Current Medical Diagnosis & Treatment 2015

41

Sports Medicine & Outpatient Orthopedics

Anthony Luke, MD, MPH
C. Benjamin Ma, MD

GENERAL APPROACH TO MUSCULOSKELETAL INJURIES

 ESSENTIALS OF DIAGNOSIS

 History is most important in diagnosing musculoskeletal problems.

 The mechanism of injury can explain the pathology and symptoms.

 Determine whether the injury is traumatic or atraumatic, acute or chronic, high or low velocity (greater velocity suggests more structural damage), or whether any movement aggravates or relieves pain associated with the injury.

 General Considerations

Musculoskeletal problems account for about 10–20% of outpatient primary care clinical visits. Orthopedic problems can be classified as traumatic (ie, injury-related) or atraumatic (ie, degenerative or overuse syndromes) as well as acute or chronic. The mechanism of injury is usually the most helpful part of the history in determining the diagnosis.

The onset of symptoms should be elicited. With acute traumatic injuries, patients typically seek medical attention within 6 weeks of onset. The patient should describe the exact location of symptoms, which helps determine anatomic structures that may be damaged. If the patient is vague, the clinician can ask the patient to point with one finger only to the point of maximal tenderness.

 Clinical Findings

  1. Symptoms and Signs

The chief musculoskeletal complaints are typically pain (most common), instability or dysfunction around the joints. Since symptoms and signs are often nonspecific, recognizing the expected combination of symptoms and physical examination signs can help facilitate the clinical diagnosis. Patients may describe symptoms of “locking” or “catching,” suggesting internal derangement in joints. Symptoms of “instability” or “giving way” suggest ligamentous injury; however, these symptoms may also be due to pain causing muscular inhibition. Constitutional symptoms of fever or weight loss, swelling with no injury, or systemic illness suggest medical conditions (such as infection, cancer, or rheumatologic disease).

Initial evaluation should follow routine trauma guidelines to rule out serious joint injury. However, typical evaluations in the clinic follow the traditional components of the physical examination and should include inspectionpalpation, and assessment of range of motion and neurovascular status.

Inspection includes observation of swelling, erythema, atrophy, deformity, and (surgical) scars (mnemonic, “SEADS”). The patient should be asked to move joints of concern (for example, see Table 41–1). If motion is asymmetric, the clinician should assess the passive range of motion for any physical limitation.

Table 41–1. Shoulder examination.

There are special tests to assess each joint. Typically, provocative tests recreate the mechanism of injury with the goal to reproduce the patient’s pain. Stress tests apply load to ligaments of concern. Typically, 10 to 15 pounds of force should be applied when performing stress tests. Functional testing, including simple tasks performed during activities of daily living, is useful to assess injury severity.

  1. Imaging

Bony pathology can be assessed using standard radiographs, although there also may be characteristic soft tissue findings. However, CT scans are the most effective method for visualizing any bony pathology, including morphology of fractures. Nuclear bone scans are now less commonly used but are still valuable for identifying stress injuries, infection, malignancy, or multisite pathology. Positron emission tomography (PET) scans are useful in identifying metastatic malignant lesions. MRI provides excellent visualization of ligaments, cartilage, and soft tissues. High Field 3.0 Tesla MRI is available clinically and allows higher image resolution and decreased examination times compared to the standard 1.5 Tesla machines. Gadolinium contrast can be injected as an MRI arthrogram to increase sensitivity of detecting certain internal derangements in joints such as labral injuries. Musculoskeletal ultrasound, where available, can be useful for identifying superficial tissue problems, including tendinopathies and synovial problems.

  1. Special Tests

Arthrocentesis must be performed promptly to rule out an infection when acute knee pain with effusion and inflammation are present and the patient is unable to actively flex the joint (see Tables 20–2 and20–3). The joint fluid should be sent for cell count, crystal analysis, and culture. Arthrocentesis and joint fluid analysis demonstrating crystals can lead to the diagnosis of gout (negatively birefringent, needle-shaped crystals) or pseudogout (positively birefringent, rectangular-shaped crystals). In large, uncomfortable knee joint effusions, removal of excessive joint fluid may improve joint range of motion (flexion) and patient comfort. To avoid infecting the joint, arthrocentesis should not be performed when there is an active cellulitis or abscess overlying the joint. It appears the risk of bleeding after arthrocentesis or joint injection is extremely low even if the patient is taking anticoagulants. Caution should be practiced if the INR is > 3.0; however, even a supratherapeutic INR did not suggest an increased risk of hemarthrosis in one study. Markers of inflammation such as complete blood cell count, erythrocyte sedimentation rate, and C-reactive protein, and rheumatologic tests are useful in evaluating for infectious, oncologic, or rheumatologic processes. Electrodiagnostic studies such as electromyography and nerve conduction studies are useful when there are neurologic concerns; they can also help with prognostication in chronic conditions.

 Treatment

While most outpatient musculoskeletal problems are best treated conservatively, the first consideration is whether there is an immediate surgical need. Surgical treatment is chosen when the outcome promises better health, restoration of function, and improved quality of life. During surgery, the musculoskeletal problem is usually repaired, removed, realigned, reconstructed, or replaced (eg, joint replacement).

If surgery is not immediately indicated, conservative treatment in the outpatient setting usually includes modification of activities, ice, compression, and elevation (remembered by the mnemonic, “MICE”). Controlling pain is an early concern for most patients. Commonly prescribed medications are analgesics (nonsteroidal anti-inflammatory drugs [NSAIDs], acetaminophen, or opioids). Other medications that may also be prescribed, albeit less commonly, are muscle relaxants or co-analgesics for neuropathic pain (which include the calcium channel alpha-2-delta ligands [eg, gabapentin] or tricyclic antidepressants). Topical medications, such as capsaicin cream or patch, lidocaine patches, and NSAID patches or gels, can help provide superficial local pain relief.

Immobilization by casting, slings, and braces is helpful to protect an injured limb. Crutches are useful to reduce weight bearing. Rehabilitation and physical therapy are frequently needed. Other modalities commonly used by patients include chiropractic manipulation, massage therapy, acupuncture, heat, and osteopathy.

 When to Refer

Indications for emergency referral (immediate)

  • Neurovascular injury.
  • Fractures (open, unstable).
  • Unreduced joint dislocation.
  • Septic arthritis.

Indications for urgent referral (within 7 days)

  • Fractures (closed, stable).
  • After reduction of a joint dislocation.
  • “Locked” joint (inability to fully extend a joint due to mechanical derangement, usually a loose body or torn cartilage).
  • Tumor.

Indications for early orthopedic assessment (2–4 weeks)

  • Motor weakness (neurologic).
  • Constitutional symptoms (eg, weight loss, fever not due to septic arthritis).
  • Multiple joint involvement.

Indications for routine orthopedic assessment (for further management)

  • Failure of conservative treatment (persistent symptoms > 3 months).
  • Persistent numbness and tingling in an extremity.

Ahmed I et al. Safety of arthrocentesis and joint injection in patients receiving anticoagulation at therapeutic levels. Am J Med. 2012 Mar;125(3):265–9. [PMID: 22340924]

Patel KV et al. Prevalence and impact of pain among older adults in the United States: findings from the 2011 National Health and Aging Trends Study. Pain. 2013 Dec;154(12):2649–57. [PMID: 24287107]

Shapiro L et al. Advances in musculoskeletal MRI: technical considerations. J Magn Reson Imaging. 2012 Oct;36(4):775–87. [PMID: 22987756]

SHOULDER

  1. Subacromial Impingement Syndrome

 ESSENTIALS OF DIAGNOSIS

 Shoulder pain with overhead motion.

 Night pain with sleeping on shoulder.

 Pain with internal rotation.

 Numbness and pain radiation below the elbow are usually due to cervical spine disease.

 General Considerations

The subacromial impingement syndrome describes a collection of diagnoses that cause mechanical inflammation in the subacromial space. Causes of impingement syndrome can be related to muscle strength imbalances, poor scapula control, rotator cuff tears, and subacromial bone spurs.

The chief complaints for shoulder problems are usually pain, instability, weakness, or loss of range of motion. With any shoulder problem, it is important to establish the patient’s hand dominance, occupation, and recreational activities because shoulder injuries may present differently depending on the demands placed on the shoulder joint. For example, baseball pitchers with impingement syndrome may complain of pain while throwing. Alternatively, elders with even full thickness rotator cuff tears may not complain of any pain because the demands on the joint are low.

 Clinical Findings

  1. Symptoms and Signs

Shoulder problems classically present with one or more of the following: pain with overhead activities, nocturnal pain with sleeping on the shoulder, or pain on internal rotation (eg, putting on a jacket or bra). On inspection, there may be appreciable atrophy in the supraspinatus or infraspinatus fossa. The patient with impingement syndrome can have mild scapula winging or “dyskinesis.” The patient often has a rolled-forward shoulder posture or head-forward posture. On palpation, the patient can have tenderness over the anterolateral shoulder at the edge of the greater tuberosity. The patient may lack full active range of motion (Table 41–1) but should have preserved passive range of motion. Impingement symptoms can be elicited with the Neer and Hawkins impingement signs (Table 41–1).

  1. Imaging

The following four radiographic views should be ordered to evaluate subacromial impingement syndrome: the anteroposterior (AP) scapula, the AP acromioclavicular joint, the lateral scapula (scapular Y), and the axillary lateral. The AP scapula view can rule out glenohumeral joint arthritis. The AP acromioclavicular view evaluates the acromioclavicular joint for inferior spurs. The scapula Y view evaluates the acromial shape, and the axillary lateral view visualizes the glenohumeral joint as well and for the presence of os acromiale.

MRI of the shoulder may demonstrate full or partial thickness tears or tendinosis. Ultrasound evaluation may demonstrate thickening of the rotator cuff tendons and tendinosis. Tears may also be visualized, although it is more difficult to identify partial tears from small full thickness on ultrasound than on MRI.

 Treatment

  1. Conservative

The first-line treatment for impingement syndrome is usually a conservative approach with education, activity modification, and physical therapy exercises. Impingement syndrome can be caused by muscle weakness or tear. Rotator cuff muscle strengthening can alleviate weakness or pain, unless the tendons are seriously compromised, which may cause more symptoms. Physical therapy is directed at rotator cuff muscle strengthening, scapula stabilization, and postural exercises. There is no strong evidence supporting the effectiveness of ice and NSAIDs as a prolonged therapy. In a Cochrane review, corticosteroid injections produced slightly better relief of symptoms in the short-term when compared with placebo. Most patients respond well to conservative treatment.

  1. Surgical

Procedures include arthroscopic acromioplasty with coracoacromial ligament release, bursectomy, or debridement or repair of rotator cuff tears.

 When to Refer

  • Failure of conservative treatment over 3 months.
  • Young and active patients with impingement due to full thickness rotator cuff tears.

Hegedus EJ et al. Which physical examination tests provide clinicians with the most value when examining the shoulder? Update of a systematic review with meta-analysis of individual tests. Br J Sports Med. 2012 Nov;46(14):964–78. [PMID: 22773322]

  1. Rotator Cuff Tears

 ESSENTIALS OF DIAGNOSIS

 A common cause of shoulder impingement syndrome after age 40.

 Difficulty lifting the arm with limited active range of motion.

 Weakness with resisted strength testing suggests full thickness tears.

 General Considerations

Rotator cuff tears can be caused by acute injuries related to falls on an outstretched arm or to pulling on the shoulder. It can also be related to chronic repetitive injuries with overhead movement and lifting.Partial rotator cuff tears are one of the most common reasons for impingement syndrome. Full thickness rotator cuff tears are usually more symptomatic and may require surgical treatment. The most commonly torn tendon is the supraspinatus.

 Clinical Findings

  1. Symptoms and Signs

Most patients complain of weakness or pain with overhead movement. Night pain is also a common complaint. The clinical findings with rotator cuff tears include those of the impingement syndrome except that with full-thickness rotator cuff tears there may be more obvious weakness noted with light resistance testing of specific rotator cuff muscles. Supraspinatus tendon strength is tested with resisted shoulder abduction at 90 degrees with slight forward flexion to around 45 degrees (“open can” test) (Table 41–1). Infraspinatus/teres minor strength is tested with resisted shoulder external rotation with shoulder at 0 degrees abduction, elbow by side (Table 41–1). Subscapularis strength is tested with the “lift-off” or “belly-press” tests (Table 41–1). The affected patient usually also has positive Neer and Hawkins impingement tests.

  1. Imaging

Recommended radiographs are very similar to impingement syndrome: AP scapula (glenohumeral), axillary lateral, supraspinatus outlet, and AP acromioclavicular joint views. The AP scapula view is useful in visualizing rotator cuff tears because degenerative changes can appear between the acromion and greater tuberosity of the shoulder. Axillary lateral views show superior elevation of the humeral head in relation to the center of the glenoid. Supraspinatus outlet views allow evaluation of the shape of the acromion. High-grade acromial spurs are associated with a higher incidence of rotator cuff tears. The AP acromioclavicular joint view evaluates for the presence of acromioclavicular joint arthritis, which can mimic rotator cuff tears, and for spurs that can cause rotator cuff injuries.

MRI is the best method for visualizing rotator cuff tears. The MR arthrogram can show partial or small (< 1 cm) rotator cuff tears. For patients who cannot undergo MRI testing or when postoperative artifacts limit MRI evaluations, ultrasonography can be helpful.

 Treatment

Partial rotator cuff tears may heal with scarring. Most partial rotator cuff tears can be treated with physical therapy and scapular and rotator cuff muscle strengthening. However, research suggests that that 40% of the partial thickness tears progress to full thickness tears in 2 years. Physical therapy can strengthen the remaining muscles to compensate for loss of strength and can have high rate of success for chronic tears. Physical therapy is also an option for older sedentary patients. On the contrary, full-thickness rotator cuff tears do not heal well and also have a tendency to increase in size with time. Fatty infiltration progresses in full thickness rotator cuff tears and it is a negative prognostic factor for successful surgical treatment. Most young active patients with acute, full-thickness tears should be treated with operative fixation. In particular, subscapularis tendon injuries warrant different treatment. Full-thickness subscapularis tendon tears should undergo surgical repair as they usually lead to premature osteoarthritis of the shoulder.

 When to Refer

  • Young and active patients with full thickness rotator cuff tears.
  • Partial tears with > 50% involvement and with significant pain.
  • Older and sedentary patients with full-thickness rotator cuff tears who have not responded to nonoperative treatment.
  • Full thickness subscapularis tears.

Kuhn JE et al; MOON Shoulder Group. Effectiveness of physical therapy in treating atraumatic full-thickness rotator cuff tears: a multicenter prospective cohort study. J Shoulder Elbow Surg. 2013 Oct;22(10):1371–9. [PMID: 23540577]

Longo UG et al. Conservative treatment and rotator cuff tear progression. Med Sport Sci. 2012;57:90–9. [PMID: 21986048]

Pedowitz RA et al; American Academy of Orthopaedic Surgeons. Optimizing the management of rotator cuff problems. J Am Acad Orthop Surg. 2011 Jun;19(6):368–79. [PMID: 21628648]

  1. Shoulder Dislocation & Instability

 ESSENTIALS OF DIAGNOSIS

 Most dislocations (95%) are in the anterior direction.

 Pain and apprehension with an unstable shoulder that is abducted and externally rotated.

 Acute shoulder dislocations should be reduced as quickly as possible, using manual relocation techniques if necessary.

 General Considerations

The shoulder is a ball and socket joint, similar to the hip. However, the bony contours of the shoulder bones are much different than the hip. Overall, the joint has much less stability than the hip, allowing greater movement and action. Stabilizing the shoulder joint relies heavily on rotator cuff muscle strength and also scapular control. If patients have poor scapular control or weak rotator cuff tendons or tears, their shoulders are more likely to have instability. Ninety-five percent of the shoulder dislocations/instability occur in the anterior direction. Dislocations usually are caused by a fall on an outstretched and abducted arm. Patients complain of pain and feeling of instability when the arm is in the abducted and externally rotated position. Posterior dislocations are usually caused by falls from a height, epileptic seizures, or electric shocks. Traumatic shoulder dislocation can lead to instability. The rate of repeated dislocation is directly related to the patient’s age: patients age 21 years or younger have a 70–90% risk of redislocation, whereas patients age 40 years or older have a much lower rate (20–30%). Ninety percent of young active individuals who had traumatic shoulder dislocation have labral injuries often described as Bankart lesions when the anterior inferior labrum is torn, which can lead to continued instability. Older patients (over age 55 years) are more likely to have rotator cuff tears or fractures following dislocation. Atraumatic shoulder dislocations are usually caused by intrinsic ligament laxity or repetitive microtrauma leading to joint instability. This is often seen in swimmers, gymnasts, and pitchers as well as other athletes involved in overhead and throwing sports.

 Clinical Findings

  1. Symptoms and Signs

For acute traumatic dislocations, patients usually have an obvious deformity with the humeral head dislocated anteriorly. The patient holds the shoulder and arm in an externally rotated position. The patient complains of acute pain and deformity that are improved with manual relocation of the shoulder. Reductions are usually performed in the emergency department. Even after reduction, the patient will continue to have limited range of motion and pain for 4–6 weeks, especially following a first-time shoulder dislocation.

Patients with recurrent dislocations can have less pain with subsequent dislocations. Posterior dislocations can be easily missed because the patient usually holds the shoulder and arm in an internally rotated position, which makes the shoulder deformity less obvious. Patients complain of difficulty pushing open a door.

Atraumatic shoulder instability is usually well tolerated with activities of daily living. Patients usually complain of a “sliding” sensation during exercises or strenuous activities such as throwing. Such dislocations may be less symptomatic and can often undergo spontaneous reduction of the shoulder with pain resolving within days after onset. The clinical examination for shoulder instability includes the apprehension test (Table 41–1), the load and shift test (Table 41–1) and the O’Brien test (Table 41–1). Most patients with persistent shoulder instability have preserved range of motion.

  1. Imaging

Radiographs for acute dislocations should include a standard trauma series of AP and axillary lateral scapula (glenohumeral) views to determine the relationship of the humerus and the glenoid and to rule out fractures. Orthogonal views are used to identify a posterior shoulder dislocation, which can be missed easily with one AP view of the shoulder. An axillary lateral view of the shoulder can be safely performed even in the acute setting of a patient with a painful shoulder dislocation. For chronic injuries or symptomatic instability, these recommended radiographic views are helpful to identify bony injuries and Hill-Sachs lesions (indented compression fractures at the posterior-superior part of the humeral head associated with anterior shoulder dislocation). MRI is commonly used to show soft tissue injuries to the labrum and to visualize associated rotator cuff tears. MRI arthrograms better identify labral tears and ligamentous structures. Three-dimensional CT scans are being used to determine the significance of bone loss.

 Treatment

For acute dislocations, the shoulder should be reduced as soon as possible. The Stimson procedure is the least traumatic method and is quite effective. The patient lies prone with the dislocated arm hanging off the examination table with a weight applied to the wrist to provide traction for 20–30 minutes. Afterward, gentle medial mobilization can be applied manually to assist the reduction. The shoulder can also be reduced with axial “traction” on the arm with “counter-traction” along the trunk. The patient should be sedated and relaxed. The shoulder can then be gently internally and externally rotated to guide it back into the socket.

Initial treatment of acute shoulder dislocations should include sling immobilization for 2–4 weeks along with pendulum exercises. Early physical therapy can be used to maintain range of motion and strengthening of rotator cuff muscles. Patients can also modify their activities to avoid active and risky sports. For patients with a traumatic incident and unilateral shoulder dislocation, a Bankart lesion is commonly present (remembered by the mnemonic, “TUBS”) and surgical treatment is often required.

The treatment of atraumatic shoulder instability is different than traumatic shoulder instability. Patients with chronic, recurrent shoulder dislocations should be managed with physical therapy and a regular maintenance program, consisting of scapular stabilization and postural and rotator cuff strengthening exercises. Activities may need to be modified. In patients with an atraumatic, multidirectional,bilateral shoulder instability, rehabilitation is the mainstay for treatment; inferior capsular shift surgery is rarely required (remembered by the mnemonic, “AMBRI”).

 When to Refer

  • Patients who are at risk for second dislocation, such as young patients, certain jobholders (eg, police officers, fire fighters, and rock climbers) to avoid recurrent dislocation or dislocation while at work.
  • Patients who have not responded to conservative approach or who have chronic instability.

Bishop JY et al; MOON Shoulder Group. 3-D CT is the most reliable imaging modality when quantifying glenoid bone loss. Clin Orthop Relat Res. 2013 Apr;471(4):1251–6. [PMID: 22996361]

Chahal J et al. Anatomic Bankart repair compared with nonoperative treatment and/or arthroscopic lavage for first-time traumatic shoulder dislocation. Arthroscopy. 2012 Apr;28(4):565–75. [PMID: 22336435]

Rerko MA et al. Comparison of various imaging techniques to quantify glenoid bone loss in shoulder instability. J Shoulder Elbow Surg. 2013 Apr;22(4):528–34. [PMID: 22748926]

  1. Adhesive Capsulitis (“Frozen Shoulder”)

 ESSENTIALS OF DIAGNOSIS

 Very painful shoulder triggered by minimal or no trauma.

 Pain out of proportion to clinical findings during the inflammatory phase.

 Stiffness during the “freezing” phase and resolution during the “thawing” phase.

 General Considerations

Adhesive capsulitis (“frozen shoulder”) is seen commonly in patients 40 to 65 years old. It is more commonly seen in women than men, especially in perimenopausal women or in patients with endocrine disorders, such as diabetes mellitus or thyroid disease. Adhesive capsulitis is a self-limiting but very debilitating disease.

 Clinical Findings

  1. Symptoms and Signs

Patients usually present with a painful shoulder that has a limited range of motion with both passive and active movements. A useful clinical sign is limitation of movement of external rotation with the elbow by the side of the trunk (Table 41–1). Strength is usually normal but it can appear diminished when the patient is in pain.

There are three phases: the inflammatory phase, the “freezing” phase, and the “thawing” phase. During the inflammatory phase, which usually lasts 4–6 months, patients complain of a very painful shoulder without obvious clinical findings to suggest trauma, fracture, or rotator cuff tear. During the “freezing” phase, which also usually lasts 4–6 months, the shoulder becomes stiffer and stiffer even though the pain is improving. The “thawing” phase can take up to a year as the shoulder slowly regains its motion. The total duration of an idiopathic frozen shoulder is usually about 24 months; it can be much longer for patients who have trauma or an endocrinopathy.

  1. Imaging

Standard AP, axillary, and lateral glenohumeral radiographs are useful to rule out glenohumeral arthritis, which can also present with limited active and passive range of motion. However, adhesive capsulitis is usually a clinical diagnosis, and it does not need an extensive diagnostic work-up.

 Treatment

Adhesive capsulitis is caused by acute inflammation of the capsule followed by scarring and remodeling. During the acute “freezing” phase, NSAIDs and physical therapy are recommended to maintain motion. There is also evidence of short-term benefit from intra-articular corticosteroid injection or oral prednisone. One study demonstrated improvement at 6 weeks but not 12 weeks following 30 mg of daily prednisone for 3 weeks. During the “freezing” phase, the shoulder is less painful but remains stiff. Anti-inflammatory medication is not as helpful during the “thawing” phase as it is during the “freezing” phase, and the shoulder symptoms usually resolve with time. Surgical treatments include manipulation under anesthesia and arthroscopic release.

 When to Refer

  • When the patient does not respond after more than 6 months of conservative treatment.
  • When there is no progress or worsening range of motion over 3 months.

Rill BK et al. Predictors of outcome after nonoperative and operative treatment of adhesive capsulitis. Am J Sports Med. 2011 Mar;39(3):567–74. [PMID: 21160014]

Robinson CM et al. Frozen shoulder. J Bone Joint Surg Br. 2012 Jan;94(1):1–9. [PMID: 22219239]

SPINE PROBLEMS

  1. Low Back Pain

 ESSENTIALS OF DIAGNOSIS

 The cause of back pain may be categorized by pain on flexion versus pain on extension.

 Nerve root impingement is suspected when pain is leg-dominant rather than back-dominant.

 Alarming signs for serious spinal disease include unexplained weight loss, failure to improve with treatment, severe pain for more than 6 weeks, and night or rest pain.

 The cauda equina syndrome often presents with bowel or bladder symptoms (or both) and is an emergency.

 General Considerations

Low back pain remains the most common cause of disability for patients under the age of 45 and is the second most common cause for primary care visits. The annual prevalence of low back pain is 15–45%, and the annual cost in the United States is over $50 billion. Approximately 80% of episodes of low back pain resolve within 2 weeks and 90% resolve within 6 weeks. The exact cause of the low back pain is often difficult to diagnose; its cause is often multifactorial, although there are usually degenerative changes in the lumbar spine.

Alarming symptoms for back pain caused by cancer include unexplained weight loss, failure to improve with treatment, pain for more than 6 weeks, and pain at night or rest. History of cancer and age > 50 years are other risk factors for malignancy. Alarming symptoms for infection include fever, rest pain, recent infection (urinary tract infection, cellulitis, pneumonia), or history of immunocompromise or injection drug use. The cauda equina syndrome is suggested by urinary retention or incontinence, saddle anesthesia, decreased anal sphincter tone or fecal incontinence, bilateral lower extremity weakness, and progressive neurologic deficits. Risk factors for back pain due to vertebral fracture include use of corticosteroids, age > 70 years, history of osteoporosis, recent significant trauma, or very severe focal pain. Back pain may also be the presenting symptom in other serious medical problems, including abdominal aortic aneurysm, peptic ulcer disease, kidney stones, or pancreatitis.

 Clinical Findings

  1. Symptoms and Signs

The physical examination is best done with the patient in the standing, sitting, supine, and then prone positions to avoid frequent repositioning of the patient. In the standing position, the patient’s posture can be observed. Commonly encountered spinal asymmetries include scoliosis, thoracic kyphosis, and lumbar hyperlordosis. The active range of motion of the lumbar spine can be assessed. The common directions include flexion, rotation, and extension. The one-leg standing extension test assesses for pain as the patient stands on one leg while extending the spine. A positive test can be caused by pars interarticularis fractures (spondylolysis or spondylolisthesis) or facet joint arthritis, although sensitivity and specificity of the test is limited.

Motor strength, reflexes, and sensation can be tested in the sitting position (Table 41–2). The major muscles in the lower extremities are assessed for weakness by eliciting a resisted isometric contraction for approximately 5 seconds. It is important to compare the strength bilaterally to detect subtle muscle weakness. Similarly, sensory testing to light touch can be checked in specific dermatomes for corresponding nerve root function. Finally, the knee (femoral nerve L2–4), ankle (deep peroneal nerve L4–L5), and Babinski (sciatic nerve L5–S1) reflexes can be checked with the patient sitting.

Table 41–2. Neurologic testing of lumbosacral nerve disorders.

In the supine position, the hip should be evaluated for range of motion, focusing on internal rotation. The straight leg raise test puts traction and compression forces on the lower lumbar nerve roots (Table 41–3).

Table 41–3. Spine: back examination.

Finally, in the prone position, the clinician can carefully palpate each level of the spine and sacroiliac joints for tenderness. A rectal examination is required if the cauda equina syndrome is suspected. Superficial skin tenderness to a light touch over the lumbar spine, overreaction to maneuvers in the regular back examination, low back pain on axial loading of spine in standing, inconsistency in thestraight leg raise test or on the neurologic examination suggest nonorthopedic causes for the pain or malingering.

  1. Imaging

In the absence of alarming “red flag” symptoms suggesting infection, malignancy, or cauda equina syndrome, diagnostic imaging, including radiographs, is not typically recommended in the first 6 weeks. The Agency for Healthcare Research and Quality guidelines for obtaining lumbar radiographs are summarized in Table 41–4. Most clinicians obtain radiographs for new back pain in patients older than 50 years. If done, radiographs of the lumbar spine should include AP and lateral views. Oblique views can be useful if the neuroforamina or lesions need to be visualized. MRI is the method of choice in the evaluation of symptoms not responding to conservative treatment or in the presence of red flags of serious conditions.

Table 41–4. AHRQ criteria for lumbar radiographs in patients with acute low back pain.

  1. Special Tests

Electromyography or nerve conduction studies may be useful in assessing patients with possible nerve root symptoms lasting longer than 6 weeks; back pain may or may not also be present. These tests are usually not necessary if the diagnosis of radiculopathy is clear.

 Treatment

  1. Conservative

Nonpharmacologic treatments are key in the management of low back pain. Education alone improves patient satisfaction with recovery and recurrence. Patients require information and reassurance, especially when diagnostic procedures are not necessary. Discussion must include reviewing safe and effective methods of symptom control as well as how to decrease the risk of recurrence with proper lifting techniques, abdominal wall/core strengthening, weight loss, and smoking cessation. Strengthening and stabilization effectively reduce pain and functional limitation compared with usual care.

Physical therapy exercise programs can be tailored to the patient’s symptoms and pathology. Neither spinal manipulation nor traction have shown benefits for low back pain; however, the level of evidence is low quality and limited by small sample sizes. Heat and cold treatments have not shown any long-term benefits but may be used for symptomatic treatment. The efficacy of transcutaneous electrical nerve stimulation (TENS), back braces, physical agents, and acupuncture is unproven. Improvements in posture, core stability strengthening, physical conditioning, and modifications of activities to decrease physical strain are keys for ongoing management.

NSAIDs are effective in the early treatment of low back pain (see Chapter 20). There is limited evidence that muscle relaxants can provide short-term relief; since these medications have addictive potential, they should be used with care. Muscle relaxants are best used if there is true muscle spasm that is painful rather than simply a protective response. Opioids may be necessary to alleviate pain immediately. Treatment of more chronic neuropathic pain with alpha-2-delta ligands (eg, gabapentin), serotonin-norepinephrine reuptake inhibitors (eg, duloxetine) or tricyclic antidepressants (eg, nortriptyline) may be helpful. Epidural injections may provide improved pain reduction short term, although studies are limited and lack long-term follow-up.

  1. Surgical

Surgical indications for back surgery include cauda equina syndrome, ongoing morbidity with no response to > 6 months of conservative treatment, cancer, infection, or severe spinal deformity. Prognosis is improved when there is an anatomic lesion that can be corrected and symptoms are neurologic. Spinal surgery has limitations. Patient selection is very important and the specific surgery recommended should have very clear indications. Patients should understand that surgery can improve their pain but is unlikely to cure it. Surgery is not generally indicated for radiographic abnormalities alone when the patient is asymptomatic. Depending on the surgery performed, possible complications include persistent pain; surgical site pain, especially if bone grafting is needed; infection; neurologic damage; non-union; cutaneous nerve damage; implant failure; deep venous thrombosis; and death.

 When to Refer

  • Patients with the cauda equina syndrome.
  • Patients with cancer, infection, or severe spinal deformity.
  • Patients who have not responded to conservative treatment.

Bicket MC et al. Epidural injections for spinal pain: a systematic review and meta-analysis evaluating the “control” injections in randomized controlled trials. Anesthesiology. 2013 Oct;119(4):907–31. [PMID: 24195874]

Goodman DM et al. JAMA patient page. Low back pain. JAMA. 2013 Apr 24;309(16):1738. [PMID: 23613079]

Lin CW et al. Cost-effectiveness of guideline-endorsed treatments for low back pain: a systematic review. Eur Spine J. 2011 Jul;20(7):1024–38. [PMID: 21229367]

Rubinstein SM et al. Spinal manipulative therapy for acute low back pain: an update of the Cochrane review. Spine (Phila Pa 1976). 2013 Feb 1;38(3):E158–77. [PMID: 23169072]

  1. Spinal Stenosis

 ESSENTIALS OF DIAGNOSIS

 Pain is usually worse with back extension and relieved by sitting.

 Occurs in older patients.

 May present with neurogenic claudication symptoms with walking.

 General Considerations

Osteoarthritis in the lumbar spine can cause narrowing of the spinal canal. A large disk herniation can also cause stenosis and compression of neural structures or the spinal artery resulting in “claudication” symptoms with ambulation. The condition usually affects patients aged 50 years or older.

 Clinical Findings

Patients report pain that worsens with extension. They describe reproducible single or bilateral leg symptoms that are worse after walking several minutes and that are relieved by sitting (“neurogenic claudication”). On examination, patients often exhibit limited extension of the lumbar spine, which may reproduce the symptoms radiating down the legs. A thorough neurovascular examination is recommended (Table 41–2).

 Treatment

Flexion-based exercises as demonstrated by a physical therapist can help relieve symptoms. Epidural or facet joint corticosteroid injections can also reduce pain symptoms. However, patients who received epidural corticosteroids had less improvement at 4 years among all patients with spinal stenosis and were associated with longer duration of surgery and longer hospital stay.

Surgical treatments for spinal stenosis include spinal decompression (widening the spinal canal or laminectomy), nerve root decompression (freeing a single nerve), and spinal fusion (joining the vertebra to eliminate motion and diminish pain from the arthritic joints). In an ongoing multicenter randomized trial, subgroups improved significantly more with surgery than with nonoperative treatment. Variables associated with greater treatment effects included lower baseline disability scores, not smoking, neuroforaminal stenosis, predominant leg pain rather than back pain, not lifting at work, and the presence of a neurologic deficit.

 When to Refer

  • If a patient exhibits radicular or claudication symptoms > 12 weeks.
  • MRI or CT confirmation of significant spinal stenosis.

Ammendolia C et al. Nonoperative treatment of lumbar spinal stenosis with neurogenic claudication: a systematic review. Spine (Phila Pa 1976). 2012 May 1;37(10):E609–16. [PMID: 22158059]

Pearson A et al. Who should have surgery for spinal stenosis? Treatment effect predictors in SPORT. Spine (Phila Pa 1976). 2012 Oct 1;37(21):1791–802. [PMID: 23018805]

Radcliff K et al. Epidural steroid injections are associated with less improvement in patients with lumbar spinal stenosis: a subgroup analysis of the spine patient outcomes research trial. Spine (Phila Pa 1976). 2013 Feb 15;38(4):279–91. [PMID: 23238485]

  1. Lumbar Disk Herniation

 ESSENTIALS OF DIAGNOSIS

 Pain with back flexion or prolonged sitting.

 Radicular pain with compression of neural structures.

 Lower extremity numbness.

 Lower extremity weakness.

 General Considerations

Lumbar disk herniation is usually due to bending or heavy loading (eg, lifting) with the back in flexion, causing herniation or extrusion of disk contents (nucleus pulposus) into the spinal cord area. However, there may not be an inciting incident. Disk herniations usually occur from degenerative disk disease (dessication of the annulus fibrosis) in patients between 30- and 50-years-old. The L5–S1 disk is affected in 90% of cases. Compression of neural structures, such as the sciatic nerve, causes radicular pain. Severe compression of the spinal cord can cause the cauda equina syndrome, a surgical emergency (see above).

 Clinical Findings

  1. Symptoms and Signs

Discogenic pain typically is localized in the low back at the level of the affected disk and is worse with activity. “Sciatica” causes electric shock-like pain radiating down the posterior aspect of the leg often to below the knee. Symptoms usually worsen with back flexion such as bending or sitting for long periods (eg, driving). A significant disk herniation can cause numbness and weakness, including weakness with plantar flexion of the foot (L5/S1) or dorsiflexion of the toes (L4/L5). The cauda equina syndrome should be ruled out if the patient complains of perianal numbness or bowel or bladder incontinence.

  1. Imaging

Plain radiographs are helpful to assess spinal alignment (scoliosis, lordosis), disk space narrowing, and osteoarthritis changes. MRI is the best method to assess the level and morphology of the herniation and is recommended if surgery is planned.

 Treatment

For an acute exacerbation of pain symptoms, bed rest is appropriate for up to 48 hours. Otherwise, first-line treatments include modified activities; NSAIDs and other analgesics; and physical therapy, including core stabilization and McKenzie exercises. Following nonsurgical treatment for a lumbar disk for over 1 year, the incidence of low back pain recurrence is at least 40% and is predicted by longer time to initial resolution of pain. Epidural and transforaminal corticosteroid injections can be beneficial, especially in relieving acute radicular pain, although the benefit tends to last only 3 months. These injections may be effective in delaying surgery for chronic low back pain. Oral prednisone can reduce inflammation and is useful in reducing symptoms of acute sciatica; the initial dose is approximately 1 mg/kg once daily with tapering doses over 10 days. Co-analgesics for neuropathic pain, such as the calcium channel alpha-2-delta ligands (ie, gabapentin, pregabalin) or tricyclic antidepressants, may be helpful (see Chapter 5).

A large, ongoing trial has shown that patients who underwent surgery for a lumbar disk herniation achieved greater improvement than conservatively treated patients in all primary and secondary outcomes except return to work status after 4 year follow-up. So far, disk replacement surgery has not shown benefits beyond generally accepted clinically important differences in short-term pain relief, disability, and quality of life compared with spine fusion surgery.

 When to Refer

  • Cauda equina syndrome.
  • Progressive worsening of neurologic symptoms.
  • Loss of motor function (sensory losses can be followed in the outpatient clinic).

Pinto RZ et al. Epidural corticosteroid injections in the management of sciatica: a systematic review and meta-analysis. Ann Intern Med. 2012 Dec 18;157(12):865–77. [PMID: 23362516]

Rihn JA et al. Duration of symptoms resulting from lumbar disc herniation: effect on treatment outcomes: analysis of the Spine Patient Outcomes Research Trial (SPORT). J Bone Joint Surg Am. 2011 Oct 19;93(20):1906–14. [PMID: 22012528]

Suri P et al. Recurrence of radicular pain or back pain after nonsurgical treatment of symptomatic lumbar disk herniation. Arch Phys Med Rehabil. 2012 Apr;93(4):690–5. [PMID: 22464091]

  1. Neck Pain

 ESSENTIALS OF DIAGNOSIS

 Most chronic neck pain is caused by degenerative joint disease and responds to conservative treatment.

 Cervical radiculopathy symptoms can be referred to the shoulder, arm, or upper back.

 Whiplash is the most common type of traumatic injury to the neck.

 Poor posture is often a factor for persistent neck pain.

 General Considerations

Most neck pain, especially in older patients, is due to mechanical degeneration involving the cervical disks, facet joints, and ligamentous structures and may occur in the setting of degenerative changes at other sites. Pain can also come from the supporting neck musculature, which often acts to protect the underlying neck structures. Posture is a very important factor, especially in younger patients. Many work-related neck symptoms are due to poor posture and repetitive motions over time. Acute injuries can also occur secondary to trauma. For example, whiplash occurs in 15–40% of motor vehicle accidents, with chronic pain developing in 5–7%. Neck fractures are serious traumatic injuries acutely and can lead to osteoarthritis in the long term. Ultimately, many degenerative conditions of the neck result in cervical canal stenosis or neural foraminal stenosis, sometimes affecting underlying neural structures. Cervical radiculopathy can cause neurologic symptoms in the upper extremities usually deriving from disease of the C5–C7 disks. Patients with neck pain may report associated headaches and shoulder pain. Thoracic outlet syndrome, in which there is mechanical compression of the brachial plexus and neurovascular structures with overhead positioning of the arm, should be considered in the differential diagnosis of neck pain.

Other causes of neck pain include rheumatoid arthritis, fibromyalgia, osteomyelitis, neoplasms, polymyalgia rheumatica, compression fractures, pain referred from visceral structures (eg, angina), and functional disorders. Amyotrophic lateral sclerosis, multiple sclerosis, syringomyelia, spinal cord tumors, and tropical spastic paresis from HTLV-1 infection can mimic myelopathy from cervical arthritis.

 Clinical Findings

  1. Symptoms and Signs

Neck pain may be limited to the posterior region or, depending on the level of the symptomatic joint, may radiate segmentally to the occiput, anterior chest, shoulder girdle, arm, forearm, and hand. It may be intensified by active or passive neck motions. The general distribution of pain and paresthesias corresponds roughly to the involved dermatome in the upper extremity.

The patient’s posture should be assessed, checking for shoulder rolled forward or head forward posture as well as scoliosis in the thoracolumbar spine. Patients with discogenic neck pain often complain of pain with flexion, which causes cervical disks to herniate posteriorly. Extension of the neck usually affects the neural foraminal and facet joints of the neck. Rotation and lateral flexion of the cervical spine should be measured both to the left and the right. Limitation of cervical movements is the most common objective finding.

A detailed neurovascular examination of the upper extremities should be performed, including sensory input to light touch and temperature; motor strength testing, especially the hand intrinsic muscles (thumb extension strength [C6], opponens strength (thumb to pinky) [C7], and finger abductors and adductors strength [C8–T1]); and upper extremity reflexes (biceps, triceps, brachioradialis). True cervical radiculopathy symptoms should match an expected dermatomal or myotomal distribution. The Spurling test involves asking the patient to rotate and extend the neck to one side (Table 41–5). The clinician can apply a gentle axial load to the neck. Reproduction of the cervical radiculopathy symptoms is a positive sign of nerve root compression. Palpation of the neck is best performed with the patient in the supine position where the clinician can palpate each level of the cervical spine with the muscles of the neck relaxed.

Table 41–5. Spine: neck examination.

  1. Imaging

Radiographs of the cervical spine can assist in determining the area of degenerative changes. Useful views include the AP and lateral view of the cervical spine. The odontoid view is usually added to rule out traumatic fractures and congenital abnormalities. Oblique views of the cervical spine can provide further information about arthritis changes and assess the neural foramina for narrowing. Many plain radiographs are completely normal in patients who have suffered an acute cervical strain. Loss of cervical lordosis is often seen but is nonspecific. Comparative reduction in height of the involved disk space and osteophytes are frequent findings when there are degenerative changes in the cervical spine.

CT scanning is the most useful method if bony abnormalities, such as fractures, are suspected. MRI is the best method to assess the cervical spine since the soft tissue structures (such as the disks, spinal cord, and nerve roots) can be evaluated. If the patient has signs of cervical radiculopathy with motor weakness, these more sensitive imaging modalities should be obtained urgently.

 Treatment

In the absence of trauma or evidence of infection, malignancy, neurologic findings, or systemic inflammation, the patient can be treated conservatively. A course of neck stretching, strengthening and postural exercises in physical therapy have demonstrated benefit in relieving symptoms. A soft cervical collar can be useful for short-term use (up to 1–2 weeks) in acute neck injuries. Chiropractic manual manipulation and mobilization can provide short-term benefit for mechanical neck pain. Although the rate of complications is low (5–10/million manipulations), care should be taken whenever there are neurologic symptoms present. Specific patients may respond to use of home cervical traction. NSAIDs are commonly used and opioids may be needed in cases of severe neck pain. Muscle relaxants (eg, cyclobenzaprine 5–10 mg orally three times daily) can be used short-term if there is muscle spasm or as a sedative to aid in sleeping. Acute radicular symptoms can be treated with neuropathic medications (eg, gabapentin 300–1200 mg orally three times daily), and a short course of oral prednisone (5–10 days) can be considered (starting at 1 mg/kg). Cervical foraminal or facet joint injections can also reduce symptoms. Cervical spine surgery does not have clear evidence of benefit over conservative treatment. Surgeries are successful in reducing neurologic symptoms in 80–90% of cases but are still considered as treatments of last resort.

 When to Refer

  • Patients with severe symptoms with motor weakness.
  • Surgical decompression surgery if the symptoms are severe and there is identifiable, correctable pathology.

Kelly JC et al. The natural history and clinical syndromes of degenerative cervical spondylosis. Adv Orthop. 2012;2012:393642. [PMID: 22162812]

van Middelkoop M et al. Surgery versus conservative care for neck pain: a systematic review. Eur Spine J. 2013 Jan;22(1):87–95. [PMID: 23104514]

UPPER EXTREMITY

  1. Lateral & Medial Epicondylosis

 ESSENTIALS OF DIAGNOSIS

 Tenderness over the lateral or medial epicondyle.

 Diagnosis of tendinopathy is confirmed by pain with resisted strength testing and passive stretching of the affected tendon and muscle unit.

 Physical therapy and activity modification are more successful than anti-inflammatory treatments.

 General Considerations

Tendinopathy involving the wrist extensors, flexors, and pronators are very common complaints. The underlying mechanism is chronic repetitive overuse causing microtrauma at the tendon insertion, although acute injuries can occur as well if the tendon is strained due to excessive loading. The traditional term “epicondylitis” is a misnomer because histologically tendinosis or degeneration in the tendon is seen rather than acute inflammation. Therefore, these entities should be referred to as “tendinopathy” or “tendinosis.” Lateral epicondylosis involves the wrist extensors, especially the extensor carpi radialis brevis. This is usually caused be lifting with the wrist and the elbow extended. Medial epicondylosis involves the wrist flexors and most commonly the pronator teres tendon. Ulnar neuropathy and cervical radiculopathy should be considered in the differential diagnosis.

 Clinical Findings

  1. Symptoms and Signs

For lateral epicondylosis, the patient describes pain with the arm and wrist extended. For example, common complaints include pain while shaking hands, lifting objects, using a computer mouse, or hitting a backhand in tennis (“tennis elbow”). Medial epicondylosis presents with pain during motions in which the arm is repetitively pronated or the wrist is flexed. This is also known as “golfer’s elbow” due to the motion of turning the hands over during the golf swing. On examination, tenderness directly over the epicondyle is present, especially over the posterior aspect where the tendon insertion occurs. The proximal tendon and musculotendinous junction can also be sore. To confirm that the pain is due to tendinopathy, pain can be reproduced over the epicondyle with resisted wrist extension and third digit extension for lateral epicondylosis and resisted wrist pronation and wrist flexion for medial epicondylosis. The pain is also often reproduced with passive stretching of the affected muscle groups, which can be performed with the arm in extension. It is useful to check the ulnar nerve (located in a groove at the posteromedial elbow) for tenderness as well as to perform a Spurling test for cervical radiculopathy.

  1. Imaging

Radiographs are often normal, although a small traction spur may be present in chronic cases (enthesopathy). Diagnostic investigations are usually unnecessary, unless the patient does not improve after up to 3 months of conservative treatment. At that point, a patient who demonstrates significant disability due to the pain should be assessed with an MRI or ultrasound. Ultrasound and MRI can visualize the tendon and confirm tendinosis or tears.

 Treatment

Treatment is usually conservative, including patient education regarding activity modification and management of symptoms. Ice and NSAIDs can help with pain. The most important steps are to begin a good stretching program followed by strengthening exercises, particularly eccentric ones. Counterforce elbow braces might provide some symptomatic relief, although there is no published evidence to support their use. If the patient has severe or long-standing symptoms, a course of physical therapy should be performed. A randomized trial showed no differences with platelet-rich plasma, corticosteroid, or saline injections at 3 months. Corticosteroid injection had improvement at 1 month as well as evidence of decreased tendon thickness and Doppler changes. Treatments such as extracorporeal shock wave therapy and other injections have not shown clear long-term benefit. Physical therapy is still the mainstay of treatment.

 When to Refer

Patients not responding to 6 months of conservative treatment should be referred for surgical debridement or repair of the tendon.

Krogh TP et al. Comparative effectiveness of injection therapies in lateral epicondylitis: a systematic review and network meta-analysis of randomized controlled trials. Am J Sports Med. 2013 Jun;41(6):1435–46. [PMID: 22972856]

Krogh TP et al. Treatment of lateral epicondylitis with platelet-rich plasma, glucocorticoid, or saline: a randomized, double-blind, placebo-controlled trial. Am J Sports Med. 2013 Mar;41(3):625–35. [PMID: 23328738]

Raman J et al. Effectiveness of different methods of resistance exercises in lateral epicondylosis—a systematic review. J Hand Ther. 2012 Jan–Mar;25(1):5–25. [PMID: 22075055]

  1. Carpal Tunnel Syndrome

 ESSENTIALS OF DIAGNOSIS

 Pain, burning, and tingling in the distribution of the median nerve.

 Initially, most bothersome during sleep.

 Late weakness or atrophy, especially of the thenar eminence.

 Can be caused by repetitive activities using the wrist.

 Commonly seen during pregnancy and in patients with diabetes mellitus or rheumatoid arthritis.

 General Considerations

An entrapment neuropathy, carpal tunnel syndrome is a painful disorder caused by compression of the median nerve between the carpal ligament and other structures within the carpal tunnel. The contents of the tunnel can be compressed by synovitis of the tendon sheaths or carpal joints, recent or malhealed fractures, tumors, tissue infiltration, and occasionally congenital syndromes (eg, mucopolysaccharidoses). Even though no anatomic lesion is apparent, flattening or even circumferential constriction of the median nerve may be observed during operative section of the overlying carpal ligament. The disorder may occur in fluid retention of pregnancy, in individuals with a history of repetitive use of the hands, or following injuries of the wrists. There is a familial type of carpal tunnel syndrome in which no etiologic factor can be identified. Carpal tunnel syndrome can also be a feature of many systemic diseases, such as rheumatoid arthritis and other rheumatic disorders (inflammatory tenosynovitis), myxedema, amyloidosis, sarcoidosis, leukemia, acromegaly, and hyperparathyroidism.

 Clinical Findings

  1. Symptoms and Signs

The initial symptoms are pain, burning, and tingling in the distribution of the median nerve (the palmar surfaces of the thumb, the index and long fingers, and the radial half of the ring finger). Aching pain may radiate proximally into the forearm and occasionally proximally to the shoulder and over the neck and chest. Pain is exacerbated by manual activity, particularly by extremes of volar flexion or dorsiflexion of the wrist. It is most bothersome at night. Impairment of sensation in the median nerve distribution may or may not be demonstrable. Subtle disparity between the affected and opposite sides can be shown by testing for two-point discrimination or by requiring the patient to identify different textures of cloth by rubbing them between the tips of the thumb and the index finger. A Tinel or Phalen sign may be positive. A Tinel sign is tingling or shock-like pain on volar wrist percussion (Table 41–6). The Phalen sign is pain or paresthesia in the distribution of the median nerve when the patient flexes both wrists to 90 degrees for 60 seconds (Table 41–6). The carpal compression test, in which numbness and tingling are induced by the direct application of pressure over the carpal tunnel, may be more sensitive and specific than the Tinel and Phalen tests (Table 41–6). Muscle weakness or atrophy, especially of the thenar eminence, can appear later than sensory disturbances as compression of the nerve worsens.

Table 41–6. Wrist examination.

  1. Imaging

Ultrasound can demonstrate flattening of the median nerve beneath the flexor retinaculum. Sensitivity of ultrasound for carpal tunnel syndrome is variable but estimated between 54% and 98%.

  1. Special Tests

Electromyography and nerve conduction studies show evidence of sensory conduction delay before motor delay, which can occur in severe cases. This syndrome should be differentiated from other cervicobrachial pain syndromes, from compression syndromes of the median nerve in the forearm or arm, and from mononeuritis multiplex. When left-sided, it may be confused with angina pectoris.

 Treatment

Treatment is directed toward relief of pressure on the median nerve. When a causative lesion is discovered, it should be treated appropriately. Otherwise, patients in whom carpal tunnel syndrome is suspected should modify their hand activities and have the affected wrist splinted in the neutral position for up to 3 months. A series of Cochrane reviews show limited evidence for splinting, therapeutic ultrasound, exercises, and ergonomic positioning. Oral corticosteroids or NSAIDs can also be tried. Carpal tunnel release surgery can be beneficial if the patient has a positive electrodiagnostic test, at least moderate symptoms, high clinical probability, unsuccessful nonoperative treatment, and symptoms lasting longer than 12 months. A randomized, controlled trial showed both corticosteroid injection and surgery resolved symptoms but only decompressive surgery allows resolution of neurophysiologic changes.

 When to Refer

  • If symptoms persist > 3 months despite conservative treatment, including the use of a wrist splint.
  • If thenar muscle (eg, abductor pollicis brevis) weakness or atrophy develops.

Andreu JL et al. Local injection versus surgery in carpal tunnel syndrome: neurophysiologic outcomes of a randomized clinical trial. Clin Neurophysiol. 2014 Jul;125(7):1479–84. [PMID: 24321619]

Carpal Tunnel Syndrome. In: Hegmann KT (editor). Occupational Medicine Practice Guidelines. Evaluation and Management of Common Health Problems and Functional Recovery in Workers, 3rd ed. Elk Grove Village (IL): American College of Occupational and Environmental Medicine (ACOEM), 2011.

  1. Dupuytren Contracture

 ESSENTIALS OF DIAGNOSIS

 Benign fibrosing disorder of the palmar fascia.

 Contracture of one or more fingers can lead to limited hand function.

 General Considerations

This relatively common disorder is characterized by hyperplasia of the palmar fascia and related structures, with nodule formation and contracture of the palmar fascia. The cause is unknown, but the condition has a genetic predisposition and occurs primarily in white men over 50 years of age, particularly in those of Celtic descent. The incidence is higher among alcoholic patients and those with chronic systemic disorders (especially cirrhosis). It is also associated with systemic fibrosing syndrome, which includes plantar fibromatosis (10% of patients), Peyronie disease (1–2%), mediastinal and retroperitoneal fibrosis, and Riedel struma. The onset may be acute, but slowly progressive chronic disease is more common.

 Clinical Findings

Dupuytren contracture manifests itself by nodular or cord-like thickening of one or both hands, with the fourth and fifth fingers most commonly affected. The patient may complain of tightness of the involved digits, with inability to satisfactorily extend the fingers, and on occasion there is tenderness. The resulting cosmetic problems may be unappealing, but in general the contracture is well tolerated since it exaggerates the normal position of function of the hand.

 Treatment

If the palmar nodule is growing rapidly, injections of triamcinolone or collagenase into the nodule may be of benefit. The injection of collagenase Clostridium histolyticum is a promising nonoperative treatment option that lyses collagen disrupting the contracted cords. Surgical intervention is indicated in patients with significant flexion contractures, depending on the location, but recurrence is possible. Invasive options include open fasciectomy, partial fasciectomy, or percutaneous needle aponeurotomy.

 When to Refer

Referral can be considered when one or more digits are affected by severe contractures, which interfere with everyday activities and result in functional limitations.

Baltzer H et al. Cost-effectiveness in the management of Dupuytren’s contracture. A Canadian cost-utility analysis of current and future management strategies. Bone Joint J. 2013 Aug;95-B(8):1094–100. [PMID: 23908426]

Peimer CA et al. Dupuytren contracture recurrence following treatment with collagenase clostridium histolyticum (CORDLESS study): 3-year data. J Hand Surg Am. 2013 Jan;38(1):12–22. [PMID: 23200951]

Worrell M. Dupuytren’s disease. Orthopedics. 2012 Jan;35(1):52–60. [PMID: 22229922]

  1. Bursitis

 ESSENTIALS OF DIAGNOSIS

 Often occurs around bony prominences where it is important to reduce friction.

 Typically presents with local swelling that is painful acutely.

 Septic bursitis can present without fever or systemic signs.

 General Considerations

Inflammation of bursae—the synovium-like cellular membranes overlying bony prominences—may be secondary to trauma, infection, or arthritic conditions such as gout, rheumatoid arthritis, or osteoarthritis. Bursitis can result from infection. The two common sites are the olecranon (Figure 41–1) and prepatellar bursae, however, others include subdeltoid, ischial, trochanteric, and semimembranous-gastrocnemius (Baker cyst) bursae.

 Figure 41–1. Aseptic olecranon bursitis secondary to repetitive trauma. (Reproduced, with permission, from Richard P. Usatine, MD.)

 Clinical Findings

  1. Symptoms and Signs

Bursitis is more likely than arthritis to cause focal tenderness and swelling and less likely to affect range of motion of the adjacent joint. Olecranon bursitis, for example, causes an oval (or, if chronic, bulbous) swelling at the tip of the elbow and does not affect elbow motion, whereas an elbow joint inflammation produces more diffuse swelling and reduces range of motion. The absence of fever does not exclude infection; one-third of those with septic olecranon bursitis are afebrile. A bursa can also become symptomatic when it ruptures. This is particularly true for Baker cyst (see below), whose rupture can cause calf pain and swelling that mimic thrombophlebitis.

  1. Imaging

Imaging is unnecessary unless there is concern for osteomyelitis, trauma or other underlying pathology. Ruptured Baker cysts are imaged easily by sonography or MRI. It may be important to exclude a deep venous thrombosis, which can be mimicked by a ruptured Baker cyst.

  1. Special Tests

Acute swelling and redness at a bursal site calls for aspiration to rule out infection. A bursal fluid white blood cell count of > 1000/mcL indicates inflammation from infection, rheumatoid arthritis, or gout. In septic bursitis, the white cell count averages over 50,000/mcL. Most cases are caused by Staphylococcus aureus; the Gram stain is positive in two-thirds.

 Treatment

Bursitis caused by trauma responds to local heat, rest, NSAIDs, and local corticosteroid injections. Chronic, stable olecranon bursa swelling usually does not require aspiration. Aspiration of the olecranon bursa runs the risk of creating a chronic drainage site, which can be reduced by using a “zig-zag” approach with a small needle (25-gauge if possible) and pulling the skin over the bursa before introducing it. Applying a pressure bandage may also help prevent chronic drainage. Repetitive minor trauma to the olecranon bursa should be eliminated by avoiding resting the elbow on a hard surface or by wearing an elbow pad. Treatment of a ruptured Baker cyst includes rest, leg elevation, and injection of triamcinolone, 20–40 mg into the knee anteriorly (the knee compartment communicates with the cyst). Knowledge of trochanteric bursa anatomy is important for effective injection.

Treatment for septic bursitis involves incision and drainage and antibiotics usually delivered intravenously.

 When to Refer

  • Surgical removal of the bursa is indicated only for cases in which repeated infections occur.
  • Elective removal for persistent symptoms affecting activities of daily living can be considered.

Del Buono A et al. Diagnosis and management of olecranon bursitis. Surgeon. 2012 Oct;10(5):297–300. [PMID: 22503398]

McEvoy JR et al. Ultrasound-guided corticosteroid injections for treatment of greater trochanteric pain syndrome: greater trochanter bursa versus subgluteus medius bursa. AJR Am J Roentgenol. 2013 Aug;201(2):W313–7. [PMID: 23883246]

HIP

  1. Hip Fractures

 ESSENTIALS OF DIAGNOSIS

 Internal rotation of the hip is the best provocative diagnostic maneuver.

 Hip fractures should be surgically repaired as soon as possible (within 24 hours).

 Delayed treatment of hip fractures in the elderly leads to increased complications and mortality.

 General Considerations

Approximately 4% of the 7.9 million fractures that occur each year in the United States are hip fractures. There is a high mortality rate among elderly patients following hip fracture, with death occurring in 8–9% within 30 days and in approximately 25–30% within 1 year. Osteoporosis, female sex, height > 5-foot 8-inches, and age over 50 years are risk factors for hip fracture. Hip fractures usually occur after a fall. High velocity trauma is needed in younger patients. Stress fractures can occur in athletes or individuals with poor bone mineral density following repetitive loading activities.

 Clinical Findings

  1. Symptoms and Signs

Patients typically report pain in the groin, though pain radiating to the lateral hip, buttock, or knee can also commonly occur. If a displaced fracture is present, the patient will not be able to bear weight and the leg may be externally rotated. Gentle logrolling of the leg with the patient supine helps rule out a fracture. Examination of the hip demonstrates pain with deep palpation in the area of the femoral triangle (similar to palpating the femoral artery). Provided the patient can tolerate it, the clinician can, with the patient supine, flex the hip to 90 degrees with the knee flexed to 90 degrees. The leg can then be internally and externally rotated to assess the range of motion on both sides. Pain with internal rotation of the hip is the most sensitive test to identify intra-articular hip pathology. Hip flexion, extension, abduction, and adduction strength can be tested.

Patients with hip stress fractures have less pain on physical examination than described previously but typically have pain with weight bearing. The Trendelenburg test can be performed to examine for weakness or instability of the hip abductors, primarily the gluteus medius muscle (Table 41–7). Another functional test is asking the patient to hop or jump during the examination. If the patient has a compatible clinical history of pain and is unable or unwilling to hop, then a stress fracture should be ruled out. The back should be carefully examined in patients with hip complaints, including examining for signs for sciatica.

Table 41–7. Hip examination.

Following displaced hip fractures, a thorough medical evaluation and treatment should be pursued to maximize the patients’ ability to undergo operative intervention. Patients who are unable to get up by themselves may have been immobile for hours or even days following their falls. Thus, clinicians must exclude rhabdomyolysis, hypothermia, deep venous thrombosis, pulmonary embolism, and other conditions that can occur with prolonged immobilization. Delay of operative intervention leads to an increased risk of perioperative morbidity and mortality.

  1. Imaging

Useful radiographic views of the hip include AP views of the pelvis and bilateral hips and frog-leg-lateral views of the painful hip. A CT scan or MRI may be necessary to identify the hip fracture pattern or to evaluate non-displaced fractures. Hip fractures are generally described by location, including femoral neck, intertrochanteric, or subtrochanteric.

 Treatment

Almost all patients with a hip fracture will require surgery and may need to be admitted to hospital for pain control while they await surgery. Surgery is recommended within the first 24 hours because studies have shown that delaying surgery 48 hours results in at least twice the rate of major and minor medical complications, including pneumonia, decubitus ulcers, and deep venous thrombosis.

Stress fractures in active patients require a period of protected weight-bearing and a gradual return to activities, although it may take 4–6 months before a return to normal activities. Femoral neck fractures are commonly treated with hemiarthroplasty or total hip replacement. This allows the patient to begin weight-bearing immediately postoperatively. Peritrochanteric hip fractures are treated with open reduction internal fixation, where plate and screw construct or intramedullary devices are used. The choice of implant will depend on the fracture pattern. Since fracture fixation requires the fracture to proceed to union, the patient may need to have protected weight-bearing during the early postoperative period. Dislocation, periprosthetic fracture, and avascular necrosis of the hip are common complications after surgery.

Patients should be mobilized as soon as possible postoperatively to avoid pulmonary complications and decubitus ulcers. Supervised physical therapy and rehabilitation is important for the patient to regain as much function as possible. Unfortunately, most patients following hip fractures will lose some degree of independence.

 Prevention

Bone density screening can identify patients at risk for osteopenia or osteoporosis, and treatment can be planned accordingly. Nutrition (calcium and vitamin D intake) and bone health (bone densitometry, serum calcium and 25-OH vitamin D levels) should be reviewed with the patient (see Chapter 26). For patients with decreased mobility, systemic anticoagulation with low-molecular-weight heparin or warfarin should be considered to avoid deep venous thrombosis (see Table 14–13). Fall prevention exercise programs are available for elderly patients at risk for falls and hip fractures. Hip protectors are uncomfortable and have less use in preventing fractures.

 When to Refer

All patients in whom hip fracture is suspected.

Della Rocca GJ et al. Hip fracture protocols: what have we changed? Orthop Clin North Am. 2013 Apr;44(2):163–82. [PMID: 23544822]

Moja L et al. Timing matters in hip fracture surgery: patients operated within 48 hours have better outcomes. A meta-analysis and meta-regression of over 190,000 patients. PLoS One. 2012;7(10):e46175. [PMID: 23056256]

  1. Hip Osteoarthritis

 ESSENTIALS OF DIAGNOSIS

 Pain deep in the groin on the affected side.

 Swelling.

 Degeneration of joint cartilage.

 Loss of active and passive range of motion in severe osteoarthritis.

 General Considerations

In the United States, the prevalence of osteoarthritis will grow as the number of persons over age 65 years doubles to more than 70 million by 2030. Cartilage loss and osteoarthritis symptoms are preceded by damage to the collagen-proteoglycan matrix. The etiology of osteoarthritis is often multifactorial, including previous trauma, prior high-impact activities, genetic factors, obesity, and rheumatologic or metabolic conditions.

 Clinical Findings

  1. Symptoms and Signs

Osteoarthritis usually causes pain in the affected joint with loading of the joint or at the extremes of motion. Mechanical symptoms—such as swelling, grinding, catching, and locking—suggest internal derangement, which is indicated by damaged cartilage or bone fragments that affect the smooth range of motion expected at an articular joint. Pain can also produce the sensation of “buckling” or “giving way” due to muscle inhibition. As the joint degeneration becomes more advanced, the patient loses active range of motion and may lose passive range of motion as well.

Patients complain of pain deep in the groin on the affected side and have problems with weight-bearing activities such as walking, climbing stairs, and getting up from a chair. They may limp and develop a lurch during their gait, leaning toward the unaffected side as they walk to reduce pressure on the hip.

  1. Imaging

Weight-bearing radiographs of the affected hip are preferred for evaluation of hip osteoarthritis. To reduce radiation exposure, obtain an AP weight-bearing radiograph of the pelvis with a lateral view of the symptomatic hip. Joint space narrowing and sclerosis suggest early osteoarthritis, while osteophytes near the femoral head or acetabulum and subchondral bone cysts are more advanced changes. After age 35, MRI of the hips already show labral changes in almost 70% of asymptomatic patients.

 Treatment

  1. Conservative

Changes in the articular cartilage are irreversible. Therefore, a cure for the diseased joint is not possible, although symptoms or structural issues can be addressed to try to maintain activity level. Conservative treatment for patients with osteoarthritis includes activity modification, proper footwear, therapeutic exercises, weight loss, and use of assistive devices (such as a cane). In a large cohort, running significantly reduced osteoarthritis and hip replacement risk possibly since running is associated with lower BMI.

Analgesics may be effective in some cases. Corticosteroid injections can be considered for short-term relief of pain; however, hip injections are best performed under fluoroscopic, ultrasound, or CT guidance to ensure accurate injection in the joint. Use of viscosupplementation in the hip has been reported in cases with modest improvements; however, it remains an off-label use at this time.

  1. Surgical

Two randomized trials demonstrate that arthroscopy does not improve outcomes at 1 year over placebo or routine conservative treatment of osteoarthritis. Arthroscopic surgery is indicated in patients with osteoarthritis if, rather than pain, they have mechanical symptoms and internal derangement symptoms that can be removed as the main complaint. Such surgical treatments are useful to restore range of motion by removing osteophytes, cartilage fragments, or loose bodies.

Joint replacement surgeries are effective and cost-effective for patients with significant symptoms and functional limitations, providing improvements in pain, function, and quality of life.Minimally invasive surgeries and computer-assisted navigation during operation are being investigated as methods to improve techniques (eg, accurate placement of the hardware implant) and to reduce complication rates.

Hip resurfacing surgery is a newer joint replacement technique. Rather than use a traditional artificial joint implant of the whole neck and femur, only the femoral head is removed and replaced. Concerns following resurfacing surgery include the risk of femoral neck fracture and collapse of the head. The cumulative survival rate of this implant at 10 years is estimated to be 94%. Evidence so far suggests that hip resurfacing is comparable to total hip replacement and is a viable alternative for younger patients.

Guidelines recommend prophylaxis for venous thromboembolic disease for a minimum of 14 days after arthroplasty of the hip or knee using warfarin, low-molecular-weight heparin, fondaparinux, aspirin, rivaroxaban, dabigatran, apixaban, or portable mechanical compression.

 When to Refer

Patients with sufficient disability, limited benefit from conservative therapy, and evidence of severe osteoarthritis can be referred for joint replacement surgery.

Lieberman JR et al. Prevention of venous thromboembolic disease after total hip and knee arthroplasty. J Bone Joint Surg Am. 2013 Oct 2;95(19):1801–11. [PMID: 24088973]

McMinn DJ et al. Mortality and implant revision rates of hip arthroplasty in patients with osteoarthritis: registry based cohort study. BMJ. 2012 Jun 14;344:e3319. [PMID: 22700782]

Register B et al. Prevalence of abnormal hip findings in asymptomatic participants: a prospective, blinded study. Am J Sports Med. 2012 Dec;40(12):2720–4. [PMID: 23104610]

KNEE

  1. Knee Pain

 ESSENTIALS OF DIAGNOSIS

 Effusion can occur with intra-articular pathology, such as osteoarthritis, and meniscus and cruciate ligament tears.

 Acute knee swelling (due to hemarthrosis) within 2 hours may indicate ligament injuries or patellar dislocation or fracture.

 General Considerations

The knee is the largest joint in the body and is susceptible to injury from trauma, inflammation, infection, and degenerative changes. The knee is a hinge joint. The joint line exists between the femoral condyles and tibial plateaus. Separating and cushioning these bony surfaces is the lateral and medial meniscal cartilage, which functions as a shock absorber during weight bearing, protecting the articular cartilage. The patella is a large sesamoid bone anterior to the joint. It is embedded in the quadriceps tendon, and it articulates with the trochlear groove of the femur. Poor patellar tracking in the trochlear groove is a common source of knee pain especially when the cause is atraumatic in nature. The knee is stabilized by the collateral ligaments against varus (lateral collateral ligament) and valgus (medial collateral ligament) stresses. The tibia is limited in its anterior movement by the anterior cruciate ligament (ACL) and in its posterior movement by the posterior cruciate ligament (PCL). The bursae of the knee are located between the skin and bony prominences. They are sac-like structures with a synovial lining. They act to decrease friction of tendons and muscles as they move over adjacent bony structures. Excessive external pressure or friction can lead to swelling and pain of the bursae. The prepatellar bursae (located between the skin and patella), and the pes anserine bursa (which is medial and inferior to the patella, just below the tibial plateau) are most commonly affected. Joint fluid, when excessive due to synovitis or trauma, can track posteriorly through a potential space, resulting in a popliteal cyst (also called a Baker cyst). Other structures that are susceptible to overuse injury and may cause knee pain following repetitive activity include the patellofemoral joint and the iliotibial band. Osteoarthritis of the knees is common after 50 years of age and can develop due to previous trauma, aging, activities, alignment issues, and genetic predisposition.

 Clinical Findings

  1. Symptoms and Signs

Evaluation of knee pain should begin with general questions regarding duration and rapidity of symptom onset and the mechanism of injury or aggravating symptoms. Overuse or degenerative problems can occur with stress or compression from sports, hobbies, or occupation. A history of trauma, previous orthopedic problems with, or surgery to, the affected knee should also be specifically queried. Symptoms of infection (fever, recent bacterial infections, risk factors for sexually transmitted infections [such as gonorrhea] or other bacterial infections [such as staphylococcal infection]) should always be elicited.

Common symptom complaints include the following:

  1. Presence of grinding, clicking, or popping with bending, may be indicative of osteoarthritis or the patellofemoral syndrome.
  2. “Locking” or “catching” when walking suggests an internal derangement, such as meniscal injury or a loose body in the knee.
  3. Intra-articular swelling of the knee or an effusion indicates an internal derangement or a synovial pathology. Large swelling may cause a popliteal (Baker) cyst. Acute swelling within minutes to hours suggests a hemarthrosis, most likely due to an ACL injury, fracture or patellar dislocation, especially if trauma is involved.
  4. Lateral “snapping” with flexion and extension of the knee may indicate inflammation of the iliotibial band.
  5. Pain that is worsened with bending and walking downstairs suggests issues with the patellofemoral joint, usually degenerative such as chondromalacia of the patella or osteoarthritis.
  6. Pain that occurs when rising after prolonged sitting suggests a problem with tracking of the patella.

A careful history, coupled with a physical examination that includes observation, palpation and range of motion testing, as well as specific tests for particular anatomic structures is frequently sufficient to establish a diagnosis. When there is a knee joint effusion caused by increased fluid in the intra-articular space, physical examination will demonstrate swelling in the hollow or dimple around the patella and distention of the suprapatellar space.

Table 41–8 shows the differential diagnosis of knee pain, and Table 41–9 outlines possible diagnoses based on the location of pain.

Table 41–8. Differential diagnosis of knee pain.

Table 41–9. Location of common causes of knee pain.

  1. Laboratory Findings

Laboratory testing of aspirated joint fluid, when indicated, can lead to a definitive diagnosis in most patients (see Tables 20–2 and 20–3).

  1. Imaging

Knee pain is evaluated with plain (weight-bearing) radiographs and MRI most commonly, but CT and ultrasound are sometimes useful.

An acute hemarthrosis represents bloody swelling that usually occurs within the first 1–2 hours following trauma. In situations where the trauma may be activity-related and not a result of a fall or collision, the differential diagnosis most commonly includes ACL tear (responsible for almost 50% of hemarthrosis in children and > 70% in adults), fracture (patella, tibial plateau, femoral supracondylar, growth plate [physeal]), and patellar dislocation. Meniscal tears are unlikely to cause large hemarthrosis.

  1. Anterior Cruciate Ligament Injury

 ESSENTIALS OF DIAGNOSIS

 An injury involving an audible pop when the knee buckles.

 Acute swelling immediately (or within 2 hours).

 Instability occurs with lateral movement activities and going down stairs.

 General Considerations

The anterior cruciate ligament (ACL) connects the posterior aspect of the lateral femoral condyle to the anterior aspect of the tibia. Its main function is to control anterior translation of the tibia on the femur. It also provides rotationally stability of the tibia on the femur. ACL tears are common with sporting injuries. They can result from both contact (valgus blow to the knee) and non-contact (jumping, pivoting, and deceleration) activities. The patient usually falls down following the injury, has acute swelling and difficulty with weight-bearing, and complains of instability. ACL injuries are common in skiing, soccer, football, and basketball among young adolescents and middle-age patients. Prepubertal and older patients usually sustain fractures instead of ligamentous injuries.

 Clinical Findings

  1. Symptoms and Signs

Acute ACL injuries usually lead to acute swelling of the knee, causing difficulty with motion. After the swelling has resolved, the patient can walk with a “stiff-knee” gait or quadriceps avoidance gait because of the instability. More importantly, patients describe symptoms of instability while performing side-to-side maneuvers or descending stairs. Stability tests assess the amount of laxity of the knee while performing side-to-side maneuvers or descending stairs. The Lachman test (84–87% sensitivity and 93% specificity) is performed with the patient lying supine and the knee flexed to 20–30 degrees (Table 41–10). The clinician grasps the distal femur from the lateral side and the proximal tibia with the other hand on the medial side. With the knee in neutral position, stabilize the femur, and pull the tibia anteriorly using a similar force to lifting a 10- to 15-pound weight. Excessive anterior translation of the tibia compared with the other side indicates injury to the ACL. The anterior drawer test (48% sensitivity and 87% specificity) is performed with the patient lying supine and the knee flexed to 90 degrees (Table 41–10). The clinician stabilizes the patient’s foot by sitting on it and grasps the proximal tibia with both hands around the calf and pulls anteriorly. A positive test finds ACL laxity compared with the unaffected side. The pivot shift test is used to determine the amount of rotational laxity of the knee (Table 41–10). The patient is examined while lying supine with the knee in full extension. It is then slowly flexed while applying internal rotation and a valgus stress. The clinician feels for a subluxation at 20–40 degrees of knee flexion. The patient must remain very relaxed to have a positive test.

Table 41–10. Knee examination.

  1. Imaging

Plain radiographs are usually negative in ACL tears but are useful to rule out fractures. A small avulsion injury can sometimes be seen over the lateral compartment of the knee. This is called a “Segond” fracture and is pathognomonic of an ACL injury. MRI is the best method to diagnose ACL tears. It has > 95% sensitivity and specificity for ACL tears. MRI also allows evaluation of other associated structures, such as menisci and cartilages.

 Treatment

Most young and active patients will require surgical reconstruction of the ACL. Common surgical techniques use the patient’s own tissues, usually the patellar or hamstring tendons (autograft) or a cadaver graft (allograft) to arthroscopically reconstruct the torn ACL. Different patients groups experienced improved results with specific surgical graft choices. Recovery from surgery usually requires 6 months.

Nonoperative treatments are usually reserved for older patients or those with a very sedentary lifestyle. Physical therapy can focus on hamstring strengthening and core stability. An ACL brace can help stability. Longitudinal studies have demonstrated that nonoperative management of an ACL tear can lead to a higher incidence of meniscus tears. However, a small, randomized study demonstrated that acute ACL injuries may be treated nonoperatively initially, with similar clinical outcomes as those injuries that were operated on within 10 weeks of injury.

 When to Refer

  • Almost all ACL tears should be referred to an orthopedic surgeon for evaluation.
  • Individuals with instability in the setting of a chronic ACL tear (> 6 months) should be considered for surgical reconstruction.
  • Patients with an ACL tear and associated meniscus or articular injuries may benefit from surgery to address the other injuries.

Barrett AM et al. Anterior cruciate ligament graft failure: a comparison of graft type based on age and Tegner activity level. Am J Sports Med. 2011 Oct;39(10):2194–8. [PMID: 21784999]

Delincé P et al. Anterior cruciate ligament tears: conservative or surgical treatment? A critical review of the literature. Knee Surg Sports Traumatol Arthrosc. 2012 Jan;20(1):48–61. [PMID: 21773828]

  1. Collateral Ligament Injury

 ESSENTIALS OF DIAGNOSIS

 Caused by a valgus or varus blow or stress to the knee.

 Pain and instability in the affected area.

 Limited range of motion.

 General Considerations

The medial collateral ligament (MCL) is the most commonly injured ligament in the knee. It is usually injured with a valgus stress to the partially flexed knee. It can also occur with a blow to the lateral leg. The MCL is commonly injured with acute ACL injuries. The lateral collateral ligament (LCL) is less commonly injured, but this can occur with a medial blow to the knee. Since both collateral ligaments are extra-articular, injuries to these ligaments may not lead to any intra-articular effusion. Affected patients may have difficulty walking initially, but this can improve when the swelling decreases.

 Clinical Findings

  1. Symptoms and Signs

The main clinical findings for patients with collateral ligament injuries are pain along the course of the ligaments. The patient may have limited range of motion due to pain, especially during the first 2 weeks following the injury. The best tests to assess the collateral ligaments are the varus and valgus stress tests. The sensitivity of the tests is as high as 86–96%.

The valgus stress test is performed with the patient supine (Table 41–10). The clinician should stand on the outside of the patient’s knee. With one hand, the clinician should hold the ankle while the other hand is supporting the leg at the level of the knee joint. A valgus stress is applied at the ankle to determine pain and laxity of the MCL. The test should be performed at both 30 degrees and at 0 degrees of knee extension.

For the varus stress test, the patient is again placed supine (Table 41–10). For the right knee, the clinician should be standing on the right side of the patient. The clinician’s left hand should be holding the ankle while the right hand is supporting the lateral thigh. A varus stress is applied at the ankle to determine pain and laxity of the LCL. The test should be performed at both 30 degrees and at 0 degrees of knee flexion.

The test results can be graded from 1–3. Grade 1 is when the patient has pain with varus/valgus stress test but no instability. With grade 2 injuries, the patient has pain, and the knee shows instability at 30 degrees of knee flexion. In grade 3 injuries, the patient has marked instability but not much pain. The knee is often unstable at both 30 degrees and 0 degrees of knee flexion.

  1. Imaging

Radiographs are usually nondiagnostic except for avulsion injuries. However, radiographs should be used to rule out fractures that can occur with collateral ligament injuries. Isolated MCL injuries usually do not require evaluation by MRI, but MRI should be used to evaluate possible associated cruciate ligament injuries. LCL or posterolateral corner injuries should have MRI evaluation to exclude associated injuries and to determine their significance.

 Treatment

The majority of MCL injuries can be treated with protected weight-bearing and physical therapy. For grade 1 and 2 injuries, the patient can usually bear weight as tolerated with full range of motion. A hinged knee brace can be given to patients with grade 2 MCL tears to provide stability. Early physical therapy is recommended to protect range of motion and muscle strength. Grade 3 MCL injuries require long leg braces to provide stability. Patients can weight-bear but only with the knee locked in extension with a brace. The motion can then be increased with the brace unlocked. Grade 3 injuries can take up to 6–8 weeks to heal. MCL injuries rarely need surgery. LCL injuries usually require surgical repair or reconstruction.

 When to Refer

  • Symptomatic instability with chronic MCL tears or acute MCL tears with other ligamentous injuries.
  • LCL or posterolateral corner injuries require urgent surgical repair or reconstruction (within 1 week).

Pacheco RJ et al. Posterolateral corner injuries of the knee: a serious injury commonly missed. J Bone Joint Surg Br. 2011 Feb;93(2):194–7. [PMID: 21282758]

  1. Posterior Cruciate Ligament Injury

 ESSENTIALS OF DIAGNOSIS

 Usually follows an anterior trauma to the tibia, such as a dashboard injury during a motor vehicle accident.

 The knee may freely dislocate and reduce.

 One-third of multi-ligament injuries involving the PCL have neurovascular injuries.

 General Considerations

The posterior cruciate ligament (PCL) is the strongest ligament in the knee. PCL injuries usually represent significant trauma and are highly associated with multi-ligament injuries and knee dislocations. More than 70–90% of PCL injuries have associated injuries to the posterolateral corner, MCL, and ACL. Neurovascular injuries occur in up to one-third of all knee dislocations or PCL injuries. There should be high suspicion for neurovascular injuries and a thorough neurovascular examination of the limb should be performed.

 Clinical Findings

  1. Symptoms and Signs

Most patients with acute injuries have difficulty with ambulation. Patients with chronic PCL injuries can ambulate without gross instability but may complain of subjective “looseness” and often report pain and dysfunction, especially with bending. Clinical examinations of PCL injuries include the “sag sign” (Table 41–10). The patient is placed supine and both hips and knees are flexed up to 90 degrees. Because of gravity, the PCL-injured knee will have an obvious set-off at the anterior tibia that is “sagging” posteriorly. The PCL ligament can also be examined using the posterior drawer test (90% sensitivity and 99% specificity) (Table 41–10). The patient is placed supine with the knee flexed at 90 degrees. In a normal knee, the anterior tibia should be positioned about 10 mm anterior to the femoral condyle. The clinician can grasp the proximal tibia with both hands and push the tibia posteriorly. The movement, indicating laxity and possible tear of the PCL, is compared with the uninjured knee. A PCL injury is sometimes mistaken for an ACL injury during the anterior drawer test since the tibia is subluxed posteriorly in a sagged position and can be abnormally translated forward, yielding a false-positive test for an ACL injury. Pain, swelling, pallor, and numbness in the affected extremity may suggest a knee dislocation with possible injury to the popliteal artery.

  1. Imaging

Radiographs are often nondiagnostic but are required to diagnose any fractures. MRI is used to diagnose PCL and other associated injuries.

 Treatment

Isolated PCL injuries can be treated nonoperatively. Acute injuries are usually immobilized using a knee brace with the knee extension; the patient uses crutches for ambulation. Physical therapy can help achieve increased range of motion and improved ambulation. Many PCL injuries are associated with other injuries and may require operative reconstruction.

 When to Refer

  • The patient should be seen urgently within 1–2 weeks.
  • If the lateral knee is also unstable with varus stress testing, the patient should be assessed for a posterolateral corner injury, which may require an urgent surgical reconstruction.
  • Isolated PCL tears may require surgery if the tear is complete (grade 3) and the patient is symptomatic.
  1. Meniscus Injuries

 ESSENTIALS OF DIAGNOSIS

 Patient may or may not report an injury.

 Joint line pain and pain with deep squatting are the most sensitive signs.

 Difficulty with knee extension suggests an internal derangement that should be evaluated urgently with MRI.

 General Considerations

The menisci act as shock absorbers within the knee. Injuries to a meniscus can lead to pain, clicking, and locking sensation. Most meniscus injuries occur with acute injuries (usually in younger patients) or repeated microtrauma, such as squatting or twisting (usually in older patients).

 Clinical Findings

  1. Symptoms and Signs

The patient may have an antalgic (painful) gait and difficulty with squatting. He or she may complain of catching or locking of the meniscal fragment. Physical findings can include effusion or joint line tenderness. Patients can usually point out the area of maximal tenderness along the joint line. Swelling usually occurs during the first 24 hours after the injury or later. Meniscus tears rarely lead to the immediate swelling that is commonly seen with fractures and ligament tears. Meniscus tears are commonly seen in arthritic knees. However, it is often unclear whether the pain is coming from the meniscus tear or the arthritis.

Provocative tests, including the McMurray test, the modified McMurray test, and the Thessaly test, can be performed to confirm the diagnosis (Table 41–10). Most symptomatic meniscus tears cause pain with deep squatting and when waddling (performing a “duck walk”).

  1. Imaging

Radiographs are usually normal but may show joint space narrowing, early osteoarthritis changes, or loose bodies. MRI of the knee is the best diagnostic tool for meniscal injuries (93% sensitivity and 95% specificity). High signal through the meniscus (bright on T2 images) represents a meniscal tear.

 Treatment

Conservative treatment can be used for degenerative tears in older patients. The treatment is similar for patients with mild knee osteoarthritis, including analgesics and physical therapy for strengthening and core stability. Acute tears in young and active patients can be best treated arthroscopically with meniscus repair or debridement. Randomized controlled studies have demonstrated no benefit with arthroscopic meniscectomy in patients with advanced osteoarthritis.

 When to Refer

  • If the patient has symptoms of internal derangement suspected as meniscus injury. The patient should receive an MRI to confirm the injury.
  • If the patient cannot extend the knee due to a mechanical block, the patient should be evaluated as soon as possible. Certain shaped tears on MRI, such as bucket handle tears, are amenable to meniscal repair surgery.

McDermott I. Meniscal tears, repairs and replacement: their relevance to osteoarthritis of the knee. Br J Sports Med. 2011 Apr;45(4):292–7. [PMID: 21297172]

  1. Patellofemoral Pain

 ESSENTIALS OF DIAGNOSIS

 Pain experienced with bending activities (kneeling, squatting, climbing stairs).

 Lateral deviation or tilting of the patella in relation to the femoral groove.

 General Considerations

Patellofemoral pain, also known as anterior knee pain, chondromalacia, or “runner’s knee,” describes any pain involving the patellofemoral joint. The pain affects any or all of the anterior knee structures, including the medial and lateral aspects of the patella as well as the quadriceps and patellar tendon insertions. The patella engages the femoral trochlear groove with approximately 30 degrees of knee flexion. Forces on the patellofemoral joint increase up to three times body weight as the knee flexes to 90 degrees (eg, climbing stairs), and five times body weight when going into full knee flexion (eg, squatting). Abnormal patellar tracking during flexion can lead to abnormal articular cartilage wear and pain. When the patient has ligamentous hyperlaxity, the patella can sublux out of the groove, usually laterally. Patellofemoral pain is also associated with muscle strength and flexibility imbalances as well as altered hip and ankle biomechanics.

 Clinical Findings

  1. Symptoms and Signs

Patients usually complain of pain in the anterior knee with bending movements and less commonly in full extension. Pain from this condition is localized under the kneecap but can sometimes be referred to the posterior knee or over the medial or lateral inferior patella. Symptoms may begin after a trauma or after repetitive physical activity, such as running and jumping. When maltracking, palpable and sometimes audible crepitus can occur.

Intra-articular swelling usually does not occur unless there are articular cartilage defects or if osteoarthritis changes develop. On physical examination, it is important to palpate the articular surfaces of the patella. For example, the clinician can use one hand to move the patella laterally, and use the fingertips of the other hand to palpate the lateral undersurface of patella. Patellar mobility can be assessed by medially and laterally deviating the patella (deviation by one-quarter of the diameter of the kneecap is consider normal; greater than one-half the diameter suggests excessive mobility). The apprehension sign suggests instability of the patellofemoral joint and is positive when the patient becomes apprehensive when the patella is deviated laterally (Table 41–10). The patellar grind test is performed by grasping the knee superior to the patella and pushing it downward with the patient supine and the knee extended, pushing the patella inferiorly. The patient is asked to contract the quadriceps muscle to oppose this downward translation, with reproduction of pain or grinding being the positive sign for chondromalacia of the patella. There are two common presentations: (1) Patients whose ligaments and patella are too loose (hypermobility); (2) and patients who have soft tissues that are too tight leading to excessive pressure on the joint.

Evaluation of the quadriceps strength and hip stabilizers can be accomplished by having the patient perform a one-leg squat without support. Patients who are weak may display poor balance, with dropping of the pelvis (similar to a positive hip Trendelenburg sign) or excessive internal rotation of the knee medially. Normally, with a one-leg squat, the knee should align over the second metatarsal ray of the foot.

  1. Imaging

Diagnostic imaging has limited use in younger patients and is more helpful in older patients to assess for osteoarthritis or to evaluate patients who do not respond to conservative treatment. Radiographs may show lateral deviation or tilting of the patella in relation to the femoral groove. MRI may show thinning of the articular cartilage but is not clinically necessary, except prior to surgery or to exclude other pathology.

 Treatment

  1. Conservative

For symptomatic relief, use of local modalities such as ice and anti-inflammatory medications can be beneficial. If the patient has signs of patellar hypermobility, physical therapy exercises are useful to strengthen the quadriceps (especially the vastus medialis obliquus muscle) to help stabilize the patella and improve tracking. Support for the patellofemoral joint can be provided by use of a patellar stabilizer brace or special taping techniques (McConnell taping). Correcting lower extremity alignment (with appropriate footwear or over-the-counter orthotics) can help improve symptoms, especially if the patient has pronation or high arched feet. If the patient demonstrates tight peripatellar soft tissues, special focus should be put on stretching the hamstrings, iliotibial band, quadriceps, calves and hip flexors. Strengthening exercises should include the quadriceps and hip abductors.

  1. Surgical

Surgery is rarely needed and is considered a last resort for patellofemoral pain. Procedures performed include lateral release or patellar realignment surgery.

 When to Refer

Patients with persistent symptoms.

  1. Knee Osteoarthritis

 ESSENTIALS OF DIAGNOSIS

 Degeneration of joint cartilage.

 Pain with bending or twisting activities.

 Swelling.

 Loss of active and passive range of motion in severe osteoarthritis.

 General Considerations

In the United States, the prevalence of osteoarthritis will grow as the number of persons over age 65 years doubles to more than 70 million by 2030. The incidence of knee osteoarthritis in the United States is 240 per 100,000 person-years.

Cartilage loss and osteoarthritis symptoms are preceded by damage to the collagen-proteoglycan matrix. The etiology of osteoarthritis is often multifactorial including previous trauma, prior high-impact activities, genetic factors, obesity, and rheumatologic or metabolic conditions.

 Clinical Findings

  1. Symptoms and Signs

Osteoarthritis usually causes pain in the affected joint with loading of the joint or at the extremes of motion. Mechanical symptoms—such as swelling, grinding, catching, and locking—suggest internal derangement, which is indicated by damaged cartilage or bone fragments that affect the smooth range of motion expected at an articular joint. Pain can also produce the sensation of “buckling” or “giving way” due to muscle inhibition. As the joint degeneration becomes more advanced, the patient loses active range of motion and may lose passive range of motion as well.

As the condition worsens, patients with knee osteoarthritis have an increasingly limited ability to walk. Symptoms include pain with bending or twisting activities, and going up and down stairs. Swelling, limping, and pain while sleeping are common complaints with osteoarthritis, especially as it progresses.

  1. Imaging

The most commonly recommended radiographs include bilateral weight-bearing 45-degree bent knee posteroanterior, lateral, and patellofemoral joint views (Merchant view). Radiographic findings include diminished width of the articular cartilage causing joint space narrowing, subchondral sclerosis, presence of osteophytes, and cystic changes in the subchondral bone. MRI of the knee is most likely unnecessary unless other pathology is suspected, including ischemic osteonecrosis of the knee.

 Treatment

  1. Conservative

Changes in the articular cartilage are irreversible. Therefore, a cure for the diseased joint is not possible, although symptoms or structural issues can be addressed to try to maintain activity level. Conservative treatment for all patients with osteoarthritis includes activity modification, therapeutic exercises, and weight loss. Lifestyle modifications also include proper footwear and avoidance of high impact activities.

Use of a cane in the hand opposite to the affected side is mechanically advantageous. Knee sleeves or braces provide some improvement in subjective pain symptoms most likely due to improvements in neuromuscular function. If patients have unicompartmental osteoarthritis in the medial or lateral compartment, joint unloader braces are available to offload the degenerative compartment. Cushioning footwear and appropriate orthotics or shoe adjustments are useful for reducing impact to the lower extremities.

The initial medication of choice for the treatment of pain in knee osteoarthritis are oral acetaminophen and topical capsaicin. If a traditional NSAID is indicated, the choice should be based on cost, side-effect profile, and adherence. The cyclooxygenase (COX)-2 inhibitor, celecoxib, is no more effective than traditional NSAIDs; it may offer short-term, but probably not long-term, advantage in preventing gastrointestinal complications. Due to its cost and potential cardiovascular risk, celecoxib should be reserved for carefully selected patients. The role of topical NSAIDs are being considered in the osteoarthritis treatment algorithm, as they do avoid many of the traditional NSAID complications. Opioids can be used appropriately in patients with severe osteoarthritis (see Chapter 5). Glucosamine and chondroitin sulfate are supplements that have been widely used and marketed for osteoarthritis. Evidence for their effectiveness in slowing or reversing cartilage loss is limited and any effect present appears to be small. Despite some initial promise, the best-controlled studies indicate these supplements are ineffective as analgesics in osteoarthritis. However, they have minimal side effects and may be appropriate if the patient experiences subjective benefit.

Knee joint corticosteroid injections are options to help reduce pain and inflammation and can provide short-term pain relief, usually lasting about 6–12 weeks. Viscosupplementation by injections of hyaluronic acid-based products improves synovial fluid viscosity by increasing the molecular weight and quantity of hyaluronic acid beyond that naturally synthesized by the synovium. Laboratory studies also demonstrate that hyaluronic acid injections decrease inflammatory cytokines and free radicals. Studies also demonstrate more prolonged effects of viscosupplementation products compared with corticosteroid injection with symptom improvement for > 6 months in some patients with mild knee osteoarthritis. One meta-analysis questions the value of viscosupplementation suggesting only a small and clinically irrelevant benefit and an increased risk of serious adverse events. However, older meta-analyses found modest improvements and did not report similar concerns regarding serious side effects.

  1. Surgical

Two randomized trials demonstrate that arthroscopy does not improve outcomes at 1 year over placebo or routine conservative treatment of osteoarthritis. Arthroscopic surgery is indicated in patients with osteoarthritis if, rather than pain, they have mechanical symptoms and internal derangement symptoms. Such surgical treatments are useful to restore range of motion by removing osteophytes, cartilage fragments, or loose bodies.

Joint replacement surgeries are effective and cost-effective for patients with significant symptoms or functional limitations, providing improvements in pain, function, and quality of life. The number of total knee arthroplasty procedures jumped 162% from 1991 to 2010, along with an increase in complications and hospital readmissions. Minimally invasive surgeries and computer-assisted navigation during operation are being investigated as methods to improve techniques (eg, accurate placement of the hardware implant) and to reduce complication rates; however, major improvements have yet to be demonstrated.

Knee realignment surgery, such as high tibial osteotomy or partial knee replacement surgery, is indicated in patients younger than age 60 with unicompartmental osteoarthritis, who would benefit from delaying total knee replacement. Knee joint replacement surgery has been very successful in improving outcomes for patient with end-stage osteoarthritis. Recent long-term series describe > 95% survival rate of the implant at 15 years.

 When to Refer

Patients with sufficient disability, limited benefit from conservative therapy, and evidence of severe osteoarthritis can be referred for joint replacement surgery.

Cram P et al. Total knee arthroplasty volume, utilization, and outcomes among Medicare beneficiaries, 1991–2010. JAMA. 2012 Sep 26;308(12):1227–36. [PMID: 23011713]

Messier SP et al. Effects of intensive diet and exercise on knee joint loads, inflammation, and clinical outcomes among overweight and obese adults with knee osteoarthritis: the IDEA randomized clinical trial. JAMA. 2013 Sep 25;310(12):1263–73. [PMID: 24065013]

Rutjes AW et al. Viscosupplementation for osteoarthritis of the knee: a systematic review and meta-analysis. Ann Intern Med. 2012 Aug 7;157(3):180–91. [PMID: 22868835]

ANKLE INJURIES

  1. Inversion Ankle Sprains

 ESSENTIALS OF DIAGNOSIS

 Localized pain and swelling.

 The majority of ankle injuries involve inversion injuries affecting the lateral ligaments.

 Consider chronic ankle instability or associated injuries if pain persists for > 3 months following an ankle sprain.

 General Considerations

Ankle sprains are the most common sports injuries seen in outpatient clinics. Patients usually report “turning the ankle” during a fall or after landing on an irregular surface such as a hole or an opponent’s foot. The most common mechanism of injury is an inversion and plantar flexion sprain, which injures the anterior talofibular ligament (ATF) ligament rather than the calcaneofibular ligament (CF) ligament. Other injuries that can occur with inversion ankle injuries are listed in (Table 41–11). Women appear to sustain an inversion injury more frequently than men.

Table 41–11. Injuries associated with ankle sprains.

 Clinical Findings

  1. Symptoms and Signs

The usual symptoms following a sprain include localized pain and swelling over the lateral aspect of the ankle, difficulty weight bearing, and limping. The patient’s ankle may feel unstable. On examination, there may be swelling or bruising over the lateral aspect of the ankle. The anterior, inferior aspect below the lateral malleolus is most often the point of maximal tenderness consistent with ATF and CF ligament injuries. The swelling may limit motion of the ankle. Special stress tests for the ankle include the anterior drawer test (Table 41–12) and subtalar tilt test (Table 41–12). In order to grade the severity of ankle sprains, no laxity on stress tests is considered a grade 1 injury, laxity of the ATF ligament on anterior drawer testing but a negative tilt test is a grade 2 injury, and both positive drawer and tilt tests signify a grade 3 injury.

Table 41–12. Ankle examination.

  1. Imaging

Routine ankle radiographic views include the AP, lateral, and oblique (mortise) views. Less common views requested include the calcaneal view and subtalar view. Ottawa Ankle Rules are clinical prediction rules to guide the need for radiographs and have a 97% sensitivity and 99% negative predictive value. If the patient is unable to bear weight immediately in the office setting or emergency department for four steps, then the clinician should check for (1) bony tenderness at the posterior edge of the medial or lateral malleolus and (2) bony tenderness over the navicular (medial midfoot) or at the base of the fifth metatarsal. If either malleoli demonstrates pain or deformity, then ankle radiographs should be obtained. If the foot has bony tenderness, obtain foot radiographs. An MRI is helpful when considering the associated injuries.

 Treatment

Immediate treatment of an ankle sprain follows the MICE mnemonic: modified activities, ice, compression, and elevation. Subsequent treatment involves protected weight bearing with crutches and use of an ankle stabilizer brace, especially for grade 2 and 3 injuries. Early motion is essential, and patients should be encouraged to do home exercises or physical therapy. Proprioception and balance exercises (eg, “wobble board”) are useful to restore function to the ankle and prevent future ankle sprains. Regular use of an ankle support with activities can reduce the risk of lateral ankle sprains. Chronic instability can develop after acute ankle sprain in 10–20% of people and may require surgical stabilization with ligament reconstruction surgery.

 When to Refer

  • Ankle fractures.
  • Recurrent ankle sprains or signs of chronic ligamentous ankle instability.
  • No response after more than 3 months of conservative treatment.
  • Suspicion of associated injuries.

Doherty C et al. The incidence and prevalence of ankle sprain injury: a systematic review and meta-analysis of prospective epidemiological studies. Sports Med. 2014 Jan;44(1):123–40. [PMID: 24105612]

Kemler E et al. A systematic review on the treatment of acute ankle sprain: brace versus other functional treatment types. Sports Med. 2011 Mar 1;41(3):185–97. [PMID: 21395362]

  1. Eversion (“High”) Ankle Sprains

 ESSENTIALS OF DIAGNOSIS

 Severe and prolonged pain.

 Limited range of motion.

 Mild swelling.

 Difficulty with weight bearing.

 General Considerations

A syndesmotic injury or “high ankle” sprain involves the anterior tibiofibular ligament in the anterolateral aspect of the ankle, superior to the anterior talofibular (ATF) ligament. The injury mechanism often involves the foot being turned out or externally rotated and everted (eg, when being tackled). This injury is commonly missed or misdiagnosed as an ATF ligament sprain on initial visit.

 Clinical Findings

  1. Symptoms and Signs

Symptoms of a high ankle sprain include severe and prolonged pain over the anterior ankle at the anterior tibiofibular ligament, worse with weight bearing. This is often more painful than the typical ankle sprain. The point of maximal tenderness involves the anterior tibiofibular ligament, which is higher than the ATF ligament. It is also important to palpate the proximal fibula to rule out any proximal syndesmotic ligament injury and associated fracture known as a “maisonneuve fracture.” There is often some mild swelling in this area, and the patient may or may not have an ankle effusion. The patient usually has limited range of motion in all directions. The external rotation stress test reproduces the mechanism of injury (Table 41–12). (Note: The patient’s foot should have an intact neurovascular examination before undertaking this test.)

  1. Imaging

Radiographs of the ankle should include the AP, mortise, and lateral views. The mortise view may demonstrate loss of the normal overlap between the tibia and fibula, which should be at least 1–2 mm. Asymmetry in the joint space around the tibiotalar joint suggests disruption of the syndesmotic ligaments. If there is proximal tenderness in the lower leg especially around the fibula, an AP and lateral view of the tibia and fibula should be obtained to rule out a proximal fibula fracture. Radiographs during an external rotation stress test may visualize instability at the distal tibiofibular joint. MRI is the best method to visualize injury to the tibiofibular ligament and to assess status of the other ligaments and the articular cartilage.

 Treatment

Whereas most ankle sprains are treated with early motion and weight bearing, treatment for a high ankle sprain should be conservative with a cast or walking boot for 4–6 weeks. Thereafter, protected weight bearing with crutches is recommended until the patient can walk pain-free. Physical therapy can start early to regain range of motion and maintain strength with limited weight-bearing initially.

 When to Refer

If there is widening of the joint space and asymmetry at the tibiotalar joint, the patient should be referred urgently to a foot and ankle surgeon. Severe or prolonged persistent cases that do not heal may require internal fixation to avoid chronic instability at the tibiofibular joint.

Scheyerer MJ et al. Diagnostics in suspicion of ankle syndesmotic injury. Am J Orthop (Belle Mead NJ). 2011 Apr;40(4):192–7. [PMID: 21731928]

Valkering KP et al. Isolated syndesmosis ankle injury. Orthopedics. 2012 Dec;35(12):e1705–10. [PMID: 23218625]