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Considerations for Evaluation of Patients with Low Back Pain

in Guildelines for Orthopedic Rehabilitation of Back Pain, Orthopedic Rehabilitation for Back Pain

This entry is part 3 of 9 in the series Low Back Pain

Evaluation of Patients with Low Back Pain

A thorough history and examination allows an accurate working diagnosis to be made in 90% of patients with LBP.

Be wary of constant pain unrelated to activity or position, nocturnal pain, pain refractory to treatment, or concomitant constitutional symptoms (Table 9–1).

History should also include questioning of nonmusculoskeletal symptoms (e.g., colic symptoms, penile discharge) (Table 9–2).

General History

  1. Demographic information
    1. Age
      1. Younger—often discogenic pain.
      2. Older—stenosis, osseous, lateral disc herniation.
    2. Gender
      1. Male—discogenic, ankylosing spondylitis, Reiter’s syndrome more common.
      2. Female—osteoporosis, fibromyalgia.
    3. Occupation
      1. Specific physical duties—possible increased incidence of back injury with repetitive lifting, twisting, vibration.
      2. Emotional, work-related stresses—if significant, monitor for nonorganic component to pain.
      3. Lack of job satisfaction—high correlation with time off work.
      4. Last date patient worked—the longer the interval off work, the lower the likelihood of return to work.
      5. Feasibility of finding “light” or “clerical” duty at work—we have had much more success with rapid return to work having our patients sit at a desk hours a day (often in a very boring setting), rather than having them stay at home.
      6. Time left to retirement.
  2. Recreational sports

History of Present Illness

  1. Onset of pain
    1. When did episode begin?
    2. How did pain begin?
      1. Spontaneously
        1. Sudden onset.
        2. Gradual onset.
      2. Traumatically
        1. Motor vehicle, work-related, nonlegal setting.
        2. Mechanism—flexion, extension, twist, lift, fall, sneeze, cough, strain, other.
    3. Motor vehicle accidents
      1. Types of cars involved.
      2. Direction of impact.
      3. Extent of vehicle damage—however, significant injury can occur with minor damage to vehicle.
      4. Seat belt used? Lap belt versus shoulder harness—flexion injuries with lap belts, torsional injuries with harness.
      5. Loss of consciousness.
      6. Did head hit windshield, or did chest hit steering wheel?
      7. Specific location of immediate pain, if any.
      8. Visit to emergency department? Diagnostic and therapeutic measures performed.
    5. Work-related injuries
      1. Details of specific injury.
      2. Litigation pending.
      3. Compensation for time off work.
    6. Sports-related injuries
      1. Sports involving torsion (e.g., golf, racquet sports, baseball)—higher incidence of discogenic pain.
      2. Sports involving repetitive hyperextension (e.g., gymnastics, dance, crew)—greater loading of posterior elements (e.g., spondolysis, facet syndrome).
      3. Details of specific injury.
  2. Time course of pain
    1. Intensity of pain—use of sual analog pain scale may be helpful
      1. Overall improvement or worsening overall: quantitate with visual analog pain scale or have patient assign a numerical or percent value to pain.
      2. Response to specific treatment.
    2. Recurrences: frequency and duration.
  3. Location of pain
    1. Pain diagram is helpful (have patient draw on pain diagram)
      1. Structural lesions.
      2. Possibility of functional component.
    2. Ask about area of most intense pain—back versus leg: right, left, or bilateral?
    3. Primarily back pain—think of annular tear, facet syndrome, local muscular pathology, bony lesion.
    4. Primarily distal lower extremity pain—think of lateral or extruded herniated nucleus pulposis (HNP), stenosis, nerve lesion.
    5. How has location changed over time and in response to specific treatments?
  4. Relationship of pain to daily routine
    1. What positions increase the pain?
      1. Prone—pain is increased with facet pain, lateral HNP, systemic process.
      2. Sitting—increased with annular tear, paramedian HNP.
      3. Standing—increased with central stenosis, facet syndrome, lateral HNP.
    2. Is there pain on arising from a seat? A positive answer is typical of discogenic pain.
    3. How does walking affect the pain?
      1. How far can the patient walk? Is the distance variable (lumbar stenosis) or constant (vascular claudication)?
      2. Is there more pain with uphill or downhill walking?
        1. Patients with spinal stenosis or facet pain have less pain while walking uphill because the lumbar spine is flexed, which increases foraminal and central canal space.
        2. Discogenic symptoms decrease while walking downhill because the lumbar spine is extended and discs are unloaded.
      3. Is it more comfortable to walk holding a wagon or carriage or in a flexed posture? A positive answer is typical of stenosis.
    4. How is the pain affected by time of day?
      1. Is the patient awakened from sleep? Consider a systemic process if so.
      2. Is there morning stiffness? Of what duration? Discogenic patients are stiff for 0 to 0 minutes, whereas rheumatic patients may be stiff for hours.
      3. Does the pain increase or decrease as the day progresses? The response helps guide treatment.
    5. Is pain intensified by coughing, sneezing, laughing, or Valsalva maneuver? In which location?
      1. Suggests disc disease or, rarely, an intraspinal tumor.
      2. Reproduction of distal pain strongly supports discogenic pain.
    6. What activities is the patient unable to perform?
    7. Do any positions or maneuvers relieve the pain or other symptoms?
  5. Associated neurologic symptoms
    1. Location of anesthesia, hypoesthesia, hyperesthesia, paresthesias
      1. Regional.
      2. Dermatomal.
      3. Sclerotomal.
      4. Nonphysiologic.
    2. Does the patient note weakness?
      1. Differentiate inability to perform a task owing to pain from actual weakness.
      2. Has the patient noted a dragging foot, buckling knee, difficulty with stairs or curbs? Suggestive of myotomal, plexus, cord, or non-physiologic process.
    3. Has the patient noted bladder, bowel, or sexual dysfunction? If so, consider cauda equina syndrome.
    4. Does the patient have associated upper extremity, central nervous system, or brain stem symptoms?
  6. Diagnostic studies
    1. Patient should be requested to bring in all images and reports.
    2. Patient should report the results of unavailable studies.
  7. Response to prior treatments—ask for specifics (answer helps guide treatment)
    1. Bedrest—may be of limited benefit in stenosis.
    2. Medications
      1. Benefits.
      2. Side effects.
    3. Modalities
      1. Superficial heating and cooling.
      2. Electric stimulation.
      3. Ultrasound.
      4. Transcutaneous electrical nerve stimulation (TENS).
    4. Manual or mechanical therapy
      1. Centralization techniques—passive and active extension, shift correction. Positive response suggests discogenic pain.
      2. Traction.
      3. Stretching.
      4. Mobilization.
        1. Relief with specific facet mobilization suggests facet disease.
        2. Mobilization may also treat other causes of pain (e.g., segmental dysfunction).
      5. Manipulation may treat facet pain and other sources of lumbar spine pain.
      6. Rapid response to facet manipulation suggests a facet syndrome.
    5. Exercises
      1. Flexibility.
      2. Strengthening and stabilization.
      3. Aerobic conditioning.
    6. Education in proper body mechanics.
    7. Corset or bracing.
    8. Biofeedback.
      1. Soft tissue injections
      2. Trigger points.
      3. Tendon.
      4. Ligament.
    10. Spinal injections
      1. Anesthetic phase relief or steroid phase relief.
      2. Fluoroscopy and/or contrast used?
    11. Percutaneous rhizolysis.
    12. Acupuncture.
    13. Surgery
      1. Specific procedure and date performed.
      2. Immediate change in symptoms and/or signs.
      3. Long-term change in symptoms and/or signs.
      4. Complications.

Medical History

  1. Prior and current medical conditions
    1. Diabetes.
    2. Hypertension.
    3. Cardiac disease.
    4. Cancer.
    5. Infections.
    6. Rheumatologic diseases.
    7. Gastrointestinal disorders (tolerance for non-steroidal anti-inflammatory drugs [NSAID] use).
  2. Present medications and drug allergies.
  3. Operations, injuries, and previous hospitalizations, with names, addresses, phone numbers of all practitioners involved in patient’s care.
  4. Review of systems, asked selectively
    1. Constitutional symptoms
      1. Weight loss.
      2. Loss of appetite.
      3. Fever or night sweats.
      4. Chills.
      5. Fatigue.
      6. Night pain.
    2. Integument—rheumatologic disorders (e.g., rashes, psoriasis).
    3. Lymph nodes
      1. Malignancy.
      2. Infection.
    4. Hematopoietic system
      1. Anemia.
      2. Bleeding.
    5. Endocrine system—symptoms suggestive of
      1. Diabetes.
      2. Thyroid dysfunction.
    6. Eyes
      1. Visual loss.
      2. Inflammation.
    7. Mouth
      1. Pain.
      2. Ulcerations.
    8. Bones, joints, muscles
      1. Pathologic fractures.
      2. Peripheral or cervicothoracic joint symptoms.
      3. Muscle pain or weakness.
    9. Breasts
      1. Pain.
      2. Lumps.
      3. Discharge.
    10. Respiratory system
      1. Pain.
      2. Shortness of breath.
      3. Cough.
    11. kCardiovascular system
      1. Chest pain.
      2. Palpitations.
      3. Orthopnea.
      4. Dyspnea on exertion.
      5. Intermittent claudication.
      6. Distal skin lesions.
      7. Edema.
    12. Gastrointestinal system
      1. Dysphagia.
      2. Nausea.
      3. Vomiting.
      4. Hematemesis.
      5. Jaundice.
      6. Change in bowel habits.
      7. Bowel incontinence.
    13. Genitourinary system
      1. Urologic
        1. Nocturia.
        2. Dysuria.
        3. Hematuria.
        4. Pyuria.
        5. Urinary frequency.
        6. Retention.
        7. Incontinence.
      2. Gynecologic
        1. Number of full-term pregnancies.
        2. Last menstrual period (currently pregnant?).
        3. Are menses regular or irregular?
        4. Date and results of last pelvic examination and Papanicolaou smear.
        5. Back or lower extremity pain associated with menses.
    14. Nervous system
      1. Cranial nerves.
      2. Movement disorders.
      3. Coordination.
      4. Convulsions.
      5. Mental status.

Family History

  1. Familial conditions.
  2. Family members with chronic pain syndromes and/or spine pain.
  3. Family members on disability.

Social History

  1. Open-ended: “Tell me about your family.”
  2. Marital status—impact of condition on relationship and vice versa.
  3. Children—impact of condition on relationship and vice versa.
  4. Substance abuse history
    1. Alcohol intake.
    2. Smoking history.
    3. Illicit drug usage.
  5. Social and economic status
    1. Extent of education.
    2. Special financial problems.

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The Development of Low Back Pain

in Guildelines for Orthopedic Rehabilitation of Back Pain, Orthopedic Rehabilitation for Back Pain

This entry is part 2 of 9 in the series Low Back Pain

Risk Factors Previously Associated with the Development of Low Back Pain

Almost all of us (70 to 85%) will develop LBP at some point. For this reason, it is inappropriate for physicians to tell patients that LBP results from being obese, inactive, or other factors.

Gordon Waddell’s recommended text (1998) critically reviews the poor methodology and science behind studies that have described risks for LBP including:

  • Heavy manual labor.
  • Repetitive lifting and twisting.
  • Postural stress.
  • Whole body vibration.
  • Monotonous work.
  • Lack of personal control at work.
  • Low job satisfaction.
  • Poor physical fitness.
  • Poor or inadequate trunk strength.
  • Smoking.

Waddell, after critical review of these studies, reached several interesting conclusions.

  • Most people get back pain; heredity, gender, and body build make little difference.
  • It is good general health advice to stop smoking, avoid or correct obesity, and get physically fit. These may possibly help reduce the likelihood of developing new episodes of back pain.

Waddell asserts that “social class” is probably the strongest personal predictor of incurring back trouble. This is in part related to heavy manual labor and in part to “social disadvantage.”

“Social class” in Waddell’s discussion reflects occupation (manual rather than clerical labor) and social disadvantage (e.g., poor medical care). The prevalence of back pain appears to be slightly higher in those patients who perform more manual types of labor. It is unclear which particular aspect of work, social disadvantage (e.g., poor medical care), lifestyle, attitudes, or behavior influences this “social class” finding.

Back pain does have a greater impact on people in heavy manual labor jobs. They are more likely to stay off work and stay off longer than “clerical” laborers. This may be a reflection of the effect of their back pain (i.e., patient cannot lift the heavy loads required at work) or may reflect the medical advice given to them by their physicians (stay off work because of the possibility of aggravating the back pain with resumption of heavy labor).

The examiner should evaluate and rule out potential emergent causes of LBP during history and physical examination. Careful history and review of systems may detect nonmusculoskeletal origin of LBP. Our approach to the work-up of LBP is to first rule out emergent or nonmusculoskeletal causes of LBP. Once this is done, the appropriate examinations and tests are performed to confirm or rule out mechanical, nerve root, tumor, infectious, traumatic, systemic, or inflammatory etiology.

Predictors of Return-to-Work Status of Patients with Back Pain (Chronicity)

Cats-Barril and Frymoyer (1991) followed 250 patients to evaluate which of numerous factors best predicted who was still off work (no return to work) after 6 months. They found the best predictors, in order of decreasing accuracy, were

  1. Job characteristics: work history, occupation, job satisfaction, satisfaction with policies and benefits.
  2. Patient beliefs about whether back pain was compensable, party at fault, and legal involvement (social factors).
  3. Past hospitalization for back pain.
  4. Educational level.

Workplace and social factors were by far the most powerful influences on chronicity (84% accurate in predicting who will be chronically disabled). These were more predictive than type of injury, health behavior, or other factors.

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About Low Back Pain

in Guildelines for Orthopedic Rehabilitation of Back Pain, Orthopedic Rehabilitation for Back Pain

This entry is part 1 of 9 in the series Low Back Pain

Acute Mechanical Low Back Pain

The pain is “mechanical”—that is, it varies with physical activity (e.g., prolonged sitting, bending forward) and with time. This pain is located in the lumbosacral region, buttocks, and thighs, with no radiation to foot or toes.

Sciatica (Nerve Root Pain)

The term nerve root pain is preferable to the use of “sciatica” because it more accurately describes the pathologic origin. Nerve root pain may arise from disc herniation, spinal stenosis, or postoperative scarring. Nerve root pain radiates down one leg in a dermatomal pattern.

The leg pain (unilateral) is described by the patient as worse than the back pain. Numbness and paresthesia (if present) are found in the same nerve root distribution. Straight-leg raise (SLR) testing reproduces the leg pain. Motor, sensory, or reflex changes are classically limited to a single nerve root.
Thus, the term “sciatica,” or nerve root pain, is used to describe leg pain that predominates in the distribution of a lumbosacral nerve root, with or without neurologic deficit.

Disc Herniation

Disc herniation describes the protrusion of the gelatinous material of the disc (nucleus pulposus) through the annulus fibrosis (Figs. 9–1 and 9–2).

Several studies have shown gradual resorption and disappearance of herniated discs on serial MRIs without surgical intervention. The larger disc herniations were found to have had more resorption. This favorable natural history shows why up to 50% of patients with confirmed, painful herniated discs recover without surgery within 1 to 6 months.

Incidence of Low Back Pain

Mechanical LBP is very common, affecting between 70 and 85% of American adults at some point during their lives. An estimated 1.3 billion days a year are lost from work in the United States because of LBP. Back pain complaints are second only to upper respiratory conditions as a cause of work absenteeism. Back pain is also the most common cause of disability in patients younger than 40 years.

In 90% of patients, LBP resolves within 6 weeks (self-limited). In another 5% of patients, the pain resolves by 12 weeks after initiation. Less than 1% of back pain is due to “serious” spinal disease (e.g., tumor, infection). Less than 1% of back pain stems from inflammatory disease (rheumatologic work-up and treatment required). Less than 5% of back pain is true nerve root pain. Most patients with LBP have one or more of four symptoms:

  1. Back pain.
  2. Leg pain.
  3. Neurologic symptoms.
  4. Spinal deformity.

False-positive Radiographic Studies in Low Back Pain Evaluation

Diagnostic triage of back pain should be based primarily on an accurate, focused clinical assessment (history and physical examination) rather than the growing trend of cursory examination and overreliance on imaging techniques. Asymptomatic patients with no back pain have been found to have a high incidence of “positive” MRI or CT findings. Jensen and coworkers (1994) found that 64% of asymptomatic individuals who underwent an MRI had “abnormal”-appearing lumbar discs at some level. Overreliance on the “shotgun approach” of diagnosis with a cursory examination and “knee-reflex” MRI imaging will often obtain an incorrect diagnosis.

Because of the high incidence of false-positive results on MRI (e.g., MRI reading a right-sided L2–3 disc “herniation” in a patient with mechanical LBP only), the physician must correctly correlate the clinical symptoms (right leg L5 sensory and motor changes) with the MRI findings (right herniated disc at the L4–5 level).

“Abnormalities” seen on MRI or CT scan (e.g., age-related disc changes) often are not the origin for the patient’s back pain (i.e., these tests are highly sensitive, but not specific). The crucial part of accurate diagnosis is the physician’s clinical findings and their correlation with imaging findings.

We recommend that the primary care physician allow the “back specialist” to order the MRI, CT, or myelogram because different radiologic studies are employed for different suspected clinical diagnosis (e.g., spinal stenosis versus disc space infection versus herniated disc).

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Morton’s Neuroma (Interdigital Neuroma)

in Guildelines for Orthopedic Rehabilitation of Toe Injuries, Orthopedic Rehabilitation for Ankle and Foot Injuries

This entry is part 1 of 1 in the series Morton's Neuroma

Presentation

The most common presentation of an interdigital (Morton’s) neuroma is pain located between the third and the fourth metatarsal heads (in the third interspace) (Fig. 5–79) that radiates into the third and fourth toes. Patients often describe this as a burning pain that intermittently “moves around.” Usually, the pain is exacerbated by tight-fitting and/or high-heeled shoes or increased activity on the foot. The pain is often relieved by removing the shoe and rubbing the forefoot. Occasionally, these symptoms occur in the second interspace with radiation into the second and third toes. Seldom do neuromas occur in both interspaces simultaneously.

Table 5–11 presents a list of the preoperative symptoms given by patients (percentage) with an interdigital neuroma in Mann’s series (1997).

Anatomy and Pathophysiology

The “classic” Morton neuroma is a lesion of the common digital nerve that supplies the third and fourth toes (see Fig. 5–79). This is not a true neuroma, but rather an irritated perineural fibrosis where the nerve passes plantar to the transverse metatarsal ligament (Fig. 5–80).

It has been speculated that because the common digital nerve to the third interspace has branches from the medial and lateral plantar nerves (and thus increased thickness) that this accounts for the third interspace being the one most commonly involved. The occasional involvement of the second interspace may be a result of anatomic variation in the distribution of the common digital nerves.

The incidence of interdigital neuromas is 8 to 10 times more common in females.

The mechanism is probably chronic hyperextension of the MTP joints (in high heels) with tethering and irritation of the nerve across the transverse metatarsal ligament. This results in an entrapment neuropathy.

Diagnosis

The diagnosis of a Morton neuroma is clinical. There are no useful radiographic or electrodiagnostic tests. Serial examinations may be necessary to establish the correct diagnosis.

Examination

Direct palpation and palpation with a stripping motion (Fig. 5–81) of the interspace will usually reproduce the patient’s pain. This maneuver, called “Mulder’s sign,” often reproduces a clicking or popping sensation and pain in the third (or second) interspace. The examiner places the index finger and thumb proximal to the metatarsal heads in the interspace, and while pushing firmly into the interspace, “strips” distally to the end of the interspace, often feeling a click or pop that elicits pain (Mulder’s click).

Widening of the involved (third and fourth) toes may be noted on occasion as a result of the neuroma mass in the interspace. Subjective numbness of the involved toes is often noted, but sensory examination may reveal partial, complete, or no sensory deficit in the nerve’s distribution (see Fig. 5–79).

The patient with a Morton neuroma does not have pain over the metatarsal heads.

Occasionally, the examination will be positive only after a vigorous workout or tight shoewear. Often, the patient’s physical examination is inconclusive and requires several serial examinations and a ruling out of related pathology.

Differential Diagnosis

Morton’s neuroma may be mimicked by a number of other conditions. The following differential diagnoses should be considered to rule out an incorrect diagnosis of a Morton neuroma.

  1. Neurogenic pain, tingling, or numbness
  2. Peripheral neuropathy typically has more global numbness (entire foot or glove and stocking rather than in the interspace and its two toes) and is numb (not painful) unless early in the onset of neuropathy.
    • Degenerative disc disease often has accompanying motor, sensory, and reflex changes rather than numbness in a single interspace and its corresponding two toes.
    • Tarsal tunnel syndrome has a positive Tinel sign over the tarsal tunnel (medial ankle) and numbness limited to the plantar aspect of the foot (no dorsal foot numbness) (Figs. 5–82 and 5–83).
    • Lesions of the medial or lateral plantar nerves (see above).
  3. MTP joint pathology
    • Synovitis of the lesser MTP joint(s) from rheumatoid arthritis or nonspecific synovitis has tenderness over the metatarsal head or MTP joint rather than the interspace (see Fig. 5–55).
    • Fat pad atrophy or degeneration of the plantar fat pad or capsule has tenderness over the metatarsal head or MTP joint rather than the interspace.
    • Subluxation or dislocation of the lesser MTP joints has tenderness over the metatarsal head or MTP joint rather than the interspace.
    • Arthritis of the MTP joint has tenderness over the metatarsal head or MTP joint rather than the interspace.
  4. Plantar foot lesions
    • Synovial cysts is usually a tender mass but no numbness or tingling.
    • Soft tissue tumors of the interspace: ganglion, synovial cyst, lipoma, soft tissue neoplasm; usually a tender mass but no numbness or tingling.
    • Abscess. Plantar abscess foot. Usually, a tender mass but no numbness or tingling.

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Classification of Hallux Rigidus

in Guildelines for Orthopedic Rehabilitation of Toe Injuries, Orthopedic Rehabilitation for Ankle and Foot Injuries

This entry is part 2 of 2 in the series Hallux Rigidis

Mark M. Casillas, MD and Margaret Jacobs, PT

A useful classification system grades clinical and radiographic findings from mild to end stage (Table 5–6).

Diagnosis

Clinical Examination

Patients with hallux rigidus complain of dorsal pain, swelling, and stiffness localized to the hallux MTP joint. The sitting examination may reveal decreased ROM in dorsiflexion and, to a lesser degree, in plantar flexion. The ROM becomes more and more painful as the condition advances. Forced dorsiflexion reveals an abrupt dorsal bony block associated with pain. Also, forced plantar flexion produces pain as the dorsal capsule and the extensor hallucis longus tendon are stretched across the dorsal osteophyte. The dorsal osteophyte is easily palpable and typically exquisitely tender.

Radiographic Evaluation

Standard radiographic evaluation includes AP and lateral views of the weight-bearing foot (Fig. 5–64). Bone scanning, CT, and MRI are capable of demonstrating the condition, but these are not part of a routine work-up.

The differential diagnosis of hallux rigidius is shown in Table 5–7.

Treatment

The treatment of hallux rigidus is symptom-based. Acute exacerbations are treated with the RICE (rest, ice, compression, and elevation) method followed by a gentle ROM program and protected weight-bearing. The chronic condition is treated with a ROM program and protected weight-bearing. The hallux MTP joint is supported by shoe modifications (e.g., rocker bottom sole), a rigid shoe insert (Fig. 5–65), a stiff-soled shoe, or various taping methods that resist forced dorsiflexion (Fig. 5–66). A soft upper and deep toe box reduce pressure over the dorsal osteophyte. The joint is also protected by reducing activity levels, increasing rest intervals and duration, and avoiding excessively firm play surfaces. Occasionally, a patient with excessive pronation will benefit from an antipronation orthotic. NSAIDs and cold therapy are used to reduce swelling and inflammation. Occasionally, corticosteroid injection to the MTP joint is used as an adjunctive therapy.

Operative treatment is indicated for symptoms that fail to respond to a reasonable period of well-supervised conservative management (Fig. 5–67). Hallux MTP débridement and exostectomy are standard treatment for hallux rigidus. Ideally, the intraoperative and postoperative passive ROM approaches 90 degrees of dorsiflexion. If the arthrosis is extensive and this ROM not obtainable, a dorsiflexion osteotomy may be added to the surgical repair. The osteotomy is designed to place the functional ROM of the hallux within the newly established pain-free arc of motion. Patients with severe findings must be warned that outcomes become less predictable with advanced stages. CT images are useful in discriminating between severe hallux rigidus and frank degenerative joint disease. A hallux arthrodesis (fusion) is a more predictable reconstruction method for the most advanced cases of hallux rigidus. Pain relief is provided at the expense of permanent loss of joint motion.

Authors’ Recommended Treatment (Figure 5–68)

The acutely swollen and painful hallux rigidus is treated with the RICE method for several days. For chronic conditions, a stiff-soled shoe with a soft upper is prescribed along with a rigid low-profile carbon insert. We often rocker-bottom the shoe. NSAIDs and ice are used as adjunct to reduce inflammation. Adequate rest and recovery are scheduled with increasing frequency and duration. If symptoms persist, or if the patient presents with moderate to severe findings, a hallux rigidus repair is considered. Adequate débridement and soft tissue release are done to achieve 90 degrees of intraoperative dorsiflexion. If the joint is globally affected (hallux arthrosis), a hallux arthrodesis is performed.

Nonoperative Rehabilitative Treatment of Hallux Rigidus

Occasionally, hallus rigidus is associated with a synovitis that is improved with nonoperative treatment. Fundamental to the protocol is the prevention of recurrent injury by limiting dorsiflexion of the hallux MTP with appropriate shoewear, rigid shoe inserts, or taping. Taping (by the trainer) is useful in athletic events, but is limited by time-related failure and the poor results with self-application. Off-the-shelf devices are readily available, and custom devices can be used for difficult sizes or specialty shoewear. The phases of rehabilitation are variable in length and depend completely on the reestablishment of ROM and resolution of pain. Flexibility is emphasized throughout the protocol.

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The Treatment of Hallux Rigidis

in Guildelines for Orthopedic Rehabilitation of Toe Injuries, Orthopedic Rehabilitation for Ankle and Foot Injuries

This entry is part 1 of 2 in the series Hallux Rigidis

Mark M. Casillas, MD and Margaret Jacobs, PT

Clinical Background

The term hallux rigidus describes a limited arthrosis of the first MTP joint. The first MTP joint and the great toe (hallux) provide significant weight transfer from the foot to the ground as well as active push-off. An intact first MTP joint implies a complete and pain-free ROM, and full intrinsic and extrinsic motor strength.

The first MTP joint ROM is variable. The neutral position is described by 0 (or 180) degrees angulation between a line through the first metatarsal and a line through the hallux (Fig. 5–61). Dorsiflexion, the ROM above the neutral position, varies between 60 and 100 degrees (Fig. 5–62A). Plantar flexion, the ROM below the neutral position, varies between 10 and 40 degrees (see Fig. 5–62B). The ROM is noncrepitant and painfree in the uninjured joint.

Two sesamoid bones (the medial, or tibial, sesamoid and the lateral, or fibular, sesamoid) provide mechanical advantage to the intrinsic plantar flexors by increasing the distance between the empirical center of the joint and the respective tendons.

Hallux rigidus is an arthritic condition limited to the dorsal aspect of the first MTP joint. Also known as a dorsal bunion or hallux limitus, the condition is most commonly idiopathic (but may be associated with posttraumatic OCD of the metatarsal head) and is characterized by an extensive dorsal osteophyte and dorsal third cartilage damage and loss. An associated synovitis may further aggravate the limited and painful ROM.

A foot with increased first ray ROM and increased pronation may be predisposed to the condition. Excessive flexibility of the shoe forefoot increases the potential for hyperdorsiflexion of the hallux MTP joint (Fig. 5–63). For this reason, this type of shoewear should be avoided.

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Radiographic Evaluation of Metarsalgia

in Guildelines for Orthopedic Rehabilitation of Toe Injuries, Orthopedic Rehabilitation for Ankle and Foot Injuries

This entry is part 3 of 3 in the series Metarsalgia

Radiographic Evaluation

Radiographs are important to define forefoot deformities and identify neoplasms, fractures, dislocations, and arthritic joints that may contribute to pain in the metatarsal area. The relative lengths of adjacent metatarsals should be compared, because discrepancies in metatarsal length can cause concentration of stress. Patients with significant shortening of the first metatarsal after a bunion operation sometimes develop pain under the second metatarsal (transfer metatarsalgia). When combined with lead markers placed on the IPK skin, the radiographs help to identify prominent condyles or sesamoids under the metatarsal head that cause plantar keratoses. Isolated second metatarsal pain may be caused by Freiberg’s infraction (Fig. 5–59).

Other imaging techniques, such as MRI and CT, are helpful only when specifically indicated and are not a routine part of the evaluation of metatarsalgia.

Although exercise and stretching offer little relief for most patients with metatarsalgia, pedorthic management can figure prominently in the initial treatment. For most patients who present with inappropriate (high heels) or tight shoewear, a discussion of the fit of the shoes should focus on the shape and room in the toe box for the toes. In addition, shoes with laces, stiff soles, and low heels help disperse and reduce the pressure on the forefoot. Occasionally, patients have severe fixed forefoot deformities that require prescription extradepth shoewear.

Full-length PPT and Plastizote or silicone insoles are very helpful in dispersing the pressure on tender areas in the forefoot. If this is unsuccessful, more sophisticated orthotic devices may be necessary. Soft metatarsal pads made of felt or silicone (Fig. 5–60A) by themselves or added to a Spenco insert can be used to relieve pressure. Correct placement of the pad is crucial. The crest of the pad should be approximately 1 cm proximal to the tender area (see Fig. 5–60B). To help position the insert, lipstick or magic marker can be applied to the tender area on the foot and the patient asked to step on the insole, making apparent where to place the pad (1 cm proximal). A custom-molded accomodative insert can also be fabricated with a well-excavated well beneath the tender metatarsal to unload it (relief well).

Metatarsal bars can be built onto the shoe to unload the forefoot, but these tend to wear out quickly and encounter resistance from patients for cosmetic reasons. A rocker-bottom sole, along with a stiffener placed into the sole, helps reduce toe motion and disperse pressure away from the metatarsal heads.

Steroid injections combined with 1% lidocaine have a definite, but limited, role in diagnosing and treating pain due to synovitis or irritation of a Morton’s neuroma from intermetatarsal bursitis.

Surgery is offered to patients in whom nonoperative treatment fails to relieve pain.

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Diagnosing Metarsalgia

in Guildelines for Orthopedic Rehabilitation of Toe Injuries, Orthopedic Rehabilitation for Ankle and Foot Injuries

This entry is part 2 of 3 in the series Metarsalgia

History and Physical Examination

A careful history and physical examination are the most important tools for differentiating the etiologies of metatarsalgia. This should begin with an evaluation of suitability of footwear in relation to the size of the foot. Measure the patient’s true shoe size and width, and then see what size shoe he or she wears into the office. A complete evaluation of the foot and ankle can disclose problems in other areas of the foot that may make the forefoot painful. For instance, medial foot disorders can cause lateral forefoot pain because of lateral weight shifting. Weakness in the anterior tibial tendon can cause toe deformity through adaptive overuse of the extrinsic toe extensors, resulting in forefoot pain.

The plantar skin should be inspected for plantar keratoses. Paring these lesions is important, not only to decrease pressure but also to differentiate them from plantar warts. Plantar warts, unlike plantar keratoses, contain vessels within the keratinized tissue that are easily seen open and bleeding after paring. The interdigital spaces should also be inspected for soft corns. Sensation should be tested and pulses palpated. Careful palpation of the metatarsal heads and intermetatarsal spaces, localizing the exact area of tenderness, narrows the differential diagnosis.

Manual compression of the interspace (Mulder’s click) can elicit crepitus, tenderness, and radiating pain from a Morton’s neuroma (see Morton’s neuroma section). A drawer maneuver of the MTP joint (Fig. 5–58) can detect articular stability problems. It is done by applying dorsally directed pressure to the plantar base of the proximal phalanx while stabilizing the metatarsal with the opposite hand.

The contralateral toes as well as the other toes on the ipsilateral foot should be evaluated to establish a baseline degree of normal translation on MTP joint drawer testing for each patient. MTP joint tenderness, swelling, and bogginess usually signify synovitis of the MTP joint, whereas pain with a relative increase in translation during MTP drawer testing usually signifies joint instability.

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Background of Metarsalgia

in Guildelines for Orthopedic Rehabilitation of Toe Injuries, Orthopedic Rehabilitation for Ankle and Foot Injuries

This entry is part 1 of 3 in the series Metarsalgia

Metatarsalgia

Brett R. Fink, MD, and Mark S. Mizel, MD

Background

Metatarsalgia describes an assortment of conditions that cause plantar pain in the forefoot around the MTP joints.

Metatarsalgia is not, in itself, a diagnosis, but rather an anatomic description of where the patient is experiencing discomfort. Successful treatment of this condition hinges on identifying the underlying cause. A clear understanding of its etiologies and a systematic approach to examination are necessary to accomplish this. Metatarsalgia is best characterized by pain under the metatarsal heads exacerbated by weight-bearing.

The fatty cushion of the forefoot is a highly specialized tissue. Fibrous septae beneath the dermis compartmentalize the subcutaneous fat. When weight is applied, hydrostatic pressure builds within the compartments, dampening and dispersing forces on the plantar skin. This mechanism acts as a cushion, protecting the area from potentially damaging focal concentrations in pressure.

Inflammatory arthritis, trauma, or neuromuscular disorders can cause imbalances of flexion and extension forces around the small joints of the toes. Toe deformity is a consequence of this imbalance. Hyperextension at the MTP joint is a common component of these deformities and draws the fatty cushion of the forefoot distally and dorsally with the proximal phalanx (Fig. 5–53). When this occurs, the weight transferred through the metatarsal heads is applied to the thinner proximal skin without the intervening fatty cushion. Increases in local pressure result in a hyperkeratotic reaction of the plantar skin. This causes further increases in pressure, and eventually, a painful intractable plantar keratosis (IPK) forms (Fig. 5–54).

IPKs are often confused with plantar warts. Both cause hyperkerotic lesions of the plantar surface of the skin, which can be painful. However, plantar warts occur as a result of infection of the epidermis with papillomavirus. Whereas the treatment of IPKs is mechanical (shaving, cushioning, relief pads), the treatment of symptomatic plantar warts is directed toward eradicating the infected tissue. Care should be used to ensure that the sometimes-caustic plantar wart preparations do not cause scarring of the plantar skin, which can be more painful than the initial wart. IPKs, unlike plantar warts, are almost always found directly below a weight-bearing area of the foot (e.g., metatarsal head). Plantar warts bleed with a characteristic “punctate” fashion when shaved, with multiple punctate areas of bleeding.

Synovitis and instability (Fig. 5–55) of the MTP joints can also cause pain along the metatarsal heads. Although inflammatory arthritides can incite this, the etiology of the instability is commonly mechanical. Chronic hyperextension of the MTP joints (claw toes) and flexion at the interphalangeal (IP) joints can occur in an attempt to accommodate a shoe toe box that is too small (Fig. 5–56). Eventually, this attenuates the plantar plate and collateral ligaments, leading to instability and subluxation (Fig. 5–57). The toes can develop varus or valgus malalignment in relation because of this. Dorsal MTP joint dislocation is sometimes seen in severe cases.

Extra-articular cause of pain in the metatarsal region should also be considered. Morton’s neuroma is a hypertrophy and subsequent irritation of the common interdigital nerve as it passes between the metatarsal heads. Inflammation of the intermetatarsal bursa and impingement by the intermetatarsal ligament are thought to contribute to the development of this condition. It most commonly affects the nerve of the third web space. It is often mistaken for synovitis (see Morton’s neuroma section) and can coexist with it. It rarely involves more than one common digital nerve. The tenderness from a stress fracture of the metatarsal is typically in the metatarsal neck or shaft. These can be invisible on radiographs for several weeks after onset. Finally, pain from a herniated lumbar disc, tarsal tunnel, or other neurologic problem can be appreciated in the forefoot and is often mistaken for pain from a disorder originating in the foot.

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Signs and Treatment of Achilles Tendon Rupture

in Guildelines for Orthopedic Rehabilitation of Foot Injuries, Orthopedic Rehabilitation for Ankle and Foot Injuries

This entry is part 1 of 1 in the series Achilles Tendon Rupture

Achilles Tendon Rupture

Background

Complete ruptures tend to occur in middle-aged patients and those without preexisting complaints. Partial ruptures occur in well-trained athletes and involve the lateral aspect of the tendon. Acute ruptures commonly result from acute eccentric overload on a dorsiflexed ankle that has chronic tendinosis. Patients should be questioned about previous steroid injection and fluoroquinolones (possible association with tendon weakening and rupture).

Clinical Signs and Symptoms

Sharp pain and a pop heard at the time of complete rupture are commonly reported. Patients often describe a sensation of being kicked in the Achilles tendon. Most have an immediate inability to bear weight or return to activity. A palpable defect may be present in the tendon initially.

Partial rupture is associated with an acutely tender, localized swelling that occasionally involves an area of nodularity.
The Thompson test (see Fig. 5–39) is positive with complete Achilles tendon rupture. A positive test occurs when squeezing the calf fails to plantar flex the foot because of a lack of continuity of the tendon (rupture).

Thompson Test
The patient is placed prone, with both feet extended off the end of the table. Both calf muscles are squeezed by the examiner. If the tendon is intact, the foot will plantar flex when the calf is squeezed. If the tendon is ruptured, normal plantar flexion will not occur (a positive Thompson test).

In some patients, an accurate diagnosis of a complete rupture is difficult through physical examination alone. The tendon defect can be disguised by a large hematoma. A false-negative Thompson test can occur because of plantar flexion of the ankle caused by extrinsic foot flexors when the accessory ankle flexors are squeezed together with the contents at the superficial posterior leg compartment. It is important to critically compare the test with results in the normal side.

Partial ruptures are also difficult to accurately diagnose, and MRI should be used to confirm the diagnosis.

Treatment of Acute Rupture of the Achilles Tendon
Both conservative and operative treatments are commonly used to restore length and tension to the tendon to optimize strength and function. Both methods are reasonable, and treatment should be individualized based on operative candidacy. High-level and competitive athletes usually undergo primary repair. Operative repair is associated with lower re-rupture rates, quicker return to full activity, and a theoretically higher level of function. However, the difference in outcomes between conservative and operative treatment is variable. The main surgical risk is wound breakdown. Generally, surgery should be avoided in patients with poor wound healing potential (diabetics); smoking is a relative contraindication.

Regardless of definitive treatment, initial treatment is a short-leg splint in a comfortable position of plantar flexion, ice, elevation, and crutch ambulation.

Nonoperative treatment of complete Achilles tendon ruptures in a 20-degree plantar flexed cast is usually reserved for chronically ill patients, poor operative candidates, elderly patients, and low-demand patients. The re-rupture rate is much higher in patients treated nonoperatively (with a plantar flexed cast for 8 weeks of non-weight-bearing) than in those treated operatively. A review of multiple studies found an average re-rupture rate of 17.5% in nonoperative patients compared with 1.2% in operatively treated patients. However, major and minor complications were more frequent with operative treatment.

Nonoperative Treatment of Acute Achilles Tendon Rupture

Nonoperative treatment for poor operative candidates requires immobilization to allow hematoma consolidation. Ultrasound is used to confirm that tendon end apposition occurs with 20 degrees or less of plantar flexion. Conservative treatment is best for small partial ruptures. Surgical repair is indicated if a diastasis or gap remains with the leg placed in 20 degrees of plantar flexion.

A 20-degree non–weight-bearing plantar flexed short-leg cast (preference) or a removable boot (not to be removed by the patient) with an elevated heel is used for 8 weeks. The patient remains non–weight-bearing in the cast for 8 weeks.

At 6 to 8 weeks, plantar flexion of the cast is slowly decreased (most easily done in a commercial cam boot with adjustable ankle angle setting). An initial heel lift of 2 to 2.5 cm should be worn for 1 month when progressive weight-bearing is begun. Gentle non–weight-bearing active ROM exercises and gentle passive stretching with rubber tubing are begun. At 10 to 12 weeks, the heel lift is decreased to 1 cm and, over the next month, is progressively decreased so that the patient is walking without a heel lift by 3 months.

Progressive resistance exercises for the calf muscles should be started between 8 and 10 weeks. Running may be resumed after 4 to 6 months if strength is 70% of the uninvolved leg. Maximal plantar flexion power may not return for 12 months or more.

Operative Treatment for Complete Achilles Tendon Rupture

Operative treatment is generally preferred for young, athletic, and active patients. The incision and approach are the same as for paratenonitis and tendi-nosis. A medial approach is used to expose the tendon ends, and a modified Bunnell technique is used to repair the rupture.

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