in those who continue to “work through the pain.” By the time such individuals seek treatment, they almost always have pain with weight bearing and an antalgic gait.

Symptoms consistent with a femoral neck stress fracture can be further evaluated with plain radiographs. However, x-rays are often negative for up to 4 weeks after the onset of pain.⁸ In cases in which radiographs are negative but the physical exam is suggestive of a stress fracture, MRI—which can detect an abnormality within a day or 2 of injury^8,9—should be used to confirm the diagnosis (FIGURE 1).

FIGURE 1
MRI reveals a femoral neck stress fracture

Treatment. A complete femoral neck fracture portends impending displacement and requires emergent evaluation by an orthopedist, and superior neck changes, also known as tension-sided stress fractures, require urgent treatment with percutaneous screw fixation.⁹ However, compression-sided, or inferior, stress fractures can be treated with restricted weight bearing and activity modification. Gradual resumption of activity is allowed only after the patient has been asymptomatic for 6 weeks; recurrent pain indicates residual stress reaction, and signals that activities should be abated.

Osteonecrosis has many causes

Necrosis of the femoral head is a debilitating and progressive condition primarily affecting patients between the ages of 20 and 50 years.¹⁰ It has multiple (and diverse) causes, including trauma, steroids, alcohol, smoking, lupus, sickle cell anemia, and coagulopathies, as well as scuba diving. But about 20% of cases have no apparent cause.^11,12

Patients with osteonecrosis of the hip typically present with groin pain, often described as a deep, intermittent ache that interferes with activities of daily living. Exam findings depend on the stage of presentation. Early on, pain will occur only with extreme ROM; in advanced cases, ROM is restricted and pain occurs even with limited motion.

Femoral head collapse due to loss of the structural integrity of the subchondral bone—which occurs in 80% of cases¹²—is thought to be caused by decreased blood flow. Plain radiography can confirm a diagnosis of osteonecrosis in patients with advanced disease, but MRI is useful for evaluating patients with earlier clinical presentations.

Treatment of osteonecrosis is dictated by the stage of the disease, but remains controversial because no intervention has been shown to prevent progression in all cases.¹² All patients should be referred to a specialist. Those without collapse or cartilage damage can be treated surgically with core decompression, possibly with additional vascularized bone grafting,^13,14 while those with more advanced disease typically require a total hip replacement at a relatively young age. Results for total hip replacement in patients with osteonecrosis are thought to be inferior to hip replacement in patients with osteoarthritis, although comparison is difficult because of the differences in age and activity levels in these 2 groups.^15,16

Femoral acetabular impingement can occur on the cam or pincer side
FAI pathology can exist on either the femoral (cam) or acetabular (pincer) side,¹⁷ or both.¹⁸ In pure cam impingement, the anterior femoral neck loses its normal concave anatomy and develops a “bump,” which impinges on the anterosuperior labrum during hip flexion, causing labral tears and delamination of the adjacent cartilage.

Pure pincer impingement arises from a prominent acetabular rim, causing overcoverage of the femoral head. Acetabular labral tears result from the repetitive impaction with flexion and internal rotation.

Patients report an insidious onset of groin pain that is exacerbated by flexion-type sports, such as hockey, football, and golf,¹⁹ as well as activities of daily living. In patients with cartilage damage, even walking can be painful. Physical examination of patients with FAI reveals findings that are similar to those of patients with acetabular labral tears. Abnormally large cam lesions or acetabular overcoverage will result in restriction of hip ROM, especially internal rotation and flexion due to a mechanical block.

Radiographs (FIGURE 2) are essential to diagnose FAI and to distinguish this condition from an isolated labral tear.²⁰ Cam impingement will be best demonstrated on a cross-table lateral radiograph, which shows an asphericity of the femoral head/neck junction anteriorly, while pincer impingement will show overcoverage of the femoral head on an AP radiograph. MRI or magnetic resonance arthrography (MRA) is frequently obtained to see whether any cartilage deterioration has occurred. Computed tomography, which can provide a 3-dimensional reproduction of the hip morphology, is often used for preoperative planning when surgical intervention is required.

FIGURE 2
Femoral acetabular impingement with a prominent pincer lesion

Treatment. Surgical intervention is often needed to correct or remove the abnormal anatomy, and both arthroscopic and open surgery are recommended.²⁰ Both methods include osteoplasty at the femoral head/neck junction and/or the acetabular rim to allow the proximal femur to articulate with the acetabulum without injury to the labrum with flexion and internal rotation.²¹

Results of both open and arthroscopic osteoplasty of the femur and acetabulum are still preliminary, with only a few studies reporting mid-term results. Open surgery typically has longer recovery and rehabilitation, but advocates emphasize the improved ability to contour the femur or acetabulum. Both open and arthroscopic procedures have about an 8% to 13% rate of revision in short-term follow-up.¹⁷

Labral tears occur with trauma and certain sports

In addition to FAI, causes of labral tears include dysplasia, instability, trauma, and degeneration, as well as sports that require repetitive hip flexion and/or pivoting, such as hockey, soccer, and football.^22,23

Patients with labral tears typically present with anterior hip pain radiating to the groin, worsening with twisting motions, running, walking, and sitting for prolonged periods. Clicking or catching may occur, as well. Patients may exhibit what one researcher called the “c-sign”—so named for the shape patients make with their hand as they grip their hip just above the greater trochanter to indicate where it hurts.⁴ The work-up for labral tears includes radiographs and, often, MRA, which is nearly 100% specific.²⁴

Treatment. Conservative treatment, which may include activity modification or rest and ice, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy, is often effective for labral tears; when such measures fail, surgical intervention is indicated. A systematic review found a 67% satisfaction rate after 3.5 years in patients who had undergone labral debridement, and complete resolution of mechanical symptoms in nearly 50%.²⁵ Another study showed similar results for hip arthroscopy, with symptom relief continuing for 4.8 years after surgery, on average, and 84% of patients able to return to their previous level of activity.²⁶

The long-term results of labral debridement are unknown, however, and the possibility of an association between this procedure and the development of arthritis remains. Most specialists prefer anatomic repair to restore normal hip kinematics and, potentially, long-term hip function,^27,28 but structural abnormalities must also be addressed to prevent failure of the repair or recurrent tears.

Iliopsoas tendonitis: You know the snap
Often referred to as internal snapping of the hip or internal coxa saltans, iliopsoas tendonitis/bursitis can be a recalcitrant cause of anterior hip pain. Snapping of the iliopsoas leading to bursitis or tendonitis can occur at the iliopectineal eminence, the femoral head, or the lesser trochanter.²⁹ Runners and ballet dancers are often affected.^30,31

Snapping in itself is not an indication of pathology, but chronicity of symptoms is. Patients with relatively acute symptoms typically have only bursitis, while a longer duration of symptoms leads to tendonitis or tendinopathy.³²

Treatment. First-line therapy is nonoperative, and includes activity modification, rest, ice, NSAIDs, and physical therapy. Advise patients to refrain from activities causing pain, and to apply ice to the affected every 20 minutes (with a 20- to 30-minute off period) for one to 2 hours. Physical therapy focuses on stretching the iliopsoas and rectus femoris muscles and strengthening the hamstring muscles to relieve the stress on the anterior pelvis. If such treatment is unsuccessful, ultrasound can be used to guide a therapeutic injection of cortisone.³³ If this fails to bring relief, fractional lengthening of the iliopsoas tendon can be performed to eliminate snapping and relieve pain.³⁴

Muscular strains/avulsion fractures: Sports and age play a role
Although strains can affect any of the anterior muscles around the hip, in active individuals the adductors are most commonly affected. Skeletally immature patients are an exception: apophyseal fractures at the origin of the sartorius and rectus femoris muscles are more common than muscular strains in this patient population.

Athletes who experience adductor strains often play sports in which kicking or frequent changes in direction are required—eg, football, hockey, and soccer³⁵—and generally are able to tell you exactly what they were doing when the injury occurred. Physical examination can reveal focal findings, with swelling and tenderness confined to the anteromedial aspect of the hip along the adductor muscle group. MRI can help differentiate the site of true pathology.³⁶

Treatment of adductor strains is nonoperative, with rest, ice, and activity modification until the tendon heals. In the rare case in which complete tendon avulsion is found, surgical reattachment is needed.

Apophyseal fracture in skeletally immature patients typically occurs during participation in a sport that requires rapid acceleration and deceleration with the hip in an extended position. In such patients, stretching the affected muscle should reproduce the pain. Radiographs are diagnostic and will often show minimal displacement of the apophysis. Treatment is almost always nonoperative. Surgical intervention is rarely needed, and only indicated with displacement >2 cm.³⁷

Athletic pubalgia: A challenging Dx
Also referred to as sports hernia, athletic pubalgia is an enigmatic cause of anterior hip pain in athletes. Diagnosis can be especially challenging, and patients may have lingering symptoms for years before the cause is discovered.³⁸ A sports hernia, unlike other hernias, does not involve a bulge of tissue protruding through one body part into another. In contrast, a sports hernia occurs when the oblique abdominal muscles strain or completely tear away from the pubis. A recent systematic review found that the underlying etiology involves posterior inguinal wall weakening, which can be a result of poorly balanced hip adductor and abdominal muscle activation.³⁹

Patients with sports hernia will often present with anterior hip and/or groin pain, especially with hip extension, twisting, and turning. In addition, patients can have pain in the lower abdomen and, in males, in the testicles. Physical examination will usually show pubic point tenderness, which is exacerbated by resisted hip adduction.⁴⁰ MRI and ultrasound are extremely helpful in diagnosing and forming a treatment plan.³⁹

The initial treatment of choice for sports hernias is nonoperative, and the first step is always activity modification or temporary avoidance of symptom-producing activities. Additional modalities include NSAIDs, ice, and physical therapy to strengthen the surrounding muscles. Surgical intervention, if needed, may be done laparoscopically or via an open approach with direct repair.^40,41

Less common causes to consider
While the conditions detailed here account for most anterior hip etiologies, there are other less common causes to consider. One such cause is osteitis pubis, an umbrella term for conditions that affect the area surrounding the symphysis pubis. Patients with osteitis pubis present with pain over the anterior aspect of the pelvis that is worse with sit-ups, rising from a chair, or any activity where contraction of the rectus muscles occurs.²⁹ Tenderness is found directly over and just lateral to the pubic symphysis. Radiographs are frequently negative, but occasionally chronic degenerative changes at the symphysis are present in addition to symphyseal narrowing. Additional imaging is often necessary for diagnosis.

Neuropathies. When history, physical examination, and imaging studies have ruled out other causes, neuropathies (ilioinguinal, genitofemoral, and obturator) should be considered, particularly in patients with vague, radiating anterior hip and/or groin pain.⁴² In pediatric patients, Legg-Calve-Perthes disease and slipped capital femoral epiphysis are possibilities, as well.

Getting patients back on track

Rehabilitation after hip injury resulting in anterior hip pain will be determined by the site, type, and mechanism of injury, as well as the severity. Restrictions in weight bearing and the use of an assistive device may be needed to prevent excessive stress on bone and supporting soft-tissue structures in the early stages of healing. Physical therapy, as needed, should initially focus on early controlled ROM of the hip joint to prevent both intra- and extra-articular adhesions and excessive scar tissue formation.²

For patients who undergo surgery, much of the focus will be on strengthening the supporting musculature—the hip abductor group, anterior and posterior thigh musculature, and core stabilizing muscles. Neuromuscular training may be needed to promote normal biomechanics and minimize compensatory movement patterns. For athletes, cardiovascular training and a return-to-play program should be implemented, as well.^2,43,44

CASE Mr. Q was diagnosed with right hip pain due to a labral tear secondary to a cam femoral acetabular impingement. Given that he had failed nonoperative treatment and had long-standing pain, we recommended surgery for this patient. He underwent right hip arthroscopic labral repair, acetabular rim trimming, acetabular microfracture, femoral osteochondroplasty with capsular plication. At 12-month follow-up, he was doing well, with resolution of the presurgical pain and return to all athletic activities.

CORRESPONDENCE Rachel M. Frank, MD, Department of Orthopedic Surgery, Rush University Medical Center, 1611 West Harrison Street, Suite 300, Chicago, IL 60612; [email protected]

Hip pain is a common complaint, and commonly misunderstood. Although the pain can be associated with a broad spectrum of conditions, the presentation is often vague and nonspecific.

Thus, hip pain and injury are frequently attributed, often incorrectly, to a “hip pointer”—a contusion of soft tissues against the iliac crest. It’s not unusual for patients who receive this diagnosis to be treated conservatively for prolonged periods, leading some previously active individuals to abandon their favorite sport or self-impose limits on the activities they engage in.¹

But it doesn’t have to be this way.

Minimally invasive hip arthroscopy and advances in imaging, instrumentation, and devices have made it easier to identify and address underlying pathology associated with hip pain, helping patients return to their previous level of activity more rapidly.^2,3 And, while many conditions associated with hip pain can be treated conservatively, family physicians—whom patients often go to first—should not hesitate to provide a referral when more aggressive treatment or diagnostic confirmation is needed.

We created this guide with family physicians in mind. Our focus here is primarily on anterior hip pain—the most common presentation—in active, or athletic, patients.

When did the pain begin? Where does it hurt?

Before performing a physical examination, find out as much as possible about the onset of pain and when and under what circumstances it occurs. (A review of hip anatomy is provided here.) Did it begin suddenly, after an acute injury or a particular physical maneuver? Or is the pain insidious, as was the case with one of our patients?

Hip anatomy: A brief review

Osseous morphology of the hip includes the anterior superior iliac spine, the origin of the sartorius muscle and the ilioinguinal ligament. The anterior inferior iliac spine attaches to the rectus femoris, a major hip flexor and knee extender. The adductors of the hip originate in the anterior pelvic region.

The inguinal canal contains the ilioinguinal nerve, which is responsible for radiation of pain to the anterior hip. The hip joint itself is a spheroid comprising the femoral head and acetabulum, with most of the articular hip innervated by the femoral or obturator nerves.

Most intra-articular conditions radiate to the anterior groin or hip, although there are cases in which the pain is referred to either the lateral aspect of the hip or the buttocks. The iliopsoas muscle is the major hip flexor, and crosses under the ilioinguinal ligament to insert on the lesser tuberosity after crossing over the anterior capsule of the hip. A large bursa surrounds it, helping the tendon glide smoothly over the hip.

CASE Mack Q, a 27-year-old man with an 8-month history of right hip pain, sought care at our medical center for an achy pain in his right groin; he also described an occasional “clicking and popping sensation” in his groin but denied any trauma. The pain worsened with prolonged sitting and certain activities, such as squatting, twisting, and putting on shoes and socks. Our patient had stopped playing soccer because it hurt too much. He had tried physical therapy, oral anti-inflammatories, and a corticosteroid injection, with little relief.

Start with a gait assessment
The physical examination should begin with a gait assessment. Consider the patient’s ability to bear weight and his or her foot angle.

An individual with a stress fracture will have difficulty bearing weight on the affected side, resulting in a limp, or antalgic gait. A patient with femoral acetabular impingement (FAI) will often exhibit greater external rotation of the foot on the affected side compared with the other foot. And a patient with weakened abductor muscles, typically because of severe osteoarthritis, will exhibit the Trendelenburg sign—a pelvic tilt when the weight is shifted to the affected extremity.

Although most individuals with hip pain will not have an obvious gait abnormality, any patient who walks with a limp or needs crutches requires an immediate referral to an orthopedic surgeon.

Include these elements in the physical exam
Examine the hip with the patient sitting on the side of the exam table. Assess range of motion (ROM), comparing the range of flexion, extension, and internal/external rotation on the affected and unaffected sides. Include the following maneuvers:

Impingement testing. In patients with FAI and osteoarthritis, impingement testing—encompassing Flexion, ADDuction, and Internal Rotation (FADDIR)—will elicit pain. The maneuver can be tested starting at 45° of hip flexion, increasing to approximately 120°. Pain with <45° of hip flexion indicates that the impingement is severe.

Such testing can also reveal labral tears, which may be caused by FAI or other structural abnormalities. In a patient with anterior labral tears, FADDIR will produce groin pain; posterior labral tears will produce pain when the patient is sitting with legs hanging off the exam table and the contralateral leg is brought to the chest and the affected limb fully extended.

In patients with hip pain and bursitis, applying downward pressure will elicit a snapping sound as the iliopsoas snaps over the iliopectineal eminence or femoral head. Flexion, ABduction, and External Rotation (FABER) can also be used to diagnose iliopsoas tendonitis: The test is positive if it elicits pain in the affected extremity or in the sacroiliac joint on the opposite side.

Log roll. A painful response to this test, which involves internally and externally rotating the affected hip while it is relaxed and the knee fully extended, is an indication of synovitis of the hip caused by intra-articular pathology. To test hip stability, externally rotate the leg while it is extended. If the hip is stable, the leg will return to a neutral position; microinstability of the hip is likely if the leg remains in the rotated position.

Muscular strength testing. To assess for tendinopathy in the hip area, the patient should be in a seated position and contract the internal and external rotators and the adductor muscles while you apply resistance. To test abductor strength, have the patient assume a lateral position and hold and abduct the leg on the affected side while you apply resistance.

Hip flexion strength should be tested with the patient in both supine and seated positions. A patient with quadriceps tendonitis will have much greater pain with resisted hip flexion in the supine position vs the seated position; the opposite is true for a patient with iliopsoas tendonitis. (See “Did you know…? Hip pain facts and findings” on for additional diagnostic tips.)

Perform a neurologic evaluation to rule out a back condition that might radiate pain into the anterior hip; ask the patient to do a sit-up while you apply resistance to test for abdominal wall pathology, as well.

Hip palpation. This aspect of the physical exam is important regardless of the cause of the pain but especially crucial for pediatric and adolescent patients, whose anterior hip pain may be related to apophyseal injury. Palpate the superior iliac spine (and over the inferior iliac spine in thin patients) to determine if the sartorius or rectus femoris has been injured. The area just lateral to the symphysis will be tender to palpation in patients with osteitis pubis.

Refer or treat? Here’s what to consider

While the history and physical should provide ample information for a differential diagnosis, imaging studies are generally required for confirmation. Clinical assessment— including physical exam, imaging, and intra-articular injection—of patients with hip pain is up to 98% accurate in identifying hip abnormalities, with arthroscopy as the gold standard.⁴

CASE On physical examination, Mr. Q had right hip extension to 0°, flexion to 110°, external rotation to 50°, and internal rotation to neutral; he also had positive impingement and subspine impingement tests, a painful arc of motion from 12 to 4 o’clock, tenderness over the hip adductor, and pain with resisted hip adduction. He did not walk with a limp.

Diagnostic studies included plain radiographs, which demonstrated that the joint space was well preserved. We identified subtle anatomical abnormalities on the femoral head-neck junction, known as a cam deformity. Magnetic resonance imaging (MRI) revealed an anterior superior labral tear with cartilage delamination.

Stress fractures affect runners, military recruits
In addition to long-distance runners who have recently increased the frequency, duration, or intensity of training,^5,6 military recruits have a higher incidence of stress fractures due to the rapid onset of intensive training. Stress fractures can also occur in patients who do not have a history of intense activity but have metabolically weakened bone, in some cases as a result of an eating disorder.⁷

Patients with femoral neck stress fractures typically present with activity-related anterior groin pain that is relieved by rest; initially, they may be only mildly affected, but the condition worsens in those who continue to “work through the pain.” By the time such individuals seek treatment, they almost always have pain with weight bearing and an antalgic gait.

Symptoms consistent with a femoral neck stress fracture can be further evaluated with plain radiographs. However, x-rays are often negative for up to 4 weeks after the onset of pain.⁸ In cases in which radiographs are negative but the physical exam is suggestive of a stress fracture, MRI—which can detect an abnormality within a day or 2 of injury^8,9—should be used to confirm the diagnosis (FIGURE 1).

FIGURE 1
MRI reveals a femoral neck stress fracture

Treatment. A complete femoral neck fracture portends impending displacement and requires emergent evaluation by an orthopedist, and superior neck changes, also known as tension-sided stress fractures, require urgent treatment with percutaneous screw fixation.⁹ However, compression-sided, or inferior, stress fractures can be treated with restricted weight bearing and activity modification. Gradual resumption of activity is allowed only after the patient has been asymptomatic for 6 weeks; recurrent pain indicates residual stress reaction, and signals that activities should be abated.

Osteonecrosis has many causes

Necrosis of the femoral head is a debilitating and progressive condition primarily affecting patients between the ages of 20 and 50 years.¹⁰ It has multiple (and diverse) causes, including trauma, steroids, alcohol, smoking, lupus, sickle cell anemia, and coagulopathies, as well as scuba diving. But about 20% of cases have no apparent cause.^11,12

Patients with osteonecrosis of the hip typically present with groin pain, often described as a deep, intermittent ache that interferes with activities of daily living. Exam findings depend on the stage of presentation. Early on, pain will occur only with extreme ROM; in advanced cases, ROM is restricted and pain occurs even with limited motion.

Femoral head collapse due to loss of the structural integrity of the subchondral bone—which occurs in 80% of cases¹²—is thought to be caused by decreased blood flow. Plain radiography can confirm a diagnosis of osteonecrosis in patients with advanced disease, but MRI is useful for evaluating patients with earlier clinical presentations.

Treatment of osteonecrosis is dictated by the stage of the disease, but remains controversial because no intervention has been shown to prevent progression in all cases.¹² All patients should be referred to a specialist. Those without collapse or cartilage damage can be treated surgically with core decompression, possibly with additional vascularized bone grafting,^13,14 while those with more advanced disease typically require a total hip replacement at a relatively young age. Results for total hip replacement in patients with osteonecrosis are thought to be inferior to hip replacement in patients with osteoarthritis, although comparison is difficult because of the differences in age and activity levels in these 2 groups.^15,16

Femoral acetabular impingement can occur on the cam or pincer side
FAI pathology can exist on either the femoral (cam) or acetabular (pincer) side,¹⁷ or both.¹⁸ In pure cam impingement, the anterior femoral neck loses its normal concave anatomy and develops a “bump,” which impinges on the anterosuperior labrum during hip flexion, causing labral tears and delamination of the adjacent cartilage.

Pure pincer impingement arises from a prominent acetabular rim, causing overcoverage of the femoral head. Acetabular labral tears result from the repetitive impaction with flexion and internal rotation.

Patients report an insidious onset of groin pain that is exacerbated by flexion-type sports, such as hockey, football, and golf,¹⁹ as well as activities of daily living. In patients with cartilage damage, even walking can be painful. Physical examination of patients with FAI reveals findings that are similar to those of patients with acetabular labral tears. Abnormally large cam lesions or acetabular overcoverage will result in restriction of hip ROM, especially internal rotation and flexion due to a mechanical block.

Radiographs (FIGURE 2) are essential to diagnose FAI and to distinguish this condition from an isolated labral tear.²⁰ Cam impingement will be best demonstrated on a cross-table lateral radiograph, which shows an asphericity of the femoral head/neck junction anteriorly, while pincer impingement will show overcoverage of the femoral head on an AP radiograph. MRI or magnetic resonance arthrography (MRA) is frequently obtained to see whether any cartilage deterioration has occurred. Computed tomography, which can provide a 3-dimensional reproduction of the hip morphology, is often used for preoperative planning when surgical intervention is required.

FIGURE 2
Femoral acetabular impingement with a prominent pincer lesion

Treatment. Surgical intervention is often needed to correct or remove the abnormal anatomy, and both arthroscopic and open surgery are recommended.²⁰ Both methods include osteoplasty at the femoral head/neck junction and/or the acetabular rim to allow the proximal femur to articulate with the acetabulum without injury to the labrum with flexion and internal rotation.²¹

Results of both open and arthroscopic osteoplasty of the femur and acetabulum are still preliminary, with only a few studies reporting mid-term results. Open surgery typically has longer recovery and rehabilitation, but advocates emphasize the improved ability to contour the femur or acetabulum. Both open and arthroscopic procedures have about an 8% to 13% rate of revision in short-term follow-up.¹⁷

Labral tears occur with trauma and certain sports

In addition to FAI, causes of labral tears include dysplasia, instability, trauma, and degeneration, as well as sports that require repetitive hip flexion and/or pivoting, such as hockey, soccer, and football.^22,23

Patients with labral tears typically present with anterior hip pain radiating to the groin, worsening with twisting motions, running, walking, and sitting for prolonged periods. Clicking or catching may occur, as well. Patients may exhibit what one researcher called the “c-sign”—so named for the shape patients make with their hand as they grip their hip just above the greater trochanter to indicate where it hurts.⁴ The work-up for labral tears includes radiographs and, often, MRA, which is nearly 100% specific.²⁴

Treatment. Conservative treatment, which may include activity modification or rest and ice, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy, is often effective for labral tears; when such measures fail, surgical intervention is indicated. A systematic review found a 67% satisfaction rate after 3.5 years in patients who had undergone labral debridement, and complete resolution of mechanical symptoms in nearly 50%.²⁵ Another study showed similar results for hip arthroscopy, with symptom relief continuing for 4.8 years after surgery, on average, and 84% of patients able to return to their previous level of activity.²⁶

The long-term results of labral debridement are unknown, however, and the possibility of an association between this procedure and the development of arthritis remains. Most specialists prefer anatomic repair to restore normal hip kinematics and, potentially, long-term hip function,^27,28 but structural abnormalities must also be addressed to prevent failure of the repair or recurrent tears.

Iliopsoas tendonitis: You know the snap
Often referred to as internal snapping of the hip or internal coxa saltans, iliopsoas tendonitis/bursitis can be a recalcitrant cause of anterior hip pain. Snapping of the iliopsoas leading to bursitis or tendonitis can occur at the iliopectineal eminence, the femoral head, or the lesser trochanter.²⁹ Runners and ballet dancers are often affected.^30,31

Snapping in itself is not an indication of pathology, but chronicity of symptoms is. Patients with relatively acute symptoms typically have only bursitis, while a longer duration of symptoms leads to tendonitis or tendinopathy.³²

Treatment. First-line therapy is nonoperative, and includes activity modification, rest, ice, NSAIDs, and physical therapy. Advise patients to refrain from activities causing pain, and to apply ice to the affected every 20 minutes (with a 20- to 30-minute off period) for one to 2 hours. Physical therapy focuses on stretching the iliopsoas and rectus femoris muscles and strengthening the hamstring muscles to relieve the stress on the anterior pelvis. If such treatment is unsuccessful, ultrasound can be used to guide a therapeutic injection of cortisone.³³ If this fails to bring relief, fractional lengthening of the iliopsoas tendon can be performed to eliminate snapping and relieve pain.³⁴

Muscular strains/avulsion fractures: Sports and age play a role
Although strains can affect any of the anterior muscles around the hip, in active individuals the adductors are most commonly affected. Skeletally immature patients are an exception: apophyseal fractures at the origin of the sartorius and rectus femoris muscles are more common than muscular strains in this patient population.

Athletes who experience adductor strains often play sports in which kicking or frequent changes in direction are required—eg, football, hockey, and soccer³⁵—and generally are able to tell you exactly what they were doing when the injury occurred. Physical examination can reveal focal findings, with swelling and tenderness confined to the anteromedial aspect of the hip along the adductor muscle group. MRI can help differentiate the site of true pathology.³⁶

Treatment of adductor strains is nonoperative, with rest, ice, and activity modification until the tendon heals. In the rare case in which complete tendon avulsion is found, surgical reattachment is needed.

Apophyseal fracture in skeletally immature patients typically occurs during participation in a sport that requires rapid acceleration and deceleration with the hip in an extended position. In such patients, stretching the affected muscle should reproduce the pain. Radiographs are diagnostic and will often show minimal displacement of the apophysis. Treatment is almost always nonoperative. Surgical intervention is rarely needed, and only indicated with displacement >2 cm.³⁷

Athletic pubalgia: A challenging Dx
Also referred to as sports hernia, athletic pubalgia is an enigmatic cause of anterior hip pain in athletes. Diagnosis can be especially challenging, and patients may have lingering symptoms for years before the cause is discovered.³⁸ A sports hernia, unlike other hernias, does not involve a bulge of tissue protruding through one body part into another. In contrast, a sports hernia occurs when the oblique abdominal muscles strain or completely tear away from the pubis. A recent systematic review found that the underlying etiology involves posterior inguinal wall weakening, which can be a result of poorly balanced hip adductor and abdominal muscle activation.³⁹

Patients with sports hernia will often present with anterior hip and/or groin pain, especially with hip extension, twisting, and turning. In addition, patients can have pain in the lower abdomen and, in males, in the testicles. Physical examination will usually show pubic point tenderness, which is exacerbated by resisted hip adduction.⁴⁰ MRI and ultrasound are extremely helpful in diagnosing and forming a treatment plan.³⁹

The initial treatment of choice for sports hernias is nonoperative, and the first step is always activity modification or temporary avoidance of symptom-producing activities. Additional modalities include NSAIDs, ice, and physical therapy to strengthen the surrounding muscles. Surgical intervention, if needed, may be done laparoscopically or via an open approach with direct repair.^40,41

Less common causes to consider
While the conditions detailed here account for most anterior hip etiologies, there are other less common causes to consider. One such cause is osteitis pubis, an umbrella term for conditions that affect the area surrounding the symphysis pubis. Patients with osteitis pubis present with pain over the anterior aspect of the pelvis that is worse with sit-ups, rising from a chair, or any activity where contraction of the rectus muscles occurs.²⁹ Tenderness is found directly over and just lateral to the pubic symphysis. Radiographs are frequently negative, but occasionally chronic degenerative changes at the symphysis are present in addition to symphyseal narrowing. Additional imaging is often necessary for diagnosis.

Neuropathies. When history, physical examination, and imaging studies have ruled out other causes, neuropathies (ilioinguinal, genitofemoral, and obturator) should be considered, particularly in patients with vague, radiating anterior hip and/or groin pain.⁴² In pediatric patients, Legg-Calve-Perthes disease and slipped capital femoral epiphysis are possibilities, as well.

Getting patients back on track

Rehabilitation after hip injury resulting in anterior hip pain will be determined by the site, type, and mechanism of injury, as well as the severity. Restrictions in weight bearing and the use of an assistive device may be needed to prevent excessive stress on bone and supporting soft-tissue structures in the early stages of healing. Physical therapy, as needed, should initially focus on early controlled ROM of the hip joint to prevent both intra- and extra-articular adhesions and excessive scar tissue formation.²

For patients who undergo surgery, much of the focus will be on strengthening the supporting musculature—the hip abductor group, anterior and posterior thigh musculature, and core stabilizing muscles. Neuromuscular training may be needed to promote normal biomechanics and minimize compensatory movement patterns. For athletes, cardiovascular training and a return-to-play program should be implemented, as well.^2,43,44

CASE Mr. Q was diagnosed with right hip pain due to a labral tear secondary to a cam femoral acetabular impingement. Given that he had failed nonoperative treatment and had long-standing pain, we recommended surgery for this patient. He underwent right hip arthroscopic labral repair, acetabular rim trimming, acetabular microfracture, femoral osteochondroplasty with capsular plication. At 12-month follow-up, he was doing well, with resolution of the presurgical pain and return to all athletic activities.

CORRESPONDENCE Rachel M. Frank, MD, Department of Orthopedic Surgery, Rush University Medical Center, 1611 West Harrison Street, Suite 300, Chicago, IL 60612; [email protected]

CASE Jane K, 52, comes to see you because of discomfort in her right wrist and tingling in her hand. The symptoms began 3 months ago, but have been getting progressively worse, and have started to interfere with her sleep. Ms. K often awakens with “pins and needles” in her hand, and says that she often has the urge to “shake it out.” Her sister has carpal tunnel syndrome (CTS), and Ms. K suspects that she does, too. On exam, you find that Ms. K has a positive Phalen’s and Durkan’s compression test, but normal Tinel’s test. She has normal strength and sensation in her hands. Her neck and upper extremity exam is otherwise unremarkable. You note that her hypothyroidism is well controlled, with a recent thyroid-stimulating hormone level of 1.2 mIU/L.

The patient has tried acetaminophen and ibuprofen, with little relief. She has researched CTS on the Internet and read about cold laser therapy, and wants to know whether you think it will work. What should you tell her?

Carpal tunnel syndrome is one of the most common disorders of the upper extremities and the most prevalent compression neuropathy.¹ About 3% of US adults are affected, typically those between the ages of 40 and 60 years.² Women are almost 3 times more likely than men to develop CTS.¹

Other risk factors include diabetes, hypothyroidism, rheumatoid arthritis, pregnancy, obesity, family history, and trauma. A history of hand-related repetitive motions also increases the risk.^3-5 Evidence does not support a definite link between keyboard or mouse use and CTS; however, occupations that require use of hand-operated vibratory tools or repeated and forceful movements of the hand/wrist (such as assembly work and food processing or packaging) are associated with CTS.⁶

The optimal diagnostic approach incorporates history and physical exam findings, including the results of a number of provocative maneuvers, as well as electrodiagnostic studies (EDS) in some cases.⁷ While surgery is the definitive treatment for CTS, numerous nonsurgical options exist, including splinting, corticosteroids, and a variety of alternative therapies, some of which (eg, chiropractic and cold laser therapy) have little evidence to support them.

Because family physicians are often the first to see patients with symptoms associated with CTS, you need to know what to look for, when to test, and whether to provide treatment or a referral. Here’s what to keep in mind.

Clinical presentation of CTS

Increased pressure in the carpal tunnel compresses the median nerve, leading to numbness, tingling, or pain in the palmar aspect of the first 3 fingers and the radial half of the fourth (FIGURE). Symptoms vary widely, with pain or numbness localized to the hand or wrist in some cases and pain radiating into the forearm or shoulder in others.

Figure
Compressed median nerve leads to numbness and tingling

Early in the course of CTS, symptoms are often most bothersome at night. In a scenario like that reported by Ms. K, patients are often awakened by numbness or tingling and the desire to shake out the affected hand—a phenomenon known as the flick sign.⁸ Pain and numbness may occur intermittently at first, especially with repetitive wrist motion. Activities such as driving or holding a telephone often aggravate symptoms.

As CTS progresses, the intensity and duration of symptoms increase. Patients may complain of weakness in the hand and report that they often drop things. Paradoxically, patients with more severe CTS sometimes have less pain, rather than more, because of increasing sensory loss.⁹

Late in the course of CTS, physical exam findings typically include decreased sensation in the fingers innervated by the median nerve, sparing the thenar eminence. (A loss of sensation in the thenar eminence suggests the presence of a lesion proximal to the carpal tunnel, rather than CTS itself.¹⁰) In advanced cases, weakness of thumb abduction and opposition may occur, as well as atrophy of the thenar eminence.¹¹

Sudden onset of severe symptoms with minimal trauma to the wrist should raise suspicion of a hematoma in the carpal tunnel—a particular risk for patients who have a clotting disorder or are being treated with newer anticoagulants such as dabigatran. Prompt surgical decompression is required to prevent permanent median nerve damage in such cases.¹²

Include these maneuvers in the physical exam

A thorough evaluation of the neck, shoulder, elbow, and wrist is crucial for all patients with signs and symptoms associated with CTS. Provocative maneuvers (TABLE 1)^7,13 are also important as an aid to diagnosis. The results of the following tests should be viewed with caution, however, as studies have found wide variations in their sensitivity and specificity:

TABLE 1
Diagnosing carpal tunnel syndrome, using physical maneuvers^7,13

Phalen’s maneuver. The patient flexes his or her wrist with the elbow in full extension to increase pressure on the median nerve, and holds the position for 60 seconds. The onset of pain or paresthesia is a positive test. A meta-analysis found the sensitivity and specificity of a positive Phalen’s sign to be 68% and 73%, respectively.⁷

Tinel’s test. Tap the volar surface of the patient’s wrist just proximal to, or on top of, the carpal tunnel. Pain or paresthesia in the fingers innervated by the median nerve as a result of the percussion constitutes a positive result. Tinel’s test is less sensitive than the Phalen’s maneuver, but has a similar specificity.¹³

The median nerve (Durkan’s) compression test. Apply pressure over the transverse carpal ligament; the test is positive if pain or paresthesia develops within 30 seconds.⁷

The hand elevation test. The patient raises both hands overhead for 60 seconds; here, too, pain or paresthesia is a positive result.¹⁴

Combining results of provocative maneuvers may increase sensitivity and specificity. Positive results in both the Phalen’s and median nerve compression tests, for example, have a collective sensitivity and specificity of 80% and 92%, respectively.¹³

When (or whether) to order electrodiagnostic studies

While some clinicians consider EDS to be the gold standard in CTS diagnosis,⁶ evidence is limited. One issue is the lack of universally accepted reference standards; another is that most studies have been affected by “spectrum bias.”¹⁵ What’s more, EDS—which include nerve conduction studies (NCS) and electromyography (EMG)—do not always correlate directly with symptoms, and 16% to 34% of mild cases can be missed.¹⁶

EDS are useful in many instances, however. EMG can rule out other causes of CTS symptoms (TABLE 2 details the differential diagnosis),^7,11 while NCS can aid in diagnosing CTS, gauging its severity, and arriving at a prognosis. Specifically, NCS can detect delayed distal latencies and slowed conduction velocities that can occur when the myelin sheath is damaged by prolonged compression of the median nerve.¹⁷ With more severe compression, axonal damage occurs, as evidenced by reduced action potential amplitudes on NCS. Results of the nerve conduction tests are compared to age-dependent normal values and to results from other nerves on either the same or the contralateral hand. In a 2002 systemic review, the sensitivity of NCS for CTS was 56% to 85% and the specificity was 94% to 99%.¹⁸

TABLE 2
Differential diagnosis for CTS^7,11

Before and after surgery. The American Academy of Orthopedic Surgeons (AAOS) recommends EDS when CTS surgery is being considered. ⁷ EDS may also be used after surgery, to verify neurologic improvement.

Ultrasound. In patients with CTS, ultrasound reveals an increased cross-sectional area of the median nerve, a finding that has prompted studies of this modality as a diagnostic tool.¹⁹ Although evidence suggests that ultrasound’s sensitivity and specificity for CTS would be similar to that of EDS, the optimal cutoff for an abnormal test has not been defined,¹⁹ and ultrasound does not provide information on prognosis or alternate causes.

Thus, AAOS does not currently recommend ultrasound for CTS diagnosis.⁷ Magnetic resonance imaging is inappropriate for routine CTS diagnosis, as well.⁷

Treatment: Start conservatively

Multiple nonsurgical options are available, but the best evidence supports splinting, steroid injection, and oral steroids. Splinting or steroids alone may bring long-term relief for patients with mild to moderate cases;²⁰ in fact, about a third of mild cases improve spontaneously.²¹

Conservative therapy can also provide relief for those who wish to avoid or delay surgery and for cases of transient CTS (pediatric patients, for example, or those whose condition is associated with pregnancy or hypothyroidism).¹⁸ A successful response to therapy can also help to confirm a CTS diagnosis.

Most conservative treatments begin providing relief within 2 to 6 weeks and reach the maximal benefit at 3 months.²² If there is no response after 6 weeks, it’s time to consider another approach.

In initiating splinting or corticosteroids, here’s a look at what to keep in mind:

Splinting. A splint can be used to maintain the wrist in a position with the least intracanal pressure, thereby limiting pressure on the median nerve. Splinting is equally effective whether used continually or only at night.²³

Splinting can relieve symptoms and improve functional status within 2 weeks and the effects can last for 3 to 6 months, eliminating the need for surgery for some patients with mild CTS.^19,20 Nerve gliding exercises, (see image at left), have been evaluated in combination with splinting. While evidence is limited, an at-home program involving these simple exercises may be a beneficial adjunctive treatment with minimal cost or harm.^24,25

Local corticosteroid injection. A Cochrane meta-analysis found significant improvement in symptoms and function at one month among patients with CTS who were treated with steroid injection.²⁶ In many cases, the effects last for many months.

A recent trial found that nearly half of patients with mild to moderate CTS who were treated with steroid injections had improved symptoms and EDS results at the 12-month follow-up.²⁰ However, while patients with severe CTS experienced improvement at 4 weeks postinjection, most eventually required surgery.²⁰

Evidence does not support one particular steroid dose or formulation over another, or one particular injection site.²² Injecting 4 cm proximal to the wrist flexion crease is as effective as a more distal injection.^26,27

Caution is required, however, as risks associated with local injections include tendon rupture and median nerve injury. If a patient experiences intense pain or paresthesia in the median nerve distribution when the needle is inserted, redirect the needle away from the median nerve immediately. For patients who respond well to this treatment, one additional injection can be given after 6 months if symptoms recur.

Oral corticosteroids. Oral prednisone at a dose of 20 mg/d for 2 weeks improves symptoms and function in patients with CTS, but is less effective than steroid injections.²⁸ Treatment for 2 weeks is as effective as treatment for 4 weeks; the effects tend to wane after 8 weeks in both cases.²⁹ Nonsteroidal anti-inflammatory drugs, diuretics, and vitamin B6 have not been found to be effective.³⁰

CASE Ms. K also asks about “those needle tests”—a reference to EDS—which her sister had to diagnose her CTS. You explain that these studies are not necessary at this time because her symptoms are mild and there is no need for other causes to be ruled out.

Instead, you offer her a neutral wrist splint for night-time use and recommend home-based nerve glide exercises. There is no evidence that cold laser therapy is effective, you explain to Ms. K, and it is expensive. She agrees to try the splint and the exercises, and you schedule a follow-up visit in 6 weeks.

A look at alternative therapies
There are many nontraditional treatments for CTS, with yoga, carpal bone mobilization, ergonomic keyboards, and ultrasound therapy among them. Some have limited evidence to suggest that they may have a therapeutic effect;³⁰ others have little or no evidence to support them.

Yoga. Stretching and improved joint posture with specific yoga exercises may lead to decreased compression within the carpal tunnel and increased blood flow to the median nerve. One small study found that yoga was more effective than nocturnal wrist splinting for pain relief, and had similar improvement for nocturnal symptoms and grip strength.³¹

Carpal bone mobilization. One small study found this physical therapy technique, which involves movement of the bones in the wrist, to improve symptoms such as numbness and tingling after 3 weeks of therapy. Yet carpal bone mobilization did not relieve pain or help restore function.³²

Ergonomic keyboard. Patients who use computers at work may find that an ergonomic keyboard helps to relieve pain associated with CTS, compared with a standard keyboard.³³

Therapeutic ultrasound. A recent meta-analysis found that there is only poor-quality evidence for ultrasound as an effective treatment for CTS—a process in which a round-headed instrument applied to the skin delivers sound waves that are absorbed by underlying tissues in the carpal tunnel. And there is insufficient evidence for one type of ultrasound over another, or to suggest that ultrasound is more effective than other nonsurgical treatments.³⁴ Notably, ultrasound takes several weeks to provide a therapeutic benefit.

What about acupuncture? A recent trial found that acupuncture was no more effective than sham acupuncture in relieving symptoms of CTS in patients wearing wrist splints.³⁵ Magnet therapy, chiropractic, and cold laser therapy are not supported by evidence either.²⁸

Is the patient a candidate for surgery?

Carpal tunnel release provides good long-term outcomes for 70% to 90% of patients and is a cost-effective treatment.^36,37 Evidence supports a trial of conservative therapy, however, before considering surgery for patients with mild-to-moderate CTS.²² Future studies are needed to identify prognostic characteristics of patients most likely to respond to each type of intervention, and the optimal timing for surgical release.

Patients with severe CTS—with findings such as thenar atrophy, diminished hand function, and median nerve denervation—should be referred for surgery without delay. This recommendation is based on expert opinion, however, as most clinical trials comparing surgical vs nonsurgical treatment exclude those with severe CTS.³⁸

3 surgical techniques, and a novel approach
Surgical techniques include open, endoscopic, and minimal incision carpal tunnel release, with benefits and drawbacks for each. Compared with open release, for example, patients who undergo endoscopic release have less postoperative pain at 12 weeks, quicker return to work, and fewer wound complications, but are more likely to require surgical revision. And minimal incision release is associated with improved symptoms and function compared with open release.³⁸ However, there is no long-term evidence that any one of these 3 surgical approaches is more effective than another.³⁹

Percutaneous carpal tunnel release is a novel approach that may be offered in outpatient settings, with local anesthesia and ultrasound guidance to avoid median nerve damage.⁴⁰ Because studies of the safety and efficacy of percutaneous carpal tunnel release are limited, however, this approach is considered experimental.⁴¹ Percutaneous release is not a treatment recommended by the AAOS.³⁸

What to tell patients about postop care
Regardless of the method used for carpal tunnel release, most complications are minor—eg, a painful or hypertrophic scar, stiffness, swelling, and pain or tenderness on either side of the incision—and resolve within a few months.⁴² Advise patients not to continue to wear a wrist splint after surgery; doing so can cause stiffness or adhesions and may compromise surgical outcomes.⁴¹ Postoperatively, patients should be instructed to do nerve gliding exercises and to massage their scars, both of which they can safely do at home.⁴³

Patients can expect significant symptomatic improvement within 1 week of surgery, and most will be able to return to normal activities in 2 weeks.⁴⁴ Those with severe CTS should be warned, however, that it could take up to a year to determine the extent of recovery.²² Evidence suggests that from 3% to 19% of patients may have persistent or recurrent symptoms even after carpal tunnel release, with up to 12% requiring surgical revision.⁴⁵

CASE When Ms. K returns, she reports that while there has been some improvement, some activities—such as driving long distances and talking on the phone—still cause numbness and tingling. And, if she doesn’t wear the splint at night, she awakens with tingling in her hands. You discuss 2 options—continued conservative treatment with a local steroid injection, or EDS and surgical referral. The patient opts for the injection and continued use of the nocturnal wrist splint and exercises. When she returns in another 6 weeks, Ms. K reports significant improvement. You agree to stop the wrist splint and exercises and advise her to follow-up on an as-needed basis if the symptoms return.

CORRESPONDENCE Jennifer Wipperman, MD, MPH, Via Christi Family Medicine, 1121 S. Clifton, Wichita, KS 67218; [email protected]

CASE Jane K, 52, comes to see you because of discomfort in her right wrist and tingling in her hand. The symptoms began 3 months ago, but have been getting progressively worse, and have started to interfere with her sleep. Ms. K often awakens with “pins and needles” in her hand, and says that she often has the urge to “shake it out.” Her sister has carpal tunnel syndrome (CTS), and Ms. K suspects that she does, too. On exam, you find that Ms. K has a positive Phalen’s and Durkan’s compression test, but normal Tinel’s test. She has normal strength and sensation in her hands. Her neck and upper extremity exam is otherwise unremarkable. You note that her hypothyroidism is well controlled, with a recent thyroid-stimulating hormone level of 1.2 mIU/L.

The patient has tried acetaminophen and ibuprofen, with little relief. She has researched CTS on the Internet and read about cold laser therapy, and wants to know whether you think it will work. What should you tell her?

Carpal tunnel syndrome is one of the most common disorders of the upper extremities and the most prevalent compression neuropathy.¹ About 3% of US adults are affected, typically those between the ages of 40 and 60 years.² Women are almost 3 times more likely than men to develop CTS.¹

Other risk factors include diabetes, hypothyroidism, rheumatoid arthritis, pregnancy, obesity, family history, and trauma. A history of hand-related repetitive motions also increases the risk.^3-5 Evidence does not support a definite link between keyboard or mouse use and CTS; however, occupations that require use of hand-operated vibratory tools or repeated and forceful movements of the hand/wrist (such as assembly work and food processing or packaging) are associated with CTS.⁶

The optimal diagnostic approach incorporates history and physical exam findings, including the results of a number of provocative maneuvers, as well as electrodiagnostic studies (EDS) in some cases.⁷ While surgery is the definitive treatment for CTS, numerous nonsurgical options exist, including splinting, corticosteroids, and a variety of alternative therapies, some of which (eg, chiropractic and cold laser therapy) have little evidence to support them.

Because family physicians are often the first to see patients with symptoms associated with CTS, you need to know what to look for, when to test, and whether to provide treatment or a referral. Here’s what to keep in mind.

Clinical presentation of CTS

Increased pressure in the carpal tunnel compresses the median nerve, leading to numbness, tingling, or pain in the palmar aspect of the first 3 fingers and the radial half of the fourth (FIGURE). Symptoms vary widely, with pain or numbness localized to the hand or wrist in some cases and pain radiating into the forearm or shoulder in others.

Figure
Compressed median nerve leads to numbness and tingling

Early in the course of CTS, symptoms are often most bothersome at night. In a scenario like that reported by Ms. K, patients are often awakened by numbness or tingling and the desire to shake out the affected hand—a phenomenon known as the flick sign.⁸ Pain and numbness may occur intermittently at first, especially with repetitive wrist motion. Activities such as driving or holding a telephone often aggravate symptoms.

As CTS progresses, the intensity and duration of symptoms increase. Patients may complain of weakness in the hand and report that they often drop things. Paradoxically, patients with more severe CTS sometimes have less pain, rather than more, because of increasing sensory loss.⁹

Late in the course of CTS, physical exam findings typically include decreased sensation in the fingers innervated by the median nerve, sparing the thenar eminence. (A loss of sensation in the thenar eminence suggests the presence of a lesion proximal to the carpal tunnel, rather than CTS itself.¹⁰) In advanced cases, weakness of thumb abduction and opposition may occur, as well as atrophy of the thenar eminence.¹¹

Sudden onset of severe symptoms with minimal trauma to the wrist should raise suspicion of a hematoma in the carpal tunnel—a particular risk for patients who have a clotting disorder or are being treated with newer anticoagulants such as dabigatran. Prompt surgical decompression is required to prevent permanent median nerve damage in such cases.¹²

Include these maneuvers in the physical exam

A thorough evaluation of the neck, shoulder, elbow, and wrist is crucial for all patients with signs and symptoms associated with CTS. Provocative maneuvers (TABLE 1)^7,13 are also important as an aid to diagnosis. The results of the following tests should be viewed with caution, however, as studies have found wide variations in their sensitivity and specificity:

TABLE 1
Diagnosing carpal tunnel syndrome, using physical maneuvers^7,13

Phalen’s maneuver. The patient flexes his or her wrist with the elbow in full extension to increase pressure on the median nerve, and holds the position for 60 seconds. The onset of pain or paresthesia is a positive test. A meta-analysis found the sensitivity and specificity of a positive Phalen’s sign to be 68% and 73%, respectively.⁷

Tinel’s test. Tap the volar surface of the patient’s wrist just proximal to, or on top of, the carpal tunnel. Pain or paresthesia in the fingers innervated by the median nerve as a result of the percussion constitutes a positive result. Tinel’s test is less sensitive than the Phalen’s maneuver, but has a similar specificity.¹³

The median nerve (Durkan’s) compression test. Apply pressure over the transverse carpal ligament; the test is positive if pain or paresthesia develops within 30 seconds.⁷

The hand elevation test. The patient raises both hands overhead for 60 seconds; here, too, pain or paresthesia is a positive result.¹⁴

Combining results of provocative maneuvers may increase sensitivity and specificity. Positive results in both the Phalen’s and median nerve compression tests, for example, have a collective sensitivity and specificity of 80% and 92%, respectively.¹³

When (or whether) to order electrodiagnostic studies

While some clinicians consider EDS to be the gold standard in CTS diagnosis,⁶ evidence is limited. One issue is the lack of universally accepted reference standards; another is that most studies have been affected by “spectrum bias.”¹⁵ What’s more, EDS—which include nerve conduction studies (NCS) and electromyography (EMG)—do not always correlate directly with symptoms, and 16% to 34% of mild cases can be missed.¹⁶

EDS are useful in many instances, however. EMG can rule out other causes of CTS symptoms (TABLE 2 details the differential diagnosis),^7,11 while NCS can aid in diagnosing CTS, gauging its severity, and arriving at a prognosis. Specifically, NCS can detect delayed distal latencies and slowed conduction velocities that can occur when the myelin sheath is damaged by prolonged compression of the median nerve.¹⁷ With more severe compression, axonal damage occurs, as evidenced by reduced action potential amplitudes on NCS. Results of the nerve conduction tests are compared to age-dependent normal values and to results from other nerves on either the same or the contralateral hand. In a 2002 systemic review, the sensitivity of NCS for CTS was 56% to 85% and the specificity was 94% to 99%.¹⁸

TABLE 2
Differential diagnosis for CTS^7,11

Before and after surgery. The American Academy of Orthopedic Surgeons (AAOS) recommends EDS when CTS surgery is being considered. ⁷ EDS may also be used after surgery, to verify neurologic improvement.

Ultrasound. In patients with CTS, ultrasound reveals an increased cross-sectional area of the median nerve, a finding that has prompted studies of this modality as a diagnostic tool.¹⁹ Although evidence suggests that ultrasound’s sensitivity and specificity for CTS would be similar to that of EDS, the optimal cutoff for an abnormal test has not been defined,¹⁹ and ultrasound does not provide information on prognosis or alternate causes.

Thus, AAOS does not currently recommend ultrasound for CTS diagnosis.⁷ Magnetic resonance imaging is inappropriate for routine CTS diagnosis, as well.⁷

Treatment: Start conservatively

Multiple nonsurgical options are available, but the best evidence supports splinting, steroid injection, and oral steroids. Splinting or steroids alone may bring long-term relief for patients with mild to moderate cases;²⁰ in fact, about a third of mild cases improve spontaneously.²¹

Conservative therapy can also provide relief for those who wish to avoid or delay surgery and for cases of transient CTS (pediatric patients, for example, or those whose condition is associated with pregnancy or hypothyroidism).¹⁸ A successful response to therapy can also help to confirm a CTS diagnosis.

Most conservative treatments begin providing relief within 2 to 6 weeks and reach the maximal benefit at 3 months.²² If there is no response after 6 weeks, it’s time to consider another approach.

In initiating splinting or corticosteroids, here’s a look at what to keep in mind:

Splinting. A splint can be used to maintain the wrist in a position with the least intracanal pressure, thereby limiting pressure on the median nerve. Splinting is equally effective whether used continually or only at night.²³

Splinting can relieve symptoms and improve functional status within 2 weeks and the effects can last for 3 to 6 months, eliminating the need for surgery for some patients with mild CTS.^19,20 Nerve gliding exercises, (see image at left), have been evaluated in combination with splinting. While evidence is limited, an at-home program involving these simple exercises may be a beneficial adjunctive treatment with minimal cost or harm.^24,25

Local corticosteroid injection. A Cochrane meta-analysis found significant improvement in symptoms and function at one month among patients with CTS who were treated with steroid injection.²⁶ In many cases, the effects last for many months.

A recent trial found that nearly half of patients with mild to moderate CTS who were treated with steroid injections had improved symptoms and EDS results at the 12-month follow-up.²⁰ However, while patients with severe CTS experienced improvement at 4 weeks postinjection, most eventually required surgery.²⁰

Evidence does not support one particular steroid dose or formulation over another, or one particular injection site.²² Injecting 4 cm proximal to the wrist flexion crease is as effective as a more distal injection.^26,27

Caution is required, however, as risks associated with local injections include tendon rupture and median nerve injury. If a patient experiences intense pain or paresthesia in the median nerve distribution when the needle is inserted, redirect the needle away from the median nerve immediately. For patients who respond well to this treatment, one additional injection can be given after 6 months if symptoms recur.

Oral corticosteroids. Oral prednisone at a dose of 20 mg/d for 2 weeks improves symptoms and function in patients with CTS, but is less effective than steroid injections.²⁸ Treatment for 2 weeks is as effective as treatment for 4 weeks; the effects tend to wane after 8 weeks in both cases.²⁹ Nonsteroidal anti-inflammatory drugs, diuretics, and vitamin B6 have not been found to be effective.³⁰

CASE Ms. K also asks about “those needle tests”—a reference to EDS—which her sister had to diagnose her CTS. You explain that these studies are not necessary at this time because her symptoms are mild and there is no need for other causes to be ruled out.

Instead, you offer her a neutral wrist splint for night-time use and recommend home-based nerve glide exercises. There is no evidence that cold laser therapy is effective, you explain to Ms. K, and it is expensive. She agrees to try the splint and the exercises, and you schedule a follow-up visit in 6 weeks.

A look at alternative therapies
There are many nontraditional treatments for CTS, with yoga, carpal bone mobilization, ergonomic keyboards, and ultrasound therapy among them. Some have limited evidence to suggest that they may have a therapeutic effect;³⁰ others have little or no evidence to support them.

Yoga. Stretching and improved joint posture with specific yoga exercises may lead to decreased compression within the carpal tunnel and increased blood flow to the median nerve. One small study found that yoga was more effective than nocturnal wrist splinting for pain relief, and had similar improvement for nocturnal symptoms and grip strength.³¹

Carpal bone mobilization. One small study found this physical therapy technique, which involves movement of the bones in the wrist, to improve symptoms such as numbness and tingling after 3 weeks of therapy. Yet carpal bone mobilization did not relieve pain or help restore function.³²

Ergonomic keyboard. Patients who use computers at work may find that an ergonomic keyboard helps to relieve pain associated with CTS, compared with a standard keyboard.³³

Therapeutic ultrasound. A recent meta-analysis found that there is only poor-quality evidence for ultrasound as an effective treatment for CTS—a process in which a round-headed instrument applied to the skin delivers sound waves that are absorbed by underlying tissues in the carpal tunnel. And there is insufficient evidence for one type of ultrasound over another, or to suggest that ultrasound is more effective than other nonsurgical treatments.³⁴ Notably, ultrasound takes several weeks to provide a therapeutic benefit.

What about acupuncture? A recent trial found that acupuncture was no more effective than sham acupuncture in relieving symptoms of CTS in patients wearing wrist splints.³⁵ Magnet therapy, chiropractic, and cold laser therapy are not supported by evidence either.²⁸

Is the patient a candidate for surgery?

Carpal tunnel release provides good long-term outcomes for 70% to 90% of patients and is a cost-effective treatment.^36,37 Evidence supports a trial of conservative therapy, however, before considering surgery for patients with mild-to-moderate CTS.²² Future studies are needed to identify prognostic characteristics of patients most likely to respond to each type of intervention, and the optimal timing for surgical release.

Patients with severe CTS—with findings such as thenar atrophy, diminished hand function, and median nerve denervation—should be referred for surgery without delay. This recommendation is based on expert opinion, however, as most clinical trials comparing surgical vs nonsurgical treatment exclude those with severe CTS.³⁸

3 surgical techniques, and a novel approach
Surgical techniques include open, endoscopic, and minimal incision carpal tunnel release, with benefits and drawbacks for each. Compared with open release, for example, patients who undergo endoscopic release have less postoperative pain at 12 weeks, quicker return to work, and fewer wound complications, but are more likely to require surgical revision. And minimal incision release is associated with improved symptoms and function compared with open release.³⁸ However, there is no long-term evidence that any one of these 3 surgical approaches is more effective than another.³⁹

Percutaneous carpal tunnel release is a novel approach that may be offered in outpatient settings, with local anesthesia and ultrasound guidance to avoid median nerve damage.⁴⁰ Because studies of the safety and efficacy of percutaneous carpal tunnel release are limited, however, this approach is considered experimental.⁴¹ Percutaneous release is not a treatment recommended by the AAOS.³⁸

What to tell patients about postop care
Regardless of the method used for carpal tunnel release, most complications are minor—eg, a painful or hypertrophic scar, stiffness, swelling, and pain or tenderness on either side of the incision—and resolve within a few months.⁴² Advise patients not to continue to wear a wrist splint after surgery; doing so can cause stiffness or adhesions and may compromise surgical outcomes.⁴¹ Postoperatively, patients should be instructed to do nerve gliding exercises and to massage their scars, both of which they can safely do at home.⁴³

Patients can expect significant symptomatic improvement within 1 week of surgery, and most will be able to return to normal activities in 2 weeks.⁴⁴ Those with severe CTS should be warned, however, that it could take up to a year to determine the extent of recovery.²² Evidence suggests that from 3% to 19% of patients may have persistent or recurrent symptoms even after carpal tunnel release, with up to 12% requiring surgical revision.⁴⁵

CASE When Ms. K returns, she reports that while there has been some improvement, some activities—such as driving long distances and talking on the phone—still cause numbness and tingling. And, if she doesn’t wear the splint at night, she awakens with tingling in her hands. You discuss 2 options—continued conservative treatment with a local steroid injection, or EDS and surgical referral. The patient opts for the injection and continued use of the nocturnal wrist splint and exercises. When she returns in another 6 weeks, Ms. K reports significant improvement. You agree to stop the wrist splint and exercises and advise her to follow-up on an as-needed basis if the symptoms return.

CORRESPONDENCE Jennifer Wipperman, MD, MPH, Via Christi Family Medicine, 1121 S. Clifton, Wichita, KS 67218; [email protected]

CASE Jane K, 52, comes to see you because of discomfort in her right wrist and tingling in her hand. The symptoms began 3 months ago, but have been getting progressively worse, and have started to interfere with her sleep. Ms. K often awakens with “pins and needles” in her hand, and says that she often has the urge to “shake it out.” Her sister has carpal tunnel syndrome (CTS), and Ms. K suspects that she does, too. On exam, you find that Ms. K has a positive Phalen’s and Durkan’s compression test, but normal Tinel’s test. She has normal strength and sensation in her hands. Her neck and upper extremity exam is otherwise unremarkable. You note that her hypothyroidism is well controlled, with a recent thyroid-stimulating hormone level of 1.2 mIU/L.

The patient has tried acetaminophen and ibuprofen, with little relief. She has researched CTS on the Internet and read about cold laser therapy, and wants to know whether you think it will work. What should you tell her?

Carpal tunnel syndrome is one of the most common disorders of the upper extremities and the most prevalent compression neuropathy.¹ About 3% of US adults are affected, typically those between the ages of 40 and 60 years.² Women are almost 3 times more likely than men to develop CTS.¹

Other risk factors include diabetes, hypothyroidism, rheumatoid arthritis, pregnancy, obesity, family history, and trauma. A history of hand-related repetitive motions also increases the risk.^3-5 Evidence does not support a definite link between keyboard or mouse use and CTS; however, occupations that require use of hand-operated vibratory tools or repeated and forceful movements of the hand/wrist (such as assembly work and food processing or packaging) are associated with CTS.⁶

The optimal diagnostic approach incorporates history and physical exam findings, including the results of a number of provocative maneuvers, as well as electrodiagnostic studies (EDS) in some cases.⁷ While surgery is the definitive treatment for CTS, numerous nonsurgical options exist, including splinting, corticosteroids, and a variety of alternative therapies, some of which (eg, chiropractic and cold laser therapy) have little evidence to support them.

Because family physicians are often the first to see patients with symptoms associated with CTS, you need to know what to look for, when to test, and whether to provide treatment or a referral. Here’s what to keep in mind.

Clinical presentation of CTS

Increased pressure in the carpal tunnel compresses the median nerve, leading to numbness, tingling, or pain in the palmar aspect of the first 3 fingers and the radial half of the fourth (FIGURE). Symptoms vary widely, with pain or numbness localized to the hand or wrist in some cases and pain radiating into the forearm or shoulder in others.

Figure
Compressed median nerve leads to numbness and tingling

Early in the course of CTS, symptoms are often most bothersome at night. In a scenario like that reported by Ms. K, patients are often awakened by numbness or tingling and the desire to shake out the affected hand—a phenomenon known as the flick sign.⁸ Pain and numbness may occur intermittently at first, especially with repetitive wrist motion. Activities such as driving or holding a telephone often aggravate symptoms.

As CTS progresses, the intensity and duration of symptoms increase. Patients may complain of weakness in the hand and report that they often drop things. Paradoxically, patients with more severe CTS sometimes have less pain, rather than more, because of increasing sensory loss.⁹

Late in the course of CTS, physical exam findings typically include decreased sensation in the fingers innervated by the median nerve, sparing the thenar eminence. (A loss of sensation in the thenar eminence suggests the presence of a lesion proximal to the carpal tunnel, rather than CTS itself.¹⁰) In advanced cases, weakness of thumb abduction and opposition may occur, as well as atrophy of the thenar eminence.¹¹

Sudden onset of severe symptoms with minimal trauma to the wrist should raise suspicion of a hematoma in the carpal tunnel—a particular risk for patients who have a clotting disorder or are being treated with newer anticoagulants such as dabigatran. Prompt surgical decompression is required to prevent permanent median nerve damage in such cases.¹²

Include these maneuvers in the physical exam

A thorough evaluation of the neck, shoulder, elbow, and wrist is crucial for all patients with signs and symptoms associated with CTS. Provocative maneuvers (TABLE 1)^7,13 are also important as an aid to diagnosis. The results of the following tests should be viewed with caution, however, as studies have found wide variations in their sensitivity and specificity:

TABLE 1
Diagnosing carpal tunnel syndrome, using physical maneuvers^7,13

Phalen’s maneuver. The patient flexes his or her wrist with the elbow in full extension to increase pressure on the median nerve, and holds the position for 60 seconds. The onset of pain or paresthesia is a positive test. A meta-analysis found the sensitivity and specificity of a positive Phalen’s sign to be 68% and 73%, respectively.⁷

Tinel’s test. Tap the volar surface of the patient’s wrist just proximal to, or on top of, the carpal tunnel. Pain or paresthesia in the fingers innervated by the median nerve as a result of the percussion constitutes a positive result. Tinel’s test is less sensitive than the Phalen’s maneuver, but has a similar specificity.¹³

The median nerve (Durkan’s) compression test. Apply pressure over the transverse carpal ligament; the test is positive if pain or paresthesia develops within 30 seconds.⁷

The hand elevation test. The patient raises both hands overhead for 60 seconds; here, too, pain or paresthesia is a positive result.¹⁴

Combining results of provocative maneuvers may increase sensitivity and specificity. Positive results in both the Phalen’s and median nerve compression tests, for example, have a collective sensitivity and specificity of 80% and 92%, respectively.¹³

When (or whether) to order electrodiagnostic studies

While some clinicians consider EDS to be the gold standard in CTS diagnosis,⁶ evidence is limited. One issue is the lack of universally accepted reference standards; another is that most studies have been affected by “spectrum bias.”¹⁵ What’s more, EDS—which include nerve conduction studies (NCS) and electromyography (EMG)—do not always correlate directly with symptoms, and 16% to 34% of mild cases can be missed.¹⁶

EDS are useful in many instances, however. EMG can rule out other causes of CTS symptoms (TABLE 2 details the differential diagnosis),^7,11 while NCS can aid in diagnosing CTS, gauging its severity, and arriving at a prognosis. Specifically, NCS can detect delayed distal latencies and slowed conduction velocities that can occur when the myelin sheath is damaged by prolonged compression of the median nerve.¹⁷ With more severe compression, axonal damage occurs, as evidenced by reduced action potential amplitudes on NCS. Results of the nerve conduction tests are compared to age-dependent normal values and to results from other nerves on either the same or the contralateral hand. In a 2002 systemic review, the sensitivity of NCS for CTS was 56% to 85% and the specificity was 94% to 99%.¹⁸

TABLE 2
Differential diagnosis for CTS^7,11

Before and after surgery. The American Academy of Orthopedic Surgeons (AAOS) recommends EDS when CTS surgery is being considered. ⁷ EDS may also be used after surgery, to verify neurologic improvement.

Ultrasound. In patients with CTS, ultrasound reveals an increased cross-sectional area of the median nerve, a finding that has prompted studies of this modality as a diagnostic tool.¹⁹ Although evidence suggests that ultrasound’s sensitivity and specificity for CTS would be similar to that of EDS, the optimal cutoff for an abnormal test has not been defined,¹⁹ and ultrasound does not provide information on prognosis or alternate causes.

Thus, AAOS does not currently recommend ultrasound for CTS diagnosis.⁷ Magnetic resonance imaging is inappropriate for routine CTS diagnosis, as well.⁷

Treatment: Start conservatively

Multiple nonsurgical options are available, but the best evidence supports splinting, steroid injection, and oral steroids. Splinting or steroids alone may bring long-term relief for patients with mild to moderate cases;²⁰ in fact, about a third of mild cases improve spontaneously.²¹

Conservative therapy can also provide relief for those who wish to avoid or delay surgery and for cases of transient CTS (pediatric patients, for example, or those whose condition is associated with pregnancy or hypothyroidism).¹⁸ A successful response to therapy can also help to confirm a CTS diagnosis.

Most conservative treatments begin providing relief within 2 to 6 weeks and reach the maximal benefit at 3 months.²² If there is no response after 6 weeks, it’s time to consider another approach.

In initiating splinting or corticosteroids, here’s a look at what to keep in mind:

Splinting. A splint can be used to maintain the wrist in a position with the least intracanal pressure, thereby limiting pressure on the median nerve. Splinting is equally effective whether used continually or only at night.²³

Splinting can relieve symptoms and improve functional status within 2 weeks and the effects can last for 3 to 6 months, eliminating the need for surgery for some patients with mild CTS.^19,20 Nerve gliding exercises, (see image at left), have been evaluated in combination with splinting. While evidence is limited, an at-home program involving these simple exercises may be a beneficial adjunctive treatment with minimal cost or harm.^24,25

Local corticosteroid injection. A Cochrane meta-analysis found significant improvement in symptoms and function at one month among patients with CTS who were treated with steroid injection.²⁶ In many cases, the effects last for many months.

A recent trial found that nearly half of patients with mild to moderate CTS who were treated with steroid injections had improved symptoms and EDS results at the 12-month follow-up.²⁰ However, while patients with severe CTS experienced improvement at 4 weeks postinjection, most eventually required surgery.²⁰

Evidence does not support one particular steroid dose or formulation over another, or one particular injection site.²² Injecting 4 cm proximal to the wrist flexion crease is as effective as a more distal injection.^26,27

Caution is required, however, as risks associated with local injections include tendon rupture and median nerve injury. If a patient experiences intense pain or paresthesia in the median nerve distribution when the needle is inserted, redirect the needle away from the median nerve immediately. For patients who respond well to this treatment, one additional injection can be given after 6 months if symptoms recur.

Oral corticosteroids. Oral prednisone at a dose of 20 mg/d for 2 weeks improves symptoms and function in patients with CTS, but is less effective than steroid injections.²⁸ Treatment for 2 weeks is as effective as treatment for 4 weeks; the effects tend to wane after 8 weeks in both cases.²⁹ Nonsteroidal anti-inflammatory drugs, diuretics, and vitamin B6 have not been found to be effective.³⁰

CASE Ms. K also asks about “those needle tests”—a reference to EDS—which her sister had to diagnose her CTS. You explain that these studies are not necessary at this time because her symptoms are mild and there is no need for other causes to be ruled out.

Instead, you offer her a neutral wrist splint for night-time use and recommend home-based nerve glide exercises. There is no evidence that cold laser therapy is effective, you explain to Ms. K, and it is expensive. She agrees to try the splint and the exercises, and you schedule a follow-up visit in 6 weeks.

A look at alternative therapies
There are many nontraditional treatments for CTS, with yoga, carpal bone mobilization, ergonomic keyboards, and ultrasound therapy among them. Some have limited evidence to suggest that they may have a therapeutic effect;³⁰ others have little or no evidence to support them.

Yoga. Stretching and improved joint posture with specific yoga exercises may lead to decreased compression within the carpal tunnel and increased blood flow to the median nerve. One small study found that yoga was more effective than nocturnal wrist splinting for pain relief, and had similar improvement for nocturnal symptoms and grip strength.³¹

Carpal bone mobilization. One small study found this physical therapy technique, which involves movement of the bones in the wrist, to improve symptoms such as numbness and tingling after 3 weeks of therapy. Yet carpal bone mobilization did not relieve pain or help restore function.³²

Ergonomic keyboard. Patients who use computers at work may find that an ergonomic keyboard helps to relieve pain associated with CTS, compared with a standard keyboard.³³

Therapeutic ultrasound. A recent meta-analysis found that there is only poor-quality evidence for ultrasound as an effective treatment for CTS—a process in which a round-headed instrument applied to the skin delivers sound waves that are absorbed by underlying tissues in the carpal tunnel. And there is insufficient evidence for one type of ultrasound over another, or to suggest that ultrasound is more effective than other nonsurgical treatments.³⁴ Notably, ultrasound takes several weeks to provide a therapeutic benefit.

What about acupuncture? A recent trial found that acupuncture was no more effective than sham acupuncture in relieving symptoms of CTS in patients wearing wrist splints.³⁵ Magnet therapy, chiropractic, and cold laser therapy are not supported by evidence either.²⁸

Is the patient a candidate for surgery?

Carpal tunnel release provides good long-term outcomes for 70% to 90% of patients and is a cost-effective treatment.^36,37 Evidence supports a trial of conservative therapy, however, before considering surgery for patients with mild-to-moderate CTS.²² Future studies are needed to identify prognostic characteristics of patients most likely to respond to each type of intervention, and the optimal timing for surgical release.

Patients with severe CTS—with findings such as thenar atrophy, diminished hand function, and median nerve denervation—should be referred for surgery without delay. This recommendation is based on expert opinion, however, as most clinical trials comparing surgical vs nonsurgical treatment exclude those with severe CTS.³⁸

3 surgical techniques, and a novel approach
Surgical techniques include open, endoscopic, and minimal incision carpal tunnel release, with benefits and drawbacks for each. Compared with open release, for example, patients who undergo endoscopic release have less postoperative pain at 12 weeks, quicker return to work, and fewer wound complications, but are more likely to require surgical revision. And minimal incision release is associated with improved symptoms and function compared with open release.³⁸ However, there is no long-term evidence that any one of these 3 surgical approaches is more effective than another.³⁹

Percutaneous carpal tunnel release is a novel approach that may be offered in outpatient settings, with local anesthesia and ultrasound guidance to avoid median nerve damage.⁴⁰ Because studies of the safety and efficacy of percutaneous carpal tunnel release are limited, however, this approach is considered experimental.⁴¹ Percutaneous release is not a treatment recommended by the AAOS.³⁸

What to tell patients about postop care
Regardless of the method used for carpal tunnel release, most complications are minor—eg, a painful or hypertrophic scar, stiffness, swelling, and pain or tenderness on either side of the incision—and resolve within a few months.⁴² Advise patients not to continue to wear a wrist splint after surgery; doing so can cause stiffness or adhesions and may compromise surgical outcomes.⁴¹ Postoperatively, patients should be instructed to do nerve gliding exercises and to massage their scars, both of which they can safely do at home.⁴³

Patients can expect significant symptomatic improvement within 1 week of surgery, and most will be able to return to normal activities in 2 weeks.⁴⁴ Those with severe CTS should be warned, however, that it could take up to a year to determine the extent of recovery.²² Evidence suggests that from 3% to 19% of patients may have persistent or recurrent symptoms even after carpal tunnel release, with up to 12% requiring surgical revision.⁴⁵

CASE When Ms. K returns, she reports that while there has been some improvement, some activities—such as driving long distances and talking on the phone—still cause numbness and tingling. And, if she doesn’t wear the splint at night, she awakens with tingling in her hands. You discuss 2 options—continued conservative treatment with a local steroid injection, or EDS and surgical referral. The patient opts for the injection and continued use of the nocturnal wrist splint and exercises. When she returns in another 6 weeks, Ms. K reports significant improvement. You agree to stop the wrist splint and exercises and advise her to follow-up on an as-needed basis if the symptoms return.

CORRESPONDENCE Jennifer Wipperman, MD, MPH, Via Christi Family Medicine, 1121 S. Clifton, Wichita, KS 67218; [email protected]

CASE Harry J is a 57-year-old man who came to us for evaluation and management of hypertension. He also complained of chronic headaches. Our initial examination revealed a body mass index (BMI) of 29 kg/m² and blood pressure (BP) of 150/100 mm Hg. The hypertension responded well to a combination of valsartan and hydrochlorothiazide. A few months later, he developed left breast soreness, as well as decreased libido. Examination revealed a round movable subareolar nodule 2 cm in diameter, with no associated skin changes or lymphadenopathy. Laboratory results were: total testosterone, 106 ng/dL (normal, 241-827); free testosterone, 23 pg/mL (47-244); thyroid-stimulating hormone (TSH), 2.222 mIU/mL (0.350-5.500); and prolactin, 102.7 ng/mL (2.1-17.7). Magnetic resonance imaging (MRI) of the brain revealed a nodular density <10 mm in the pituitary gland with minimal displacement of the stalk, consistent with a microadenoma.

Enlargement of the male breasts—gynecomastia—is caused by a benign proliferation of the ductal epithelium, due to a relative increase in the ratio of free estrogen to androgen locally in the breast. Gynecomastia of recent onset is often associated with pain and tenderness, as was the case with our patient.

Often self-limiting, age-related influences. Gynecomastia is common in newborns, during adolescence, and in old age.¹ In both male and female newborns, maternal and placental estrogens induce bilateral proliferation of breast tissue. This resolves within a few weeks after birth. During the early stages of male puberty, there is a relative increase in estrogens derived mostly from peripheral aromatization of testicular and adrenal androgens. If gynecomastia results, it usually regresses spontaneously as testicular testosterone production increases in late puberty.² Gynecomastia is also common in elderly men due to a decrease in testosterone production and an increase in sex hormone binding globulin (SHBG) that lowers free testosterone levels.

Deleterious contributing factors. Several other potential causes of gynecomastia exist (TABLE 1),^3,4 and these can usually be identified with a systematic approach using a careful history, physical examination, and selected laboratory studies. Many medications are associated with gynecomastia (TABLE 2),⁵ one of the most common being spironolactone due to its antiandrogenic activity at the receptor level.⁵ Some drugs, although associated with gynecomastia, cannot be linked to a direct cause-and-effect mechanism. These factors are compounded in elderly, obese men who take medications such as spironolactone, known to cause gynecomastia.

TABLE 1
Causes of gynecomastia^3,4

TABLE 2
Drugs associated with gynecomastia⁵

A patient’s medical history may reveal chronic conditions associated with gynecomastia. Such disorders include cirrhosis, hyperthyroidism, malnutrition, and chronic kidney disease. Rarely, gynecomastia can be a manifestation of a testicular, adrenal, or other neoplasm.

Despite a thorough evaluation, no detectable abnormality is found initially in 25% of gynecomastia cases.⁶ Close observation and monitoring is necessary in such instances, to ensure the earliest possible identification of the underlying cause and initiation of appropriate medical or surgical therapy.

First steps in the clinical evaluation

In cases of male breast enlargement, first determine whether you are dealing with true gynecomastia or “pseudogynecomastia,” which involves increased fat deposits typically seen in obese individuals.³ In cases of pseudogynecomastia, the tissue is uniformly enlarged and soft, with the same consistency as adipose tissue.

In about half of the cases of gynecomastia, the condition is bilateral.³ It is characteristically a rubbery or firm mass concentric with the nipple-areolar complex.

Clues to look for in the history. When examination suggests true gynecomastia, conduct a focused history to determine if medications or other substances might be causing the problem. (See “A case where drug therapy was to blame”) Some plant-derived oils used as skin care products have also been associated with gynecomastia due to weak estrogenic or anti-androgenic activity.⁷

The history may also uncover significant weight gain, because obesity is associated with increased aromatase activity resulting in a relative increase in estrogens systemically and locally in the breast. When obesity is the cause of gynecomastia, the breast examination reveals firm, rubbery tissue (unlike the findings in pseudogynecomastia, where there is a soft enlargement of the breast). Alternatively, a history of weight loss is important because it can lead to hypothalamic dysfunction and a decrease in gonadotropin (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) secretion, resulting in decreased testosterone levels.⁸

Also inquire about prior diagnoses of liver cirrhosis or thyrotoxicosis or the presence of symptoms suggestive of these disorders, such as fatigue, jaundice, bloating, heat intolerance, or heart palpitations. These conditions can alter the metabolism of sex steroids and their binding proteins. A history of decreased libido and erectile dysfunction is suggestive of low testosterone levels, also known as hypogonadism. Headaches, visual disturbances, and behavioral abnormalities suggest a hypothalamic or pituitary disorder resulting in decreased FSH and LH levels and secondary hypogonadism. A family history of gynecomastia is elicited in half the patients with persistent pubertal gynecomastia.⁹

Physical examination. For all patients (except newborns), calculate the BMI and measure arm span and upper and lower body segments. A eunuchoid proportion—arm span 2 cm or greater than height—is associated with early-onset hypogonadism that precedes fusion of the epiphyses.³ Thus, you’ll need to consider congenital disorders of the testes, such as Klinefelter syndrome, as well as hypothalamic or pituitary disease, such as Kallmann syndrome, resulting in deficient FSH and LH production.

As noted earlier, you’ll need to examine the breasts to determine if true gynecomastia exists, as opposed to increased adipose tissue or the presence of a suspicious mass. A hard or irregular mass outside the areola, especially if associated with skin changes such as dimpling or retraction, should raise the possibility of breast carcinoma. Promptly arrange for diagnostic mammography and possible biopsy in this setting.

Carefully examine the secondary sexual characteristics, including body hair distribution and muscle mass. Inspect the external genitalia, penile development, and position of the urethral meatus. Note testicular size and consistency. Small, firm testes are suggestive of dysgenetic gonads found in patients with Klinefelter syndrome (47 XXY), whereas small, soft testes suggest secondary hypogonadism. A unilateral testicular mass raises suspicion of a neoplasm. Palpate the prostate in older men, especially if contemplating androgen therapy, which could exacerbate a preexisting focal prostate cancer.

Look for signs of hyperthyroidism, such as goiter, exophthalmos, tachycardia, and hyper-reflexia. Examine the abdomen for masses, hepato- or splenomegaly, and signs of cirrhosis, such as ascites and venous congestion. The examination should also include visual fields, cranial nerves, and fundoscopy for possible pituitary (or other) central nervous system lesions. Look for spider angiomas and palmar erythema (as occur in cirrhosis); warm, moist skin and myxedema (as in Graves’ disease); and mucocutaneous lentigines (as in Peutz-Jeghers syndrome).¹⁰

When laboratory and radiologic testing may help

Most adolescents with gynecomastia are best managed by reassurance and observation¹¹ (ALGORITHM),³ and no laboratory or radiographic studies are recommended in most cases. Exceptions would be gynecomastia that develops before the onset of puberty; evidence of undervirilization on physical examination; a testicular mass; or persistence of gynecomastia beyond the usual observation period of 12 to 18 months.¹¹

ALGORITHM
Evaluating gynecomastia³

CT, computed tomography; hCG, human chorionic gonadotropin; LH, luteinizing hormone; MRI, magnetic resonance imaging; TSH, thyroid-stimulating hormone.
↑ = elevated; ↓ = lowered; ↔ = normal.

If findings on physical examination are consistent with a breast neoplasm, arrange for mammography immediately. The sensitivity and specificity of mammography for benign and malignant conditions exceed 90%.¹² A biopsy may be necessary if uncertainty remains after imaging.

No specific tests are necessary when gynecomastia is clearly associated with intake of a medication known to be associated with the condition, especially if the history and examination are otherwise negative. A prompt regression of gynecomastia after discontinuation of the offending drug will confirm the diagnosis.

If the condition persists in an adolescent or adult and the cause is still unclear, perform renal function tests and measure levels of liver enzymes, early-morning serum human chorionic gonadotropin (hCG), LH, total testosterone, estradiol, TSH, and prolactin.

What lab results may mean. If the total testosterone level is borderline or low-normal (200-350 ng/dL), repeat the test and measure the free testosterone level.

If an elevated hCG level is found, repeat the testicular examination carefully and order ultrasonography. In the absence of a testicular tumor, consider an MRI of the brain and computed tomography (CT) of the abdomen and chest to help identify an extragonadal hCG-secreting tumor.

An elevated LH level and low testosterone level are diagnostic of primary testicular hypogonadism. A karyotype may be necessary in some individuals to diagnose Klinefelter syndrome. Elevated LH and testosterone levels are seen in patients with androgen insensitivity syndromes. These conditions are caused by abnormalities in the androgen receptor with a wide range of possible phenotypes, including ambiguous genitalia.

A low testosterone level with a low or normal LH level indicates secondary hypogonadism of hypothalamic or pituitary origin. An elevated prolactin level in such cases (as was seen in Mr. J.’s case) is usually due to a prolactin secreting pituitary adenoma.

Hereditary hemochromatosis is an important and often overlooked cause of hypogonadism. Obtain iron studies and ferritin levels in this setting.¹³ Unrecognized hemochromatosis may result in fibrosis and multiple organ failure.

Patients with secondary hypogonadism are best managed by a referral to an endocrinologist, as the potential list of causes is extensive.^4,14,15

A low TSH level is consistent with thyrotoxicosis, which may result in increased levels of SHBG and altered metabolism of estrogens and androgens.¹⁶ Thus, about 10% of men with thyrotoxicosis present with gynecomastia and erectile dysfunction.¹⁶ If the estradiol level is elevated, a testicular ultrasound as well as an adrenal CT scan will help identify a neoplasm.

In a significant number of patients, the diagnostic tests are normal, leading to a diagnosis of idiopathic gynecomastia. In these cases, the alteration in androgen and estrogen levels can be subtle and intermittent.¹⁷ Continue surveillance and periodically reevaluate the patient.

Management of gynecomastia

Gynecomastia often results from transient hormonal imbalance and regresses spontaneously. Therefore, no specific treatment is necessary for neonatal, pubertal, or drug-induced gynecomastia. In other situations, prompt diagnosis and treatment are important to maximize the likelihood of successful medical therapy. It has been shown that fibrosis develops 6 to 12 months after the onset of gynecomastia, making it unlikely that medical treatments beyond that stage will result in significant regression of the breast enlargement.¹⁸ In such long-standing cases, surgical intervention with subcutaneous mastectomy or liposuction can be considered for patients who have significant psychological problems or esthetic issues. Indications for surgery also include continued growth and tenderness of breast tissue or malignancy.

Available medications include those aimed at decreasing estrogen production or estrogen effect on target breast tissue. Aromatase inhibitors such as testolactone, anastrozole, and letrozole can decrease the synthesis of estrogen by inhibiting aromatization of androgens. Although theoretically promising, results of the few controlled trials with aromatase inhibitors have been generally disappointing.¹⁹

Selective estrogen receptor modulators that alter the effect of estrogen on breast tissue are tamoxifen and raloxifene. Tamoxifen is not yet approved for treatment of gynecomastia, but has proven effective in randomized trials.²⁰ At a dose of 20 mg/d for 3 or more months, tamoxifen resulted in complete regression of gynecomastia in 60% of patients and partial regression in 20% of patients.²⁰ Tamoxifen also prevents gynecomastia after medial prostatectomy and treatment with the antiandrogen, bicalutamide.

CASE Mr. J had a pituitary prolactin-secreting microadenoma causing secondary hypogonadism and gynecomastia. He was started on cabergoline (a dopamine agonist) 0.5 mg orally once a week. Four months later, his total testosterone level was 291 ng/dL, and prolactin was 9.3 ng/mL. His headaches and gynecomastia had significantly decreased. He continued to do well on the same regimen and, 6 years later, his prolactin level was 1.4 ng/mL, indicating that treatment had been effective.

CORRESPONDENCE
Roy N. Morcos, MD, Department of Family Medicine, St. Elizabeth Health Center, 1044 Belmont Avenue, Youngstown, OH 44501; [email protected]

CASE Harry J is a 57-year-old man who came to us for evaluation and management of hypertension. He also complained of chronic headaches. Our initial examination revealed a body mass index (BMI) of 29 kg/m² and blood pressure (BP) of 150/100 mm Hg. The hypertension responded well to a combination of valsartan and hydrochlorothiazide. A few months later, he developed left breast soreness, as well as decreased libido. Examination revealed a round movable subareolar nodule 2 cm in diameter, with no associated skin changes or lymphadenopathy. Laboratory results were: total testosterone, 106 ng/dL (normal, 241-827); free testosterone, 23 pg/mL (47-244); thyroid-stimulating hormone (TSH), 2.222 mIU/mL (0.350-5.500); and prolactin, 102.7 ng/mL (2.1-17.7). Magnetic resonance imaging (MRI) of the brain revealed a nodular density <10 mm in the pituitary gland with minimal displacement of the stalk, consistent with a microadenoma.

Enlargement of the male breasts—gynecomastia—is caused by a benign proliferation of the ductal epithelium, due to a relative increase in the ratio of free estrogen to androgen locally in the breast. Gynecomastia of recent onset is often associated with pain and tenderness, as was the case with our patient.

Often self-limiting, age-related influences. Gynecomastia is common in newborns, during adolescence, and in old age.¹ In both male and female newborns, maternal and placental estrogens induce bilateral proliferation of breast tissue. This resolves within a few weeks after birth. During the early stages of male puberty, there is a relative increase in estrogens derived mostly from peripheral aromatization of testicular and adrenal androgens. If gynecomastia results, it usually regresses spontaneously as testicular testosterone production increases in late puberty.² Gynecomastia is also common in elderly men due to a decrease in testosterone production and an increase in sex hormone binding globulin (SHBG) that lowers free testosterone levels.

Deleterious contributing factors. Several other potential causes of gynecomastia exist (TABLE 1),^3,4 and these can usually be identified with a systematic approach using a careful history, physical examination, and selected laboratory studies. Many medications are associated with gynecomastia (TABLE 2),⁵ one of the most common being spironolactone due to its antiandrogenic activity at the receptor level.⁵ Some drugs, although associated with gynecomastia, cannot be linked to a direct cause-and-effect mechanism. These factors are compounded in elderly, obese men who take medications such as spironolactone, known to cause gynecomastia.

TABLE 1
Causes of gynecomastia^3,4

TABLE 2
Drugs associated with gynecomastia⁵

A patient’s medical history may reveal chronic conditions associated with gynecomastia. Such disorders include cirrhosis, hyperthyroidism, malnutrition, and chronic kidney disease. Rarely, gynecomastia can be a manifestation of a testicular, adrenal, or other neoplasm.

Despite a thorough evaluation, no detectable abnormality is found initially in 25% of gynecomastia cases.⁶ Close observation and monitoring is necessary in such instances, to ensure the earliest possible identification of the underlying cause and initiation of appropriate medical or surgical therapy.

First steps in the clinical evaluation

In cases of male breast enlargement, first determine whether you are dealing with true gynecomastia or “pseudogynecomastia,” which involves increased fat deposits typically seen in obese individuals.³ In cases of pseudogynecomastia, the tissue is uniformly enlarged and soft, with the same consistency as adipose tissue.

In about half of the cases of gynecomastia, the condition is bilateral.³ It is characteristically a rubbery or firm mass concentric with the nipple-areolar complex.

Clues to look for in the history. When examination suggests true gynecomastia, conduct a focused history to determine if medications or other substances might be causing the problem. (See “A case where drug therapy was to blame”) Some plant-derived oils used as skin care products have also been associated with gynecomastia due to weak estrogenic or anti-androgenic activity.⁷

The history may also uncover significant weight gain, because obesity is associated with increased aromatase activity resulting in a relative increase in estrogens systemically and locally in the breast. When obesity is the cause of gynecomastia, the breast examination reveals firm, rubbery tissue (unlike the findings in pseudogynecomastia, where there is a soft enlargement of the breast). Alternatively, a history of weight loss is important because it can lead to hypothalamic dysfunction and a decrease in gonadotropin (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) secretion, resulting in decreased testosterone levels.⁸

Also inquire about prior diagnoses of liver cirrhosis or thyrotoxicosis or the presence of symptoms suggestive of these disorders, such as fatigue, jaundice, bloating, heat intolerance, or heart palpitations. These conditions can alter the metabolism of sex steroids and their binding proteins. A history of decreased libido and erectile dysfunction is suggestive of low testosterone levels, also known as hypogonadism. Headaches, visual disturbances, and behavioral abnormalities suggest a hypothalamic or pituitary disorder resulting in decreased FSH and LH levels and secondary hypogonadism. A family history of gynecomastia is elicited in half the patients with persistent pubertal gynecomastia.⁹

Physical examination. For all patients (except newborns), calculate the BMI and measure arm span and upper and lower body segments. A eunuchoid proportion—arm span 2 cm or greater than height—is associated with early-onset hypogonadism that precedes fusion of the epiphyses.³ Thus, you’ll need to consider congenital disorders of the testes, such as Klinefelter syndrome, as well as hypothalamic or pituitary disease, such as Kallmann syndrome, resulting in deficient FSH and LH production.

As noted earlier, you’ll need to examine the breasts to determine if true gynecomastia exists, as opposed to increased adipose tissue or the presence of a suspicious mass. A hard or irregular mass outside the areola, especially if associated with skin changes such as dimpling or retraction, should raise the possibility of breast carcinoma. Promptly arrange for diagnostic mammography and possible biopsy in this setting.

Carefully examine the secondary sexual characteristics, including body hair distribution and muscle mass. Inspect the external genitalia, penile development, and position of the urethral meatus. Note testicular size and consistency. Small, firm testes are suggestive of dysgenetic gonads found in patients with Klinefelter syndrome (47 XXY), whereas small, soft testes suggest secondary hypogonadism. A unilateral testicular mass raises suspicion of a neoplasm. Palpate the prostate in older men, especially if contemplating androgen therapy, which could exacerbate a preexisting focal prostate cancer.

Look for signs of hyperthyroidism, such as goiter, exophthalmos, tachycardia, and hyper-reflexia. Examine the abdomen for masses, hepato- or splenomegaly, and signs of cirrhosis, such as ascites and venous congestion. The examination should also include visual fields, cranial nerves, and fundoscopy for possible pituitary (or other) central nervous system lesions. Look for spider angiomas and palmar erythema (as occur in cirrhosis); warm, moist skin and myxedema (as in Graves’ disease); and mucocutaneous lentigines (as in Peutz-Jeghers syndrome).¹⁰

When laboratory and radiologic testing may help

Most adolescents with gynecomastia are best managed by reassurance and observation¹¹ (ALGORITHM),³ and no laboratory or radiographic studies are recommended in most cases. Exceptions would be gynecomastia that develops before the onset of puberty; evidence of undervirilization on physical examination; a testicular mass; or persistence of gynecomastia beyond the usual observation period of 12 to 18 months.¹¹

ALGORITHM
Evaluating gynecomastia³

CT, computed tomography; hCG, human chorionic gonadotropin; LH, luteinizing hormone; MRI, magnetic resonance imaging; TSH, thyroid-stimulating hormone.
↑ = elevated; ↓ = lowered; ↔ = normal.

If findings on physical examination are consistent with a breast neoplasm, arrange for mammography immediately. The sensitivity and specificity of mammography for benign and malignant conditions exceed 90%.¹² A biopsy may be necessary if uncertainty remains after imaging.

No specific tests are necessary when gynecomastia is clearly associated with intake of a medication known to be associated with the condition, especially if the history and examination are otherwise negative. A prompt regression of gynecomastia after discontinuation of the offending drug will confirm the diagnosis.

If the condition persists in an adolescent or adult and the cause is still unclear, perform renal function tests and measure levels of liver enzymes, early-morning serum human chorionic gonadotropin (hCG), LH, total testosterone, estradiol, TSH, and prolactin.

What lab results may mean. If the total testosterone level is borderline or low-normal (200-350 ng/dL), repeat the test and measure the free testosterone level.

If an elevated hCG level is found, repeat the testicular examination carefully and order ultrasonography. In the absence of a testicular tumor, consider an MRI of the brain and computed tomography (CT) of the abdomen and chest to help identify an extragonadal hCG-secreting tumor.

An elevated LH level and low testosterone level are diagnostic of primary testicular hypogonadism. A karyotype may be necessary in some individuals to diagnose Klinefelter syndrome. Elevated LH and testosterone levels are seen in patients with androgen insensitivity syndromes. These conditions are caused by abnormalities in the androgen receptor with a wide range of possible phenotypes, including ambiguous genitalia.

A low testosterone level with a low or normal LH level indicates secondary hypogonadism of hypothalamic or pituitary origin. An elevated prolactin level in such cases (as was seen in Mr. J.’s case) is usually due to a prolactin secreting pituitary adenoma.

Hereditary hemochromatosis is an important and often overlooked cause of hypogonadism. Obtain iron studies and ferritin levels in this setting.¹³ Unrecognized hemochromatosis may result in fibrosis and multiple organ failure.

Patients with secondary hypogonadism are best managed by a referral to an endocrinologist, as the potential list of causes is extensive.^4,14,15

A low TSH level is consistent with thyrotoxicosis, which may result in increased levels of SHBG and altered metabolism of estrogens and androgens.¹⁶ Thus, about 10% of men with thyrotoxicosis present with gynecomastia and erectile dysfunction.¹⁶ If the estradiol level is elevated, a testicular ultrasound as well as an adrenal CT scan will help identify a neoplasm.

In a significant number of patients, the diagnostic tests are normal, leading to a diagnosis of idiopathic gynecomastia. In these cases, the alteration in androgen and estrogen levels can be subtle and intermittent.¹⁷ Continue surveillance and periodically reevaluate the patient.

Management of gynecomastia

Gynecomastia often results from transient hormonal imbalance and regresses spontaneously. Therefore, no specific treatment is necessary for neonatal, pubertal, or drug-induced gynecomastia. In other situations, prompt diagnosis and treatment are important to maximize the likelihood of successful medical therapy. It has been shown that fibrosis develops 6 to 12 months after the onset of gynecomastia, making it unlikely that medical treatments beyond that stage will result in significant regression of the breast enlargement.¹⁸ In such long-standing cases, surgical intervention with subcutaneous mastectomy or liposuction can be considered for patients who have significant psychological problems or esthetic issues. Indications for surgery also include continued growth and tenderness of breast tissue or malignancy.

Available medications include those aimed at decreasing estrogen production or estrogen effect on target breast tissue. Aromatase inhibitors such as testolactone, anastrozole, and letrozole can decrease the synthesis of estrogen by inhibiting aromatization of androgens. Although theoretically promising, results of the few controlled trials with aromatase inhibitors have been generally disappointing.¹⁹

Selective estrogen receptor modulators that alter the effect of estrogen on breast tissue are tamoxifen and raloxifene. Tamoxifen is not yet approved for treatment of gynecomastia, but has proven effective in randomized trials.²⁰ At a dose of 20 mg/d for 3 or more months, tamoxifen resulted in complete regression of gynecomastia in 60% of patients and partial regression in 20% of patients.²⁰ Tamoxifen also prevents gynecomastia after medial prostatectomy and treatment with the antiandrogen, bicalutamide.

CASE Mr. J had a pituitary prolactin-secreting microadenoma causing secondary hypogonadism and gynecomastia. He was started on cabergoline (a dopamine agonist) 0.5 mg orally once a week. Four months later, his total testosterone level was 291 ng/dL, and prolactin was 9.3 ng/mL. His headaches and gynecomastia had significantly decreased. He continued to do well on the same regimen and, 6 years later, his prolactin level was 1.4 ng/mL, indicating that treatment had been effective.

CORRESPONDENCE
Roy N. Morcos, MD, Department of Family Medicine, St. Elizabeth Health Center, 1044 Belmont Avenue, Youngstown, OH 44501; [email protected]

CASE Harry J is a 57-year-old man who came to us for evaluation and management of hypertension. He also complained of chronic headaches. Our initial examination revealed a body mass index (BMI) of 29 kg/m² and blood pressure (BP) of 150/100 mm Hg. The hypertension responded well to a combination of valsartan and hydrochlorothiazide. A few months later, he developed left breast soreness, as well as decreased libido. Examination revealed a round movable subareolar nodule 2 cm in diameter, with no associated skin changes or lymphadenopathy. Laboratory results were: total testosterone, 106 ng/dL (normal, 241-827); free testosterone, 23 pg/mL (47-244); thyroid-stimulating hormone (TSH), 2.222 mIU/mL (0.350-5.500); and prolactin, 102.7 ng/mL (2.1-17.7). Magnetic resonance imaging (MRI) of the brain revealed a nodular density <10 mm in the pituitary gland with minimal displacement of the stalk, consistent with a microadenoma.

Enlargement of the male breasts—gynecomastia—is caused by a benign proliferation of the ductal epithelium, due to a relative increase in the ratio of free estrogen to androgen locally in the breast. Gynecomastia of recent onset is often associated with pain and tenderness, as was the case with our patient.

Often self-limiting, age-related influences. Gynecomastia is common in newborns, during adolescence, and in old age.¹ In both male and female newborns, maternal and placental estrogens induce bilateral proliferation of breast tissue. This resolves within a few weeks after birth. During the early stages of male puberty, there is a relative increase in estrogens derived mostly from peripheral aromatization of testicular and adrenal androgens. If gynecomastia results, it usually regresses spontaneously as testicular testosterone production increases in late puberty.² Gynecomastia is also common in elderly men due to a decrease in testosterone production and an increase in sex hormone binding globulin (SHBG) that lowers free testosterone levels.

Deleterious contributing factors. Several other potential causes of gynecomastia exist (TABLE 1),^3,4 and these can usually be identified with a systematic approach using a careful history, physical examination, and selected laboratory studies. Many medications are associated with gynecomastia (TABLE 2),⁵ one of the most common being spironolactone due to its antiandrogenic activity at the receptor level.⁵ Some drugs, although associated with gynecomastia, cannot be linked to a direct cause-and-effect mechanism. These factors are compounded in elderly, obese men who take medications such as spironolactone, known to cause gynecomastia.

TABLE 1
Causes of gynecomastia^3,4

TABLE 2
Drugs associated with gynecomastia⁵

A patient’s medical history may reveal chronic conditions associated with gynecomastia. Such disorders include cirrhosis, hyperthyroidism, malnutrition, and chronic kidney disease. Rarely, gynecomastia can be a manifestation of a testicular, adrenal, or other neoplasm.

Despite a thorough evaluation, no detectable abnormality is found initially in 25% of gynecomastia cases.⁶ Close observation and monitoring is necessary in such instances, to ensure the earliest possible identification of the underlying cause and initiation of appropriate medical or surgical therapy.

First steps in the clinical evaluation

In cases of male breast enlargement, first determine whether you are dealing with true gynecomastia or “pseudogynecomastia,” which involves increased fat deposits typically seen in obese individuals.³ In cases of pseudogynecomastia, the tissue is uniformly enlarged and soft, with the same consistency as adipose tissue.

In about half of the cases of gynecomastia, the condition is bilateral.³ It is characteristically a rubbery or firm mass concentric with the nipple-areolar complex.

Clues to look for in the history. When examination suggests true gynecomastia, conduct a focused history to determine if medications or other substances might be causing the problem. (See “A case where drug therapy was to blame”) Some plant-derived oils used as skin care products have also been associated with gynecomastia due to weak estrogenic or anti-androgenic activity.⁷

The history may also uncover significant weight gain, because obesity is associated with increased aromatase activity resulting in a relative increase in estrogens systemically and locally in the breast. When obesity is the cause of gynecomastia, the breast examination reveals firm, rubbery tissue (unlike the findings in pseudogynecomastia, where there is a soft enlargement of the breast). Alternatively, a history of weight loss is important because it can lead to hypothalamic dysfunction and a decrease in gonadotropin (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) secretion, resulting in decreased testosterone levels.⁸

Also inquire about prior diagnoses of liver cirrhosis or thyrotoxicosis or the presence of symptoms suggestive of these disorders, such as fatigue, jaundice, bloating, heat intolerance, or heart palpitations. These conditions can alter the metabolism of sex steroids and their binding proteins. A history of decreased libido and erectile dysfunction is suggestive of low testosterone levels, also known as hypogonadism. Headaches, visual disturbances, and behavioral abnormalities suggest a hypothalamic or pituitary disorder resulting in decreased FSH and LH levels and secondary hypogonadism. A family history of gynecomastia is elicited in half the patients with persistent pubertal gynecomastia.⁹

Physical examination. For all patients (except newborns), calculate the BMI and measure arm span and upper and lower body segments. A eunuchoid proportion—arm span 2 cm or greater than height—is associated with early-onset hypogonadism that precedes fusion of the epiphyses.³ Thus, you’ll need to consider congenital disorders of the testes, such as Klinefelter syndrome, as well as hypothalamic or pituitary disease, such as Kallmann syndrome, resulting in deficient FSH and LH production.

As noted earlier, you’ll need to examine the breasts to determine if true gynecomastia exists, as opposed to increased adipose tissue or the presence of a suspicious mass. A hard or irregular mass outside the areola, especially if associated with skin changes such as dimpling or retraction, should raise the possibility of breast carcinoma. Promptly arrange for diagnostic mammography and possible biopsy in this setting.

Carefully examine the secondary sexual characteristics, including body hair distribution and muscle mass. Inspect the external genitalia, penile development, and position of the urethral meatus. Note testicular size and consistency. Small, firm testes are suggestive of dysgenetic gonads found in patients with Klinefelter syndrome (47 XXY), whereas small, soft testes suggest secondary hypogonadism. A unilateral testicular mass raises suspicion of a neoplasm. Palpate the prostate in older men, especially if contemplating androgen therapy, which could exacerbate a preexisting focal prostate cancer.

Look for signs of hyperthyroidism, such as goiter, exophthalmos, tachycardia, and hyper-reflexia. Examine the abdomen for masses, hepato- or splenomegaly, and signs of cirrhosis, such as ascites and venous congestion. The examination should also include visual fields, cranial nerves, and fundoscopy for possible pituitary (or other) central nervous system lesions. Look for spider angiomas and palmar erythema (as occur in cirrhosis); warm, moist skin and myxedema (as in Graves’ disease); and mucocutaneous lentigines (as in Peutz-Jeghers syndrome).¹⁰

When laboratory and radiologic testing may help

Most adolescents with gynecomastia are best managed by reassurance and observation¹¹ (ALGORITHM),³ and no laboratory or radiographic studies are recommended in most cases. Exceptions would be gynecomastia that develops before the onset of puberty; evidence of undervirilization on physical examination; a testicular mass; or persistence of gynecomastia beyond the usual observation period of 12 to 18 months.¹¹

ALGORITHM
Evaluating gynecomastia³

CT, computed tomography; hCG, human chorionic gonadotropin; LH, luteinizing hormone; MRI, magnetic resonance imaging; TSH, thyroid-stimulating hormone.
↑ = elevated; ↓ = lowered; ↔ = normal.

If findings on physical examination are consistent with a breast neoplasm, arrange for mammography immediately. The sensitivity and specificity of mammography for benign and malignant conditions exceed 90%.¹² A biopsy may be necessary if uncertainty remains after imaging.

No specific tests are necessary when gynecomastia is clearly associated with intake of a medication known to be associated with the condition, especially if the history and examination are otherwise negative. A prompt regression of gynecomastia after discontinuation of the offending drug will confirm the diagnosis.

If the condition persists in an adolescent or adult and the cause is still unclear, perform renal function tests and measure levels of liver enzymes, early-morning serum human chorionic gonadotropin (hCG), LH, total testosterone, estradiol, TSH, and prolactin.

What lab results may mean. If the total testosterone level is borderline or low-normal (200-350 ng/dL), repeat the test and measure the free testosterone level.

If an elevated hCG level is found, repeat the testicular examination carefully and order ultrasonography. In the absence of a testicular tumor, consider an MRI of the brain and computed tomography (CT) of the abdomen and chest to help identify an extragonadal hCG-secreting tumor.

An elevated LH level and low testosterone level are diagnostic of primary testicular hypogonadism. A karyotype may be necessary in some individuals to diagnose Klinefelter syndrome. Elevated LH and testosterone levels are seen in patients with androgen insensitivity syndromes. These conditions are caused by abnormalities in the androgen receptor with a wide range of possible phenotypes, including ambiguous genitalia.

A low testosterone level with a low or normal LH level indicates secondary hypogonadism of hypothalamic or pituitary origin. An elevated prolactin level in such cases (as was seen in Mr. J.’s case) is usually due to a prolactin secreting pituitary adenoma.

Hereditary hemochromatosis is an important and often overlooked cause of hypogonadism. Obtain iron studies and ferritin levels in this setting.¹³ Unrecognized hemochromatosis may result in fibrosis and multiple organ failure.

Patients with secondary hypogonadism are best managed by a referral to an endocrinologist, as the potential list of causes is extensive.^4,14,15

A low TSH level is consistent with thyrotoxicosis, which may result in increased levels of SHBG and altered metabolism of estrogens and androgens.¹⁶ Thus, about 10% of men with thyrotoxicosis present with gynecomastia and erectile dysfunction.¹⁶ If the estradiol level is elevated, a testicular ultrasound as well as an adrenal CT scan will help identify a neoplasm.

In a significant number of patients, the diagnostic tests are normal, leading to a diagnosis of idiopathic gynecomastia. In these cases, the alteration in androgen and estrogen levels can be subtle and intermittent.¹⁷ Continue surveillance and periodically reevaluate the patient.

Management of gynecomastia

Gynecomastia often results from transient hormonal imbalance and regresses spontaneously. Therefore, no specific treatment is necessary for neonatal, pubertal, or drug-induced gynecomastia. In other situations, prompt diagnosis and treatment are important to maximize the likelihood of successful medical therapy. It has been shown that fibrosis develops 6 to 12 months after the onset of gynecomastia, making it unlikely that medical treatments beyond that stage will result in significant regression of the breast enlargement.¹⁸ In such long-standing cases, surgical intervention with subcutaneous mastectomy or liposuction can be considered for patients who have significant psychological problems or esthetic issues. Indications for surgery also include continued growth and tenderness of breast tissue or malignancy.

Available medications include those aimed at decreasing estrogen production or estrogen effect on target breast tissue. Aromatase inhibitors such as testolactone, anastrozole, and letrozole can decrease the synthesis of estrogen by inhibiting aromatization of androgens. Although theoretically promising, results of the few controlled trials with aromatase inhibitors have been generally disappointing.¹⁹

Selective estrogen receptor modulators that alter the effect of estrogen on breast tissue are tamoxifen and raloxifene. Tamoxifen is not yet approved for treatment of gynecomastia, but has proven effective in randomized trials.²⁰ At a dose of 20 mg/d for 3 or more months, tamoxifen resulted in complete regression of gynecomastia in 60% of patients and partial regression in 20% of patients.²⁰ Tamoxifen also prevents gynecomastia after medial prostatectomy and treatment with the antiandrogen, bicalutamide.

CASE Mr. J had a pituitary prolactin-secreting microadenoma causing secondary hypogonadism and gynecomastia. He was started on cabergoline (a dopamine agonist) 0.5 mg orally once a week. Four months later, his total testosterone level was 291 ng/dL, and prolactin was 9.3 ng/mL. His headaches and gynecomastia had significantly decreased. He continued to do well on the same regimen and, 6 years later, his prolactin level was 1.4 ng/mL, indicating that treatment had been effective.

CORRESPONDENCE
Roy N. Morcos, MD, Department of Family Medicine, St. Elizabeth Health Center, 1044 Belmont Avenue, Youngstown, OH 44501; [email protected]

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
My patient is an officer in a large corporation. During therapy, he sometimes talks about how the company is doing. Would I risk malpractice liability if I used this information in managing my retirement investments?
Submitted by “Dr. B”

As most physicians find out within a short time of finishing medical school, doctors learn all kinds of useful things from their patients, including information that can help them manage personal matters outside their practices. But are you allowed to use nonpublic business information to make investment decisions?

As this article explains, legal rules and case law suggest that if psychiatrists or therapists act on potentially profitable business information incidentally mentioned by a patient during treatment, they may be subject to serious legal problems. To explain why, we’ll begin with a brief overview of business terms, including “securities” and “insider trading.” Then, to answer Dr. B’s question, we’ll look at what kind of legal consequences may result if mental health professionals are found guilty of “misappropriating” confidential business information.

Securities and security rules

Approximately one-half to two-thirds of Americans have money invested in the stock market—either through their retirement plans, by owning mutual funds, or by holding stocks of individual companies.¹ Stocks are a type of financial instrument, or security, that companies issue to raise capital. Companies also raise money by issuing debt, typically in the form of bonds that pay interest to the holder, who in buying the bond has in effect loaned money to the company. Derivatives refer to securities that have prices that move up or down depending on the value of some underlying asset, such as stock prices.²

Stock prices fluctuate in reaction to general economic developments—changes in the unemployment rate, in the cost of basic materials (eg, oil or metals used in manufacturing), or in government policies that influence consumers’ purchasing decisions. But the key factor in determining the price of a company’s stock is investors’ beliefs about the company’s future earnings.³ Because investors usually have to make educated guesses about a company’s future, actually knowing something about a company before the general public finds out would give an investor a huge—but possibly unfair—advantage over other investors.

Making markets fair for all investors is the key purpose of U.S. laws on trading securities. In the 1930s, Congress created the Securities and Exchange Commission (SEC), a federal agency charged with ensuring that companies report the truth about their financial situation and that potential investors receive full, fair disclosure of available public information.⁴ Among the many ways that the SEC does this is by enforcing regulations concerning “insider trading.”

‘Insider trading’

Corporate “insiders” (eg, directors or employees) often know a lot about how their businesses are doing, and they buy or sell stock in their own companies. Such trading is legal if the insiders follow federal regulations about the timing of their investments and report them publicly.

Insider trading is illegal, however, if an individual acquires material, nonpublic information about a corporation through a relationship that involves trust and confidence and then uses that information when buying or selling a security. The SEC has prosecuted corporate employees who traded securities after learning of confidential developments in their companies, friends and family members of corporate officers who bought or sold securities after getting such information, and employees of law firms who misused information they received while providing services to corporations whose securities they traded.⁵

To be guilty of insider trading, a person must:

• buy or sell a security based on information that the person realizes is material and nonpublic,⁶ and
• have received the confidential information under circumstances that create a duty of trust or confidence.⁷

If both of these conditions are met, the person has wrongfully used confidential information with which he was entrusted, or “misappropriated” that information for personal gain.⁸

Physicians sometimes gain information that, if used for investment decisions, might lead to accusations of insider trading. Stock prices of pharmaceutical companies rise before public announcements of clinical drug trials, which suggests that information about those results leaks out in advance.⁹ Recently, physicians have gotten into well-publicized legal trouble by making investment decisions based on information they obtained while participating on an institution’s board¹⁰ and from learning early results of clinical drug trials.¹¹

But would it be wrong for a psychiatrist to make a potentially profitable investment based on information obtained incidentally during a treatment encounter? After all, it’s not as though the psychiatrist would be a corporate insider or would have acquired the information improperly. Yet courts have ruled that a psychiatrist’s trading on such information might constitute malpractice and could be grounds for even more serious legal consequences.

Potential malpractice issues

The federal court ruling in United States v Willis¹² describes how a psychiatrist learned during treatment that a patient’s husband was seeking to become CEO of a large bank. Realizing that this development might make the bank more valuable, the psychiatrist told his broker what he had learned and purchased 13,000 shares of the bank’s stock for himself and his children. When the husband’s efforts were announced publicly a few weeks later, the psychiatrist sold the shares at a big profit.

Quoting the vow of confidentiality contained in the Hippocratic Oath (Box),¹³ the court held that the psychiatrist had an obligation to the patient not to disclose information learned during her treatment without her permission. The court said the patient “had an economic interest in preserving the confidentiality of the information disclosed,” and the psychiatrist’s actions “might have jeopardized her husband’s advancement” and financial benefits the wife would have gained. Also, the psychiatrist’s “disclosures jeopardized the psychiatrist-patient relationship,” which might negate the wife’s financial investment in her care, require her to find a new psychiatrist, or require additional treatment to deal with how the psychiatrist’s behavior had affected her.¹²

Box

More legal consequences

Dr. Willis had legal problems more serious than just a malpractice lawsuit. He faced criminal prosecution for insider trading and mail fraud, and the court refused to dismiss these charges. The court reasoned that the psychiatrist received the information while in a position of trust and confidence, and breached that trust when he used that confidential information for his personal benefit—behavior that meets the legal definition of “misappropriation.” Because the psychiatrist received stock trade confirmations through the U.S. mail, he also could face federal charges of mail fraud. Ultimately, Dr. Willis pled guilty and paid $137,000 in fines and penalties. Although Dr. Willis retained his New Jersey medical license and avoided a prison sentence, the district court sentenced him to 5 years of probation and required that he perform 3,000 hours of community service.^14,15

In a second case,¹⁶ a licensed clinical social worker made investments through a broker based on information learned during a therapy session about upcoming business developments (the 1994 Lockheed-Martin Marietta merger). The social worker pled guilty to insider trading, forfeited the illegal gains, and paid a large fine.

Related Resources

• Insider trading versus medical professionalism. Lancet. 2005;366(9488):781.
• Nijm LM. The online message board controversy. Physicians hit with claims of libel and insider trading by their employers. J Leg Med. 2000;21(2):223-239.

Disclosure

Dr. Mossman reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
My patient is an officer in a large corporation. During therapy, he sometimes talks about how the company is doing. Would I risk malpractice liability if I used this information in managing my retirement investments?
Submitted by “Dr. B”

As most physicians find out within a short time of finishing medical school, doctors learn all kinds of useful things from their patients, including information that can help them manage personal matters outside their practices. But are you allowed to use nonpublic business information to make investment decisions?

As this article explains, legal rules and case law suggest that if psychiatrists or therapists act on potentially profitable business information incidentally mentioned by a patient during treatment, they may be subject to serious legal problems. To explain why, we’ll begin with a brief overview of business terms, including “securities” and “insider trading.” Then, to answer Dr. B’s question, we’ll look at what kind of legal consequences may result if mental health professionals are found guilty of “misappropriating” confidential business information.

Securities and security rules

Approximately one-half to two-thirds of Americans have money invested in the stock market—either through their retirement plans, by owning mutual funds, or by holding stocks of individual companies.¹ Stocks are a type of financial instrument, or security, that companies issue to raise capital. Companies also raise money by issuing debt, typically in the form of bonds that pay interest to the holder, who in buying the bond has in effect loaned money to the company. Derivatives refer to securities that have prices that move up or down depending on the value of some underlying asset, such as stock prices.²

Stock prices fluctuate in reaction to general economic developments—changes in the unemployment rate, in the cost of basic materials (eg, oil or metals used in manufacturing), or in government policies that influence consumers’ purchasing decisions. But the key factor in determining the price of a company’s stock is investors’ beliefs about the company’s future earnings.³ Because investors usually have to make educated guesses about a company’s future, actually knowing something about a company before the general public finds out would give an investor a huge—but possibly unfair—advantage over other investors.

Making markets fair for all investors is the key purpose of U.S. laws on trading securities. In the 1930s, Congress created the Securities and Exchange Commission (SEC), a federal agency charged with ensuring that companies report the truth about their financial situation and that potential investors receive full, fair disclosure of available public information.⁴ Among the many ways that the SEC does this is by enforcing regulations concerning “insider trading.”

‘Insider trading’

Corporate “insiders” (eg, directors or employees) often know a lot about how their businesses are doing, and they buy or sell stock in their own companies. Such trading is legal if the insiders follow federal regulations about the timing of their investments and report them publicly.

Insider trading is illegal, however, if an individual acquires material, nonpublic information about a corporation through a relationship that involves trust and confidence and then uses that information when buying or selling a security. The SEC has prosecuted corporate employees who traded securities after learning of confidential developments in their companies, friends and family members of corporate officers who bought or sold securities after getting such information, and employees of law firms who misused information they received while providing services to corporations whose securities they traded.⁵

To be guilty of insider trading, a person must:

• buy or sell a security based on information that the person realizes is material and nonpublic,⁶ and
• have received the confidential information under circumstances that create a duty of trust or confidence.⁷

If both of these conditions are met, the person has wrongfully used confidential information with which he was entrusted, or “misappropriated” that information for personal gain.⁸

Physicians sometimes gain information that, if used for investment decisions, might lead to accusations of insider trading. Stock prices of pharmaceutical companies rise before public announcements of clinical drug trials, which suggests that information about those results leaks out in advance.⁹ Recently, physicians have gotten into well-publicized legal trouble by making investment decisions based on information they obtained while participating on an institution’s board¹⁰ and from learning early results of clinical drug trials.¹¹

But would it be wrong for a psychiatrist to make a potentially profitable investment based on information obtained incidentally during a treatment encounter? After all, it’s not as though the psychiatrist would be a corporate insider or would have acquired the information improperly. Yet courts have ruled that a psychiatrist’s trading on such information might constitute malpractice and could be grounds for even more serious legal consequences.

Potential malpractice issues

The federal court ruling in United States v Willis¹² describes how a psychiatrist learned during treatment that a patient’s husband was seeking to become CEO of a large bank. Realizing that this development might make the bank more valuable, the psychiatrist told his broker what he had learned and purchased 13,000 shares of the bank’s stock for himself and his children. When the husband’s efforts were announced publicly a few weeks later, the psychiatrist sold the shares at a big profit.

Quoting the vow of confidentiality contained in the Hippocratic Oath (Box),¹³ the court held that the psychiatrist had an obligation to the patient not to disclose information learned during her treatment without her permission. The court said the patient “had an economic interest in preserving the confidentiality of the information disclosed,” and the psychiatrist’s actions “might have jeopardized her husband’s advancement” and financial benefits the wife would have gained. Also, the psychiatrist’s “disclosures jeopardized the psychiatrist-patient relationship,” which might negate the wife’s financial investment in her care, require her to find a new psychiatrist, or require additional treatment to deal with how the psychiatrist’s behavior had affected her.¹²

Box

More legal consequences

Dr. Willis had legal problems more serious than just a malpractice lawsuit. He faced criminal prosecution for insider trading and mail fraud, and the court refused to dismiss these charges. The court reasoned that the psychiatrist received the information while in a position of trust and confidence, and breached that trust when he used that confidential information for his personal benefit—behavior that meets the legal definition of “misappropriation.” Because the psychiatrist received stock trade confirmations through the U.S. mail, he also could face federal charges of mail fraud. Ultimately, Dr. Willis pled guilty and paid $137,000 in fines and penalties. Although Dr. Willis retained his New Jersey medical license and avoided a prison sentence, the district court sentenced him to 5 years of probation and required that he perform 3,000 hours of community service.^14,15

In a second case,¹⁶ a licensed clinical social worker made investments through a broker based on information learned during a therapy session about upcoming business developments (the 1994 Lockheed-Martin Marietta merger). The social worker pled guilty to insider trading, forfeited the illegal gains, and paid a large fine.

Related Resources

• Insider trading versus medical professionalism. Lancet. 2005;366(9488):781.
• Nijm LM. The online message board controversy. Physicians hit with claims of libel and insider trading by their employers. J Leg Med. 2000;21(2):223-239.

Disclosure

Dr. Mossman reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
My patient is an officer in a large corporation. During therapy, he sometimes talks about how the company is doing. Would I risk malpractice liability if I used this information in managing my retirement investments?
Submitted by “Dr. B”

As most physicians find out within a short time of finishing medical school, doctors learn all kinds of useful things from their patients, including information that can help them manage personal matters outside their practices. But are you allowed to use nonpublic business information to make investment decisions?

As this article explains, legal rules and case law suggest that if psychiatrists or therapists act on potentially profitable business information incidentally mentioned by a patient during treatment, they may be subject to serious legal problems. To explain why, we’ll begin with a brief overview of business terms, including “securities” and “insider trading.” Then, to answer Dr. B’s question, we’ll look at what kind of legal consequences may result if mental health professionals are found guilty of “misappropriating” confidential business information.

Securities and security rules

Approximately one-half to two-thirds of Americans have money invested in the stock market—either through their retirement plans, by owning mutual funds, or by holding stocks of individual companies.¹ Stocks are a type of financial instrument, or security, that companies issue to raise capital. Companies also raise money by issuing debt, typically in the form of bonds that pay interest to the holder, who in buying the bond has in effect loaned money to the company. Derivatives refer to securities that have prices that move up or down depending on the value of some underlying asset, such as stock prices.²

Stock prices fluctuate in reaction to general economic developments—changes in the unemployment rate, in the cost of basic materials (eg, oil or metals used in manufacturing), or in government policies that influence consumers’ purchasing decisions. But the key factor in determining the price of a company’s stock is investors’ beliefs about the company’s future earnings.³ Because investors usually have to make educated guesses about a company’s future, actually knowing something about a company before the general public finds out would give an investor a huge—but possibly unfair—advantage over other investors.

Making markets fair for all investors is the key purpose of U.S. laws on trading securities. In the 1930s, Congress created the Securities and Exchange Commission (SEC), a federal agency charged with ensuring that companies report the truth about their financial situation and that potential investors receive full, fair disclosure of available public information.⁴ Among the many ways that the SEC does this is by enforcing regulations concerning “insider trading.”

‘Insider trading’

Corporate “insiders” (eg, directors or employees) often know a lot about how their businesses are doing, and they buy or sell stock in their own companies. Such trading is legal if the insiders follow federal regulations about the timing of their investments and report them publicly.

Insider trading is illegal, however, if an individual acquires material, nonpublic information about a corporation through a relationship that involves trust and confidence and then uses that information when buying or selling a security. The SEC has prosecuted corporate employees who traded securities after learning of confidential developments in their companies, friends and family members of corporate officers who bought or sold securities after getting such information, and employees of law firms who misused information they received while providing services to corporations whose securities they traded.⁵

To be guilty of insider trading, a person must:

• buy or sell a security based on information that the person realizes is material and nonpublic,⁶ and
• have received the confidential information under circumstances that create a duty of trust or confidence.⁷

If both of these conditions are met, the person has wrongfully used confidential information with which he was entrusted, or “misappropriated” that information for personal gain.⁸

Physicians sometimes gain information that, if used for investment decisions, might lead to accusations of insider trading. Stock prices of pharmaceutical companies rise before public announcements of clinical drug trials, which suggests that information about those results leaks out in advance.⁹ Recently, physicians have gotten into well-publicized legal trouble by making investment decisions based on information they obtained while participating on an institution’s board¹⁰ and from learning early results of clinical drug trials.¹¹

But would it be wrong for a psychiatrist to make a potentially profitable investment based on information obtained incidentally during a treatment encounter? After all, it’s not as though the psychiatrist would be a corporate insider or would have acquired the information improperly. Yet courts have ruled that a psychiatrist’s trading on such information might constitute malpractice and could be grounds for even more serious legal consequences.

Potential malpractice issues

The federal court ruling in United States v Willis¹² describes how a psychiatrist learned during treatment that a patient’s husband was seeking to become CEO of a large bank. Realizing that this development might make the bank more valuable, the psychiatrist told his broker what he had learned and purchased 13,000 shares of the bank’s stock for himself and his children. When the husband’s efforts were announced publicly a few weeks later, the psychiatrist sold the shares at a big profit.

Quoting the vow of confidentiality contained in the Hippocratic Oath (Box),¹³ the court held that the psychiatrist had an obligation to the patient not to disclose information learned during her treatment without her permission. The court said the patient “had an economic interest in preserving the confidentiality of the information disclosed,” and the psychiatrist’s actions “might have jeopardized her husband’s advancement” and financial benefits the wife would have gained. Also, the psychiatrist’s “disclosures jeopardized the psychiatrist-patient relationship,” which might negate the wife’s financial investment in her care, require her to find a new psychiatrist, or require additional treatment to deal with how the psychiatrist’s behavior had affected her.¹²

Box

More legal consequences

Dr. Willis had legal problems more serious than just a malpractice lawsuit. He faced criminal prosecution for insider trading and mail fraud, and the court refused to dismiss these charges. The court reasoned that the psychiatrist received the information while in a position of trust and confidence, and breached that trust when he used that confidential information for his personal benefit—behavior that meets the legal definition of “misappropriation.” Because the psychiatrist received stock trade confirmations through the U.S. mail, he also could face federal charges of mail fraud. Ultimately, Dr. Willis pled guilty and paid $137,000 in fines and penalties. Although Dr. Willis retained his New Jersey medical license and avoided a prison sentence, the district court sentenced him to 5 years of probation and required that he perform 3,000 hours of community service.^14,15

In a second case,¹⁶ a licensed clinical social worker made investments through a broker based on information learned during a therapy session about upcoming business developments (the 1994 Lockheed-Martin Marietta merger). The social worker pled guilty to insider trading, forfeited the illegal gains, and paid a large fine.

Related Resources

• Insider trading versus medical professionalism. Lancet. 2005;366(9488):781.
• Nijm LM. The online message board controversy. Physicians hit with claims of libel and insider trading by their employers. J Leg Med. 2000;21(2):223-239.

Disclosure

Dr. Mossman reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Background and objective Genetic test uptake and cancer risk management have been understudied in medically underserved populations. Study aims were to quantify rates of BRCA1/2 genetic testing and evidence-based cancer risk management (ie, prophylactic surgeries and surveillance practices) in women who were seen for breast and ovarian cancer genetic counseling in a public, safety net health system.

Methods We conducted a retrospective medical record abstraction of 195 women who presented for breast or ovarian genetic counseling within a 2-year period (2008-2009) at Parkland Health & Hospital System in Dallas, Texas.

Results The identified women represented a racially and ethnically diverse population: 48% Hispanic, 37% non-Hispanic black, 12% non-Hispanic white, and 3% Asian. Among the 158 women who were medically eligible for genetic testing, 134 (84.8%) received BRCA1/2 results, with most tests funded through a financial assistance program. In all, 29 women (22%) tested positive for BRCA1/2 mutations. Financial and funding barriers were identified for 20 of the untested women. Among the identified high-risk women (mutation carriers, selected variants, and noncarriers with pretest BRCAPRO scores 30 or more), 26% had prophylactic breast surgeries and 33% had prophylactic ovarian surgeries within the follow-up period averaging 35 months. Of those who opted for surveillance, 71% had at least 1 mammogram or MRI and 38% had CA-125 tests. Trends indicated lower rates of all risk management behaviors, except for mammogram or MRI, among non-Hispanic black women.

Conclusions Within this racially and ethnically diverse sample, BRCA1/2 test uptake was high, but financial barriers were identified for nontested women. The rates of breast cancer risk management were generally comparable with other studies, but risk management for ovarian cancer was limited, especially among non-Hispanic black women. The reasons for these apparen disparities should be further explored.

Click on the PDF icon at the top of this introduction to read the full article.

Background and objective Genetic test uptake and cancer risk management have been understudied in medically underserved populations. Study aims were to quantify rates of BRCA1/2 genetic testing and evidence-based cancer risk management (ie, prophylactic surgeries and surveillance practices) in women who were seen for breast and ovarian cancer genetic counseling in a public, safety net health system.

Methods We conducted a retrospective medical record abstraction of 195 women who presented for breast or ovarian genetic counseling within a 2-year period (2008-2009) at Parkland Health & Hospital System in Dallas, Texas.

Results The identified women represented a racially and ethnically diverse population: 48% Hispanic, 37% non-Hispanic black, 12% non-Hispanic white, and 3% Asian. Among the 158 women who were medically eligible for genetic testing, 134 (84.8%) received BRCA1/2 results, with most tests funded through a financial assistance program. In all, 29 women (22%) tested positive for BRCA1/2 mutations. Financial and funding barriers were identified for 20 of the untested women. Among the identified high-risk women (mutation carriers, selected variants, and noncarriers with pretest BRCAPRO scores 30 or more), 26% had prophylactic breast surgeries and 33% had prophylactic ovarian surgeries within the follow-up period averaging 35 months. Of those who opted for surveillance, 71% had at least 1 mammogram or MRI and 38% had CA-125 tests. Trends indicated lower rates of all risk management behaviors, except for mammogram or MRI, among non-Hispanic black women.

Conclusions Within this racially and ethnically diverse sample, BRCA1/2 test uptake was high, but financial barriers were identified for nontested women. The rates of breast cancer risk management were generally comparable with other studies, but risk management for ovarian cancer was limited, especially among non-Hispanic black women. The reasons for these apparen disparities should be further explored.

Click on the PDF icon at the top of this introduction to read the full article.

Background and objective Genetic test uptake and cancer risk management have been understudied in medically underserved populations. Study aims were to quantify rates of BRCA1/2 genetic testing and evidence-based cancer risk management (ie, prophylactic surgeries and surveillance practices) in women who were seen for breast and ovarian cancer genetic counseling in a public, safety net health system.

Methods We conducted a retrospective medical record abstraction of 195 women who presented for breast or ovarian genetic counseling within a 2-year period (2008-2009) at Parkland Health & Hospital System in Dallas, Texas.

Results The identified women represented a racially and ethnically diverse population: 48% Hispanic, 37% non-Hispanic black, 12% non-Hispanic white, and 3% Asian. Among the 158 women who were medically eligible for genetic testing, 134 (84.8%) received BRCA1/2 results, with most tests funded through a financial assistance program. In all, 29 women (22%) tested positive for BRCA1/2 mutations. Financial and funding barriers were identified for 20 of the untested women. Among the identified high-risk women (mutation carriers, selected variants, and noncarriers with pretest BRCAPRO scores 30 or more), 26% had prophylactic breast surgeries and 33% had prophylactic ovarian surgeries within the follow-up period averaging 35 months. Of those who opted for surveillance, 71% had at least 1 mammogram or MRI and 38% had CA-125 tests. Trends indicated lower rates of all risk management behaviors, except for mammogram or MRI, among non-Hispanic black women.

Conclusions Within this racially and ethnically diverse sample, BRCA1/2 test uptake was high, but financial barriers were identified for nontested women. The rates of breast cancer risk management were generally comparable with other studies, but risk management for ovarian cancer was limited, especially among non-Hispanic black women. The reasons for these apparen disparities should be further explored.

Click on the PDF icon at the top of this introduction to read the full article.

Dr. David Henry's podcast covers highlights of the November issue including pazopanib in soft tissue sarcoma and dasatinib in first-line treatment of chronic myeloid leukemia.

Dr. David Henry's podcast covers highlights of the November issue including pazopanib in soft tissue sarcoma and dasatinib in first-line treatment of chronic myeloid leukemia.

Dr. David Henry's podcast covers highlights of the November issue including pazopanib in soft tissue sarcoma and dasatinib in first-line treatment of chronic myeloid leukemia.

John Almquist, MD, FHM, director of hospitalist services for Ministry Health Care, a 15-hospital system serving rural Wisconsin, believes that an "e-hospitalist" pilot project now being tested at Ministry St. Mary's Hospital in Rhinelander, Wis., could be a boon for rural communities that have difficulty recruiting primary-care physicians (PCPs).

When the hospitals in those communities are unable to offer hospitalist coverage, it makes the setting less attractive to PCPs because they might have to follow their patients in the hospital day and night, he explains.

Ministry recruited and trained two nurse practitioners who will soon be deployed at a critical-access hospital in Eagle River, population 1,443, supported remotely by the eight-member HM group in Rhinelander for consultations, supervision, and multidisciplinary rounds. The training is bolstered by written order sets focused on 30 common medical conditions that lead to admissions to rural hospitals.

"The hospitalist in Rhinelander is also able to talk directly to the patient at the remote site," Dr. Almquist says.

The e-hospitalist program uses a telehealth network developed by Marshfield Clinic, a multispecialty physician group practice based in Marshfield, Wis. The clinic recently received a $1 million grant from the federal government to expand its 15-year-old telemedicine program. Part of the grant money is being used to expand the ehospitalist approach to new sites.

Visit our website for more information about hospitalists and telemedicine.

John Almquist, MD, FHM, director of hospitalist services for Ministry Health Care, a 15-hospital system serving rural Wisconsin, believes that an "e-hospitalist" pilot project now being tested at Ministry St. Mary's Hospital in Rhinelander, Wis., could be a boon for rural communities that have difficulty recruiting primary-care physicians (PCPs).

When the hospitals in those communities are unable to offer hospitalist coverage, it makes the setting less attractive to PCPs because they might have to follow their patients in the hospital day and night, he explains.

Ministry recruited and trained two nurse practitioners who will soon be deployed at a critical-access hospital in Eagle River, population 1,443, supported remotely by the eight-member HM group in Rhinelander for consultations, supervision, and multidisciplinary rounds. The training is bolstered by written order sets focused on 30 common medical conditions that lead to admissions to rural hospitals.

"The hospitalist in Rhinelander is also able to talk directly to the patient at the remote site," Dr. Almquist says.

The e-hospitalist program uses a telehealth network developed by Marshfield Clinic, a multispecialty physician group practice based in Marshfield, Wis. The clinic recently received a $1 million grant from the federal government to expand its 15-year-old telemedicine program. Part of the grant money is being used to expand the ehospitalist approach to new sites.

Visit our website for more information about hospitalists and telemedicine.

John Almquist, MD, FHM, director of hospitalist services for Ministry Health Care, a 15-hospital system serving rural Wisconsin, believes that an "e-hospitalist" pilot project now being tested at Ministry St. Mary's Hospital in Rhinelander, Wis., could be a boon for rural communities that have difficulty recruiting primary-care physicians (PCPs).

When the hospitals in those communities are unable to offer hospitalist coverage, it makes the setting less attractive to PCPs because they might have to follow their patients in the hospital day and night, he explains.

Ministry recruited and trained two nurse practitioners who will soon be deployed at a critical-access hospital in Eagle River, population 1,443, supported remotely by the eight-member HM group in Rhinelander for consultations, supervision, and multidisciplinary rounds. The training is bolstered by written order sets focused on 30 common medical conditions that lead to admissions to rural hospitals.

"The hospitalist in Rhinelander is also able to talk directly to the patient at the remote site," Dr. Almquist says.

The e-hospitalist program uses a telehealth network developed by Marshfield Clinic, a multispecialty physician group practice based in Marshfield, Wis. The clinic recently received a $1 million grant from the federal government to expand its 15-year-old telemedicine program. Part of the grant money is being used to expand the ehospitalist approach to new sites.

Visit our website for more information about hospitalists and telemedicine.

Clinical question: Does the addition of clopidogrel to aspirin reduce the risk of any type of recurrent stroke, or affect the risk of bleeding or death, in patients who recently suffered a lacunar stroke?

Background: There are no prior randomized, multicenter trials on secondary prevention of lacunar stroke; aspirin is the standard antiplatelet therapy in this setting.

Study design: Double-blind, randomized, multicenter trial.

Setting: Eighty-two clinical centers in North America, Latin America, and Spain.

Synopsis: Researchers enrolled 3,020 patients from 2003 to 2011; criteria included age >30 years old and symptomatic lacunar stroke (proven by MRI) in the preceding 180 days.

Results showed no significant difference between recurrent strokes (any type) in the aspirin-only group (2.7% per year) versus the aspirin-plus-clopidogrel group (2.5% per year). Major hemorrhage risk was much higher in the aspirin-plus-clopidogrel group (2.1% per year) versus aspirin-only group (1.1% per year). All-cause mortality also was much higher in the aspirin-plus-clopidogrel group (N=113) versus the aspirin-only group (N=77).

Bottom line: The addition of clopidogrel to aspirin for secondary prevention does not significantly reduce the risk of recurrent stroke, but it does significantly increase the risk of bleeding and death.

Citation: Benavente OR, Hart RG, McClure LA, et al. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012;367:817-825.

For more physician reviews of recent HM-relevant literature, visit our website.

Clinical question: Does the addition of clopidogrel to aspirin reduce the risk of any type of recurrent stroke, or affect the risk of bleeding or death, in patients who recently suffered a lacunar stroke?

Background: There are no prior randomized, multicenter trials on secondary prevention of lacunar stroke; aspirin is the standard antiplatelet therapy in this setting.

Study design: Double-blind, randomized, multicenter trial.

Setting: Eighty-two clinical centers in North America, Latin America, and Spain.

Synopsis: Researchers enrolled 3,020 patients from 2003 to 2011; criteria included age >30 years old and symptomatic lacunar stroke (proven by MRI) in the preceding 180 days.

Results showed no significant difference between recurrent strokes (any type) in the aspirin-only group (2.7% per year) versus the aspirin-plus-clopidogrel group (2.5% per year). Major hemorrhage risk was much higher in the aspirin-plus-clopidogrel group (2.1% per year) versus aspirin-only group (1.1% per year). All-cause mortality also was much higher in the aspirin-plus-clopidogrel group (N=113) versus the aspirin-only group (N=77).

Bottom line: The addition of clopidogrel to aspirin for secondary prevention does not significantly reduce the risk of recurrent stroke, but it does significantly increase the risk of bleeding and death.

Citation: Benavente OR, Hart RG, McClure LA, et al. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012;367:817-825.

For more physician reviews of recent HM-relevant literature, visit our website.

Clinical question: Does the addition of clopidogrel to aspirin reduce the risk of any type of recurrent stroke, or affect the risk of bleeding or death, in patients who recently suffered a lacunar stroke?

Background: There are no prior randomized, multicenter trials on secondary prevention of lacunar stroke; aspirin is the standard antiplatelet therapy in this setting.

Study design: Double-blind, randomized, multicenter trial.

Setting: Eighty-two clinical centers in North America, Latin America, and Spain.

Synopsis: Researchers enrolled 3,020 patients from 2003 to 2011; criteria included age >30 years old and symptomatic lacunar stroke (proven by MRI) in the preceding 180 days.

Results showed no significant difference between recurrent strokes (any type) in the aspirin-only group (2.7% per year) versus the aspirin-plus-clopidogrel group (2.5% per year). Major hemorrhage risk was much higher in the aspirin-plus-clopidogrel group (2.1% per year) versus aspirin-only group (1.1% per year). All-cause mortality also was much higher in the aspirin-plus-clopidogrel group (N=113) versus the aspirin-only group (N=77).

Bottom line: The addition of clopidogrel to aspirin for secondary prevention does not significantly reduce the risk of recurrent stroke, but it does significantly increase the risk of bleeding and death.

Citation: Benavente OR, Hart RG, McClure LA, et al. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012;367:817-825.

For more physician reviews of recent HM-relevant literature, visit our website.

ANSWER
This ECG demonstrates normal sinus rhythm, right-axis deviation, evidence of a lateral MI, and inferolateral ST- and T-wave abnormalities.

Right-axis deviation is indicated by an R-wave axis between 90° and 180° and QS or QR complexes in lead I and/or aVL. While the most common cause of a right-axis deviation is right ventricular hypertrophy, it is also evident in a lateral MI. Evidence for the latter includes the presence of significant Q waves in leads I and aVL. Finally, inferolateral ST- and T-wave changes are evidenced by inverted T waves in leads II, III, aVF, and precordial leads V₄ to V₆. 

ECG evidence of a lateral MI not present on a previous scan (eight months ago), in the presence of a normal troponin level, suggests a recent MI.           

ANSWER
This ECG demonstrates normal sinus rhythm, right-axis deviation, evidence of a lateral MI, and inferolateral ST- and T-wave abnormalities.

Right-axis deviation is indicated by an R-wave axis between 90° and 180° and QS or QR complexes in lead I and/or aVL. While the most common cause of a right-axis deviation is right ventricular hypertrophy, it is also evident in a lateral MI. Evidence for the latter includes the presence of significant Q waves in leads I and aVL. Finally, inferolateral ST- and T-wave changes are evidenced by inverted T waves in leads II, III, aVF, and precordial leads V₄ to V₆. 

ECG evidence of a lateral MI not present on a previous scan (eight months ago), in the presence of a normal troponin level, suggests a recent MI.           

ANSWER
This ECG demonstrates normal sinus rhythm, right-axis deviation, evidence of a lateral MI, and inferolateral ST- and T-wave abnormalities.

Right-axis deviation is indicated by an R-wave axis between 90° and 180° and QS or QR complexes in lead I and/or aVL. While the most common cause of a right-axis deviation is right ventricular hypertrophy, it is also evident in a lateral MI. Evidence for the latter includes the presence of significant Q waves in leads I and aVL. Finally, inferolateral ST- and T-wave changes are evidenced by inverted T waves in leads II, III, aVF, and precordial leads V₄ to V₆. 

ECG evidence of a lateral MI not present on a previous scan (eight months ago), in the presence of a normal troponin level, suggests a recent MI.           

ANSWER
The correct answer is all of the above (choice “d”). Prolonged injudicious use of topical steroids can cause a number of problems, including these; they are collectively termed iatrogenic since they are ultimately caused by prescribed medication. One of the more difficult aspects of this problem to deal with is the “addictive” state, in which withdrawal symptoms compel the patient to continue applying the offending steroid cream.

DISCUSSION
This is a relatively common scenario in dermatology offices. The misuse of topical steroids is well known, and something we strive to prevent—but with mixed results. It’s one of the reasons we’re stingy with refills of such medications, requiring the patient to be seen at least once a year. Unfortunately, this patient had been getting “refills” from friends in Mexico; patients often “borrow” steroid creams from household members or friends, or use products prescribed for one condition to treat others for which they were not intended.

The primary mode of action of topical steroids is vasoconstriction, a positive thing in terms of reduction of inflammation. The bad news is that continuous use of class 1 (the most powerful) steroids, such as clobetasol, can cause such profound and prolonged vasoconstriction that the skin effectively loses its blood supply and withers, sometimes down to adipose tissue. As one might suspect, this is more likely in already thin-skinned areas, including the antecubital area, face, neck, eyelids, and genitals, where the creation of striae is especially common.

Fairly early on in this process, before frank atrophy occurs, the condition being treated usually resolves. However, when the steroid is stopped, stinging and itching immediately return—which, of course, causes the patient to reapply the medication, perpetuating the vicious cycle.

The cycle is ultimately broken by gradual reduction in the frequency of application of successively weaker steroids. Usually, the skin gradually regenerates and returns to normal. In this case, the process will be lengthy and will almost certainly result in significant scarring.

Even injudicious application of weaker classes of steroids (eg, hydrocortisone 2.5% cream) to areas such as the face can result in a range of deleterious effects, including localized rosacea-like eruption or erythema. It has been reported that approximately 75% of cases of perioral dermatitis are either caused by or exacerbated by the application of topical steroids.

Topical application of even mid-strength steroids can also have systemic effects (eg, adrenal suppression, hyperglycemia) if applied over large areas. This is especially true when pediatric patients are involved.

Prevention of these iatrogenic effects lies in selecting the lowest strength steroid for the condition and area in question, then using them sparingly: no more than twice a day, and for no more than five days in a row, stopping for two consecutive days to allow the skin to regenerate. Even more caution should be exercised in treating children and when applying the product to intertriginous areas (skin-on-skin areas, such as the groin, in axillae, or under the breasts). Covering steroid-treated areas with anything—bandages, socks, even skin—effectively potentiates the positive and negative effects of steroids.

ANSWER
The correct answer is all of the above (choice “d”). Prolonged injudicious use of topical steroids can cause a number of problems, including these; they are collectively termed iatrogenic since they are ultimately caused by prescribed medication. One of the more difficult aspects of this problem to deal with is the “addictive” state, in which withdrawal symptoms compel the patient to continue applying the offending steroid cream.

DISCUSSION
This is a relatively common scenario in dermatology offices. The misuse of topical steroids is well known, and something we strive to prevent—but with mixed results. It’s one of the reasons we’re stingy with refills of such medications, requiring the patient to be seen at least once a year. Unfortunately, this patient had been getting “refills” from friends in Mexico; patients often “borrow” steroid creams from household members or friends, or use products prescribed for one condition to treat others for which they were not intended.

The primary mode of action of topical steroids is vasoconstriction, a positive thing in terms of reduction of inflammation. The bad news is that continuous use of class 1 (the most powerful) steroids, such as clobetasol, can cause such profound and prolonged vasoconstriction that the skin effectively loses its blood supply and withers, sometimes down to adipose tissue. As one might suspect, this is more likely in already thin-skinned areas, including the antecubital area, face, neck, eyelids, and genitals, where the creation of striae is especially common.

Fairly early on in this process, before frank atrophy occurs, the condition being treated usually resolves. However, when the steroid is stopped, stinging and itching immediately return—which, of course, causes the patient to reapply the medication, perpetuating the vicious cycle.

The cycle is ultimately broken by gradual reduction in the frequency of application of successively weaker steroids. Usually, the skin gradually regenerates and returns to normal. In this case, the process will be lengthy and will almost certainly result in significant scarring.

Even injudicious application of weaker classes of steroids (eg, hydrocortisone 2.5% cream) to areas such as the face can result in a range of deleterious effects, including localized rosacea-like eruption or erythema. It has been reported that approximately 75% of cases of perioral dermatitis are either caused by or exacerbated by the application of topical steroids.

Topical application of even mid-strength steroids can also have systemic effects (eg, adrenal suppression, hyperglycemia) if applied over large areas. This is especially true when pediatric patients are involved.

Prevention of these iatrogenic effects lies in selecting the lowest strength steroid for the condition and area in question, then using them sparingly: no more than twice a day, and for no more than five days in a row, stopping for two consecutive days to allow the skin to regenerate. Even more caution should be exercised in treating children and when applying the product to intertriginous areas (skin-on-skin areas, such as the groin, in axillae, or under the breasts). Covering steroid-treated areas with anything—bandages, socks, even skin—effectively potentiates the positive and negative effects of steroids.

ANSWER
The correct answer is all of the above (choice “d”). Prolonged injudicious use of topical steroids can cause a number of problems, including these; they are collectively termed iatrogenic since they are ultimately caused by prescribed medication. One of the more difficult aspects of this problem to deal with is the “addictive” state, in which withdrawal symptoms compel the patient to continue applying the offending steroid cream.

DISCUSSION
This is a relatively common scenario in dermatology offices. The misuse of topical steroids is well known, and something we strive to prevent—but with mixed results. It’s one of the reasons we’re stingy with refills of such medications, requiring the patient to be seen at least once a year. Unfortunately, this patient had been getting “refills” from friends in Mexico; patients often “borrow” steroid creams from household members or friends, or use products prescribed for one condition to treat others for which they were not intended.

The primary mode of action of topical steroids is vasoconstriction, a positive thing in terms of reduction of inflammation. The bad news is that continuous use of class 1 (the most powerful) steroids, such as clobetasol, can cause such profound and prolonged vasoconstriction that the skin effectively loses its blood supply and withers, sometimes down to adipose tissue. As one might suspect, this is more likely in already thin-skinned areas, including the antecubital area, face, neck, eyelids, and genitals, where the creation of striae is especially common.

Fairly early on in this process, before frank atrophy occurs, the condition being treated usually resolves. However, when the steroid is stopped, stinging and itching immediately return—which, of course, causes the patient to reapply the medication, perpetuating the vicious cycle.

The cycle is ultimately broken by gradual reduction in the frequency of application of successively weaker steroids. Usually, the skin gradually regenerates and returns to normal. In this case, the process will be lengthy and will almost certainly result in significant scarring.

Even injudicious application of weaker classes of steroids (eg, hydrocortisone 2.5% cream) to areas such as the face can result in a range of deleterious effects, including localized rosacea-like eruption or erythema. It has been reported that approximately 75% of cases of perioral dermatitis are either caused by or exacerbated by the application of topical steroids.

Topical application of even mid-strength steroids can also have systemic effects (eg, adrenal suppression, hyperglycemia) if applied over large areas. This is especially true when pediatric patients are involved.

Prevention of these iatrogenic effects lies in selecting the lowest strength steroid for the condition and area in question, then using them sparingly: no more than twice a day, and for no more than five days in a row, stopping for two consecutive days to allow the skin to regenerate. Even more caution should be exercised in treating children and when applying the product to intertriginous areas (skin-on-skin areas, such as the groin, in axillae, or under the breasts). Covering steroid-treated areas with anything—bandages, socks, even skin—effectively potentiates the positive and negative effects of steroids.