Kamis, 06 Desember 2007

Brachial Plexus Injury


Background

Peripheral nerve injuries are not common in noncontact sports. However, in contact and collision sports like football and rugby, brachial plexus injuries occur often. The greater incidence of brachial plexus injuries has been suggested to be the result of direct trauma from participation in contact sports.

The result of trauma to the brachial plexus can lead to the cervical "stinger" or "burner" syndrome, which is classically characterized by unilateral weakness and a burning sensation that radiates down an upper extremity. The condition may last less than a minute or as long as 2 weeks, with the latter duration described as a chronic burner syndrome.

Frequency

United States

Brachial plexus injuries are the most common peripheral nerve injuries seen in athletes. True rate of brachial plexus injuries is difficult to determine due to significant underreporting. Many stingers last briefly and players do not seek medical attention. Clancy et al reported that 33 of 67 college football players (49%) sustained at least 1 burner during collegiate play. Sallis et al surveyed Division III college football players and reported that 65% experienced brachial plexus injuries. In addition, Sallis reported an 87% recurrence rate in these individuals. Meeuwisse reported that 7.2% of all football injuries were brachial plexus injuries.

International

True measure of international occurrence of brachial plexus injuries is undetermined due to significant underreporting in athletes and lack of studies in rugby and hockey involving brachial plexus injuries.

Functional Anatomy

Injuries to the cervical spine are common. The common level of injury is at C5-C6. Damage to other areas of the spinal area can lead to an array of motor and sensory deficits. The following is a list of cervical nerve roots with the associated area of potential motor and sensory deficits:

  • C4 - Trapezius; shoulder; top of shoulders
  • C5 - Deltoid, rotator cuff; shoulder abduction; lateral upper arm or distal radius
  • C6 - Biceps, rotator cuff; elbow flexion; lateral forearm and thumb
  • C7 - Triceps; elbow extension; index and middle finger tips
  • C8 - Extension of fingers; distal thumb; fourth and fifth fingers

Sport Specific Biomechanics

The following 3 mechanisms are common to brachial plexus injury:

  1. Traction caused by lateral flexion of the neck away from the involved side (similar to the mechanism in birth trauma)
  1. Direct impact to the Erb point causing compression to the brachial plexus (often associated with poor-fitting shoulder pads)
  1. Nerve compression caused by neck hyperextension and ipsilateral rotation (The neural foramen narrows in this mechanism.)

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

At onset of injury, nonsteroidal anti-inflammatory drugs (NSAIDs), early mobilization, and moist heat packs are the favorable methods of treatment for acute injuries. In the subacute phase, a gradual progression from ROM activity to cervical and shoulder muscle strengthening is recommended.

Medical Issues/Complications

If symptoms persist (eg, persistent weakness, chronic neurapraxia) regardless of therapy, further consideration for additional imaging and referral should be undertaken.

Surgical Intervention

Surgical intervention is rarely needed, is injury-specific, and should be directed by a neurosurgical or orthopedic spine surgeon.

Consultations

Neurosurgery spine/orthopedic spine

Other Treatment

Manipulation is not recommended as a first line intervention, but it may be a helpful adjunct after full medical assessment has been completed.

Recovery Phase

Rehabilitation Program

Physical Therapy

In the recovery phase, cervical muscle strengthening and conditioning should be continued. Strength training programs are used to fully recover the strength that the athlete had prior to the injury. Training should be focused on muscles supporting the injured brachial plexus nerve, such as the shoulders and the surrounding cervical spine region. The neck also should be protected (eg, use of cervical neck rolls, cervical pillows) until strength is regained.

Consultations

If needed, continue follow-up care with a neurologist, and/or spine specialist.

Maintenance Phase

Rehabilitation Program

Physical Therapy

Continued maintenance of cervical muscle strength, conditioning, and protection is recommended.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Opiate-Narcotics

Analgesia is important to obtain in the setting of brachial plexus nerve injuries. This can be accomplished by use of anti-inflammatory and/or opiate-narcotic medications. Analgesia may facilitate further assessment of the athlete, as well as their willingness to participate in therapy sessions.

Drug NameHydrocodone and acetaminophen (Lortab, Norcet, Vicodin)
DescriptionDrug combination indicated for moderate to severe pain.
Adult Dose1-2 tab PO q4-6h prn
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; high altitude cerebral edema (HACE) or elevated intracranial pressure (ICP)
InteractionsCoadministration with phenothiazines may decrease analgesic effects; toxicity increases with CNS depressants or tricyclic antidepressants
PregnancyD - Unsafe in pregnancy
PrecautionsTablets contain metabisulfite which may cause hypersensitivity; caution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction; may cause drowsiness (Do not drive heavy machinery while taking medication)

Drug NameHydrocodone and ibuprofen (Vicoprofen)
DescriptionDrug combination indicated for short-term (less than 10 d) relief of moderate to severe acute pain
Adult Dose1-2 tab PO q4-6h prn pain; not to exceed 5 tab/d
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; 3rd trimester of pregnancy
InteractionsCoadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsCaution in impaired renal function, peptic ulcer disease, impaired thyroid function, asthma, hypertension, edema, heart failure, increased intracranial pressure, and erosive gastritis; duration of action may increase in elderly patients

Drug NameOxycodone and acetaminophen (Percocet, Roxicet, Roxilox, Tylox)
DescriptionDrug combination indicated for the relief of moderate to severe pain.
Adult Dose1-2 tab or cap PO q4-6h prn pain
Pediatric Dose0.05-0.15 mg/kg/dose oxycodone PO; not to exceed 5 mg/dose of oxycodone q4-6h prn
ContraindicationsDocumented hypersensitivity
InteractionsPhenothiazines may decrease analgesic effects of this medication; toxicity increases with coadministration of either CNS depressants or tricyclic antidepressants
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsDuration of action may increase in elderly patients; be aware of total daily dose of acetaminophen patient is receiving; do not exceed 4,000 mg/d of acetaminophen; higher doses may cause liver toxicity

Drug Category: Nonsteroidal anti-inflammatory drugs (NSAIDs)

Have analgesic and antiinflammatory activities. Their mechanism of action is not known, but may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Drug NameIbuprofen (Motrin, Ibuprin)
DescriptionDOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Adult Dose600-800 mg PO tid prn
Pediatric Dose10 mg/kg/dose PO q6h
ContraindicationsDocumented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
InteractionsCoadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsCategory D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Drug NameKetoprofen (Oruvail, Orudis, Actron)
DescriptionFor relief of mild to moderate pain and inflammation. Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.
Adult Dose25-50 mg PO q6-8h prn; not to exceed 300 mg/d
Pediatric Dose3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
ContraindicationsDocumented hypersensitivity
InteractionsCoadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsCategory D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Drug NameNaproxen (Naprosyn, Naprelan, Anaprox)
DescriptionFor relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.
Adult Dose500 mg PO, followed by 250 mg q6-8h; not to exceed 1.25 g/d
Pediatric Dose<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
ContraindicationsDocumented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
InteractionsCoadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsCategory D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Bicycle Seat Neuropathy

Background

Bicycle seat neuropathy is one of the more common injuries reported by cyclists (Weiss, 1994). The injuries and symptoms are due to the cyclist supporting his or her body weight on a narrow seat and are believed to be related to either vascular or neurologic injury to the pudendal nerve (Oberpenning, 1994).

Frequency

United States

A wide frequency range has been reported for bicycle seat neuropathy, but it is believed to be underreported. The medical literature contains several case reports of reversible neuropathy (Silbert, 1991; Oberpenning, 1994) and several retrospective studies surveying participants in long-distance cycling races and tours (Kuland, 1978; Weiss, 1985; Andersen, 1997).

Andersen and Bovim surveyed 260 cyclists participating in a long-distance bike tour that was 540 km in length. Of responding males, 22% (35 of 160) reported symptoms of either numbness or pain in the pudendal area. Thirty-three males reported penile numbness, with 10 male cyclists reporting symptoms that lasted longer than one week. Twenty-one males (13%) reported symptoms of impotence, 11 of whom experienced symptoms for longer than one week and 3 of whom reported impotence lasting longer than one month.

Kuland and Brubaker reported that during the 1976 Bikecentennial tour, there was a 7% incidence of pudendal and/or penile numbness, but this study only surveyed 89 out of 1200 participating cyclists.

Weiss studied symptoms of cyclists participating in a 500-mile bicycle tour. Of the participating cyclists, 45% reported at least mild and transient perineal numbness. Ten percent reported the symptoms as severe, and 2% of the cyclists had to temporarily stop riding. Perineal numbness also has been documented in women cyclists. LaSalle et al surveyed 282 female members of a Dallas cycling club. In this group, 34% of the women reported perineal numbness.

Sport Specific Biomechanics

The cause of bicycle seat neuropathy has been attributed to several different ischemic events. Amarenco and Oberpenning hypothesized that compression of the pudendal nerve as it passes through the Alcock canal causes the condition. The Alcock canal is enclosed laterally by the ischial bone and medially by the fascial layer of the obturator internus muscle. The pudendal nerve exits the canal ventrally, below the symphysis pubis, and innervates the genital and perineal regions.

Oberpenning et al postulated that long-distance cycling results in the indirect transmission of pressure onto the perineal nerve within the Alcock canal. Weiss and Bond separately proposed that bicycle seat neuropathy is due to temporary and transient ischemic injury to the dorsal branch of the pudendal nerve secondary to compression of the nerve between the bicycle seat and the symphysis pubis. Weiss also theorized that the genital branch of the genital-femoral nerve could be involved in cases in which scrotal paresthesia is reported.

Bicycle seat design (eg, shape) may be the major extrinsic factor for the development of bicycle seat neuropathy. Results of computer modelling reported by Spears et al in 2003 have shown that wider bicycle seats that support the ischial tuberosities decrease pressure on the perineal area. Other studies have also demonstrated the effect bicycle seat design has on penile blood flow (Jeong, 2002) and penile oxygen pressure (Schwarzer, 2002).

Treatment

Acute Phase

Rehabilitation Program

Recreational Therapy

Recreational therapy should include evaluation of the rider's position on the bicycle and could include changing the seat height and tilt position.

Medical Issues/Complications

Medical issues and complications include continued injury or insult to the area, resulting in continuation of the neuropathy and long-term sequelae such as impotence. Reevaluate the patient after making changes to the bicycle or riding style or after decreasing the training volume to ensure that improvement in symptoms is occurring. Continued symptoms despite changes in the bicycle seat position and training volume may indicate a different source of the symptoms and should warrant reevaluation by the physician.

Consultations

Possible consultants include urology and neurology, based upon the clinical presentation.

Other Treatment

The mainstay of treatment is the adjustment of the bike seat and bike position, such as tilting the nose of the seat down or lowering the seat height to relieve pressure off of the perineum. Other recommendations include having the rider change the style of riding, eg, change positions more frequently or stop riding more frequently.

Newer bicycle seats with a split nose or a center cutout also may help reduce the prevalence of neuropathy by limiting compression on the perineal area . A 2004 study by Lowe et al compared pressure measurements in the perineal area of cyclists on these different bicycle seats and found that some of the newer seats reduced perineal pressure by approximately 50%.

Medication

No medical therapy is recommended.

Bicipital Tendonitis

Background

Biceps tendonitis is an inflammatory process of the long head tendon and is a common cause of shoulder pain due to its position and function. The tendon is exposed on the anterior shoulder as it passes through the humeral bicipital groove and inserts on the superior aspect of the labrum of the glenohumeral joint. Disorders can result from impingement or as an isolated inflammatory injury. Other causes are secondary to compensation to rotator cuff disorders, labral tears, and intra-articular pathology.

Frequency

United States

Biceps tendonitis is frequently diagnosed in association with rotator cuff disease as a component of the impingement syndrome or secondary to intra-articular pathology, such as labral tears.

Functional Anatomy

As its name implies, the biceps has 2 proximal heads with a common distal insertion into the radius. The long head of the biceps merges with the short head of the biceps to form the body of the biceps brachii muscle. This muscle is a powerful supinator and flexor of the forearm.

The long head tendon lies in the bicipital groove of the humerus between the greater and lesser tuberosities and angles 90° inward at the upper end of the groove, crossing the humeral head to insert at the upper edge of the glenoid labrum and supraglenoid tubercle. The long head biceps tendon helps stabilize the humeral head, especially during abduction and external rotation.

Sport Specific Biomechanics

Overhead athletes, most commonly baseball pitchers, tennis players, and swimmers, are prone to biceps tendonitis. Trauma may occur because of direct injury to the tendon as the arm is passed into excessive abduction and external rotation.

The athletic shoulder differs qualitatively from the biomechanics of daily life because of higher energies and repetitive motions involved in athletics. Sports requiring repetitive overhead motion may cause tendon breakdown with inadequate reparative time. Biceps tendonitis frequently occurs from overuse syndromes of the shoulder, which are fairly common in swimmers, gymnasts, racquet sport enthusiasts, and rowing/kayak athletes. This pattern of shoulder injury also can occur in the left shoulder of right-handed golfers. Many overuse injuries coexist with some degree of biceps tendonitis and rotator cuff tendonitis.

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

The initial goals of the acute phase of treatment are to reduce inflammation and swelling. Patients should restrict over-the-shoulder movements, reaching, and lifting. Apply ice for 10-15 minutes, 2-3 times per day for the first 48 hours. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, are used for 3-4 weeks to treat inflammation and pain. The degree of immobilization depends upon the degree of injury and discomfort. Most authors agree that prolonged immobilization tends to result in a stiff shoulder.

Physical therapy plays a minor role in the treatment of acute bicipital tendonitis; however, some authors recommend daily weighted pendulum stretch exercises for uncomplicated and mild cases of acute biceps tendonitis. Use of transcutaneous electrical nerve stimulation (TENS) has been reported with some success.

Phonophoresis and iontophoresis are examples of methods used to deliver steroids into inflamed tissue without injection. Phonophoresis uses ultrasound, while iontophoresis uses electrical repulsion to transport medicines through the skin. In order to deliver effective steroid concentration the target area should be superficial and serial application is necessary.

Medical Issues/Complications

Analgesic and steroid injections into the bicipital groove are not performed without risks. Use care to avoid direct injection into the long head biceps tendon itself because this can result in direct trauma and may lead to atrophy and/or rupture. Other complications from injections include postinjection infection and inflammatory reaction.

Radiographic imaging should be considered if no improvement occurs after treatment in order to exclude a possible missed diagnoses.

Consultations

Consider orthopedic consultation if symptoms persist longer than 2 months or if tendon rupture occurs.

Other Treatment

A local injection can be given in the bicipital groove. A combination of 2-3 mL of anesthetic with 1 mL of methylprednisolone (Depo-Medrol) typically is recommended 3-6 weeks after acute injury. A repeat injection can be performed 4 weeks later if symptoms have not decreased by 50%. Caution is indicated with additional injections or with patients older than 40 years because they are at an increased risk of tendon rupture from repetitive injections. Restrict lifting and overhead activities for 30 days after the injection.

Recovery Phase

Rehabilitation Program

Physical Therapy

The goal of the recovery phase is to achieve and maintain full and painless ROM. Weighted pendulum stretch exercises are combined with isometric toning. Exercises are recommended 3 times per week throughout the recovery phase. Passive stretching with ROM exercises removes residual shoulder stiffness. The uninvolved shoulder can be used as a standard comparison to achieve symmetric ROM.

Occupational Therapy

Interval tennis and baseball programs have been developed for highly competitive athletes. The patient progresses in a series of steps and stages, with the goal of returning safely to competition without reinjury. Progression is dependent upon gradual, painless increase in activity without excessive fatigue. While a rehabilitation program should improve strength and flexibility, adding an interval program can help restore normal joint arthrokinematics.

Medical Issues/Complications

Failure to recognize concomitant injuries could result in delayed healing and damage from inappropriate treatment. Physical therapy for shoulder injuries or a misdiagnosed injury may aggravate other conditions in the elbow and neck.

Consultations

Consider orthopedic consultation if symptoms persist longer than 2 months or if tendon rupture occurs.

Other Treatment (Injection, manipulation, etc.)

Weighted pendulum swings should begin with moist heat application to the shoulder, followed by therapy with 5- to 10-lb weights, which are held lightly in the hand. The shoulder muscle should be relaxed and the arm kept vertical and close to the body. The arm is allowed to swing back and forth, no greater than 1 inch in any direction. This exercise is not appropriate for patients with shoulder separation or strain, upper back strain, or neck strains.

Maintenance Phase

Rehabilitation Program

Physical Therapy

The maintenance phase concentrates on developing increased strength and endurance. This phase can begin as soon as discomfort is effectively controlled and should continue for at least 3 weeks after pain has resolved completely. When performing strengthening exercises, it is safer to start out with low tension, followed by a gradual increase in force, because flare-ups can occur.

Isotonic and isokinetic stretching continues as the patient is allowed limited participation in sports activity. Monitor the patient and adjust activity as progress allows. Conditioning and proper throwing techniques are important for certain athletes because improper mechanics may result in tissue fatigue and damage.

Surgical Intervention

Surgical intervention is not recommended if the patient is making slow and gradual improvement. Surgical treatment is only indicated after a 6-month trial of conservative care is unsuccessful. Although good results have been reported using arthroscopic decompression, acromioplasty with anterior acromionectomy is the standard surgical treatment. The biceps tendon generally is not tenodesed unless severe attritional wear or eminent rupture is found. No attempt is made to repair ruptures greater than 6 weeks old.

Tenodesis is not recommended when it is believed that the tendinitis is reversible. Specific indications for tenodesis of the biceps long head include the following:

  • Greater than 25% partial thickness tendon tear


  • Severe subluxation from the bicipital groove


  • Disruption of the associated bony or ligamentous anatomy of the groove itself


  • Tendon atrophy greater than 25%


  • Failure of surgical decompression

Growing evidence has shown a shift from routine tenodesis to a more individual approach, taking into consideration physiologic age, activity level, expectations, and specific combinations of shoulder pathology. While new repair techniques are under development, preservation of the biceps-labral complex is preferred over routine surgery.

Consultations

Consider orthopedic consultation if symptoms persist longer than 2 months or if tendon rupture occurs.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Nonsteroidal anti-inflammatory drugs (NSAIDs)

Anti-inflammatory and nonnarcotic medications that have analgesic and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions. Treatment of pain tends to be patient specific.

Drug NameIbuprofen (Ibuprin, Advil, Motrin)
DescriptionDOC for mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Adult Dose400-800 mg PO tid/qid
Pediatric Dose<12 years: Not indicated
>12 years: 20-40 mg/kg/d PO divided tid/qid
ContraindicationsDocumented hypersensitivity to ibuprofen, other NSAIDs, or aspirin; avoid in peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, and high risk of bleeding
InteractionsConcomitant use with anticoagulants may potentiate anticoagulant effects; effects of oral diabetic hypoglycemic agents may be potentiated with combination use with ibuprofen, leading to hypoglycemia; may decrease clearance and absorption of methotrexate, lithium, diuretics, and antihypotensives
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsConsidered to be a class D drug in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Drug Category: Local anesthetics

Block the generation of conduction impulses in the nerve, thereby preventing the transmission of pain.

Drug NameBupivacaine (Sensorcaine, Marcaine)
DescriptionAn amide-type local anesthetic that shares similar properties with other drugs in this classification, including lidocaine (Xylocaine). Has the advantage of a longer duration of anesthesia.
Administer smallest dose and concentration required to produce desired results. Dose varies with anesthetic procedure, area to be anesthetized, vascularity of the tissues, and individual tolerance.
Adult DoseLocal anesthesia: 5-10 mL (0.25% sol) 12.5-25 mg; not to exceed 2.5 g/kg
Pediatric Dose<12 years: Not recommended
>12 years: Administer as adults
ContraindicationsDocumented hypersensitivity
InteractionsMay enhance effects of CNS depressants; coadministration may increase toxicity of MAOIs, TCAs, beta-blockers, vasopressors, and phenothiazines; have antiarrhythmic effects, which may cause additive toxicity interactions with phenytoin, procainamide, propanolol, and quinidine
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsSystemic absorption produces effects on the cardiovascular and CNS; rate of absorption dependent upon the dose, rate of administration, and vascularity of the injection site; aspirate for blood prior to injection to avoid accidental intravenous administration; adverse reactions include restlessness, anxiety, dizziness, blurred vision, tremors, confusion, seizure, hypotension, palpitations, and syncope; consider reduced dose in patients with lowered hepatic clearance from disease or age

Drug Category: Glucocorticoids

Stimulate synthesis of enzymes that decrease inflammatory response and suppress the immune system.

Drug NameMethylprednisolone acetate (Depo-Medrol)
DescriptionMethylprednisolone is a potent intermediate acting glucocorticoid, which has no mineralocorticoid activity. A useful anti-inflammatory and immunosuppressant agent.
Adult Dose4-80 mg/d intra-articular, intrasynovial, intrabursal, intralesional, or soft tissue injection
Pediatric Dose140-835 mcg/kg/d intra-articular, intrasynovial, intrabursal, intralesional, or soft tissue injection
ContraindicationsDocumented hypersensitivity to ingredients of adrenocorticoid preparations; systemic fungal infections
InteractionsGlucocorticoids may decrease effects of PO anticoagulants, isoniazid, insulin, PO hypoglycemic agents, and salicylates
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsCaution in hypertension, diabetes mellitus, tuberculosis, psychiatric disorders, glaucoma, and gastric ulcers; glucocorticoids suppress the immune system, which may result in complications in patients receiving live vaccines and in patients with concomitant infectious disease

Atlantoaxial Injury and Dysfunction


Background

Disability and instability of the unique atlantoaxial joint result in controversies regarding the management of acute trauma and also the screening evaluation of particular at-risk individuals. The purposes of this article are to define atlantoaxial instability; describe the relatively rare symptomatic lesions with significant morbidity and mortality; and, finally, discuss the rationale for and against screening and restricting activities of at-risk individuals.

Definition

Atlantoaxial instability (AAI), also known as atlantoaxial subluxation, is radiologically identified increased mobility or laxity between the body of the first cervical vertebra (atlas) and the odontoid process of the second cervical vertebra (axis). Subluxation can be anterior, posterior, or lateral, and symptoms occur as a result of cervical cord impingement.

Epidemiology

Although traumatic lesions involving the atlantoaxial region are relatively rare, certain disease states and conditions present a higher theoretical risk of instability due to increased atlantoaxial joint laxity.

Surveys indicate 10-25% of patients with trisomy 21 have AAI. Two thirds of these cases are due to laxity of transverse ligament, whereas one third are due to abnormal odontoid development. Although this association has been depicted on radiographs, the clinical incidence of serious cervical spine injury is not increased in this population compared with other populations.

About 25% of patients with rheumatoid arthritis have atlantoaxial instability, which is thought to be due to chronic inflammation. Congenital skeletal dysplasias may cause resultant odontoid hypoplasia. Marfan syndrome may involve to ligamentous laxity, and acute inflammatory processes can affect the retropharyngeal, neck or pharyngeal spaces.

Frequency

United States

Approximately 15-25% of all patients with trisomy 21 and about 25% of patients with rheumatoid arthritis have atlantoaxial injury or dysfunction.

Functional Anatomy

The articulation of the odontoid process of C2 (axis) with the anterior arch of C1 (atlas) allows for 50% of cervical lateral rotation. The transverse and alar ligaments maintain joint integrity and limit posterior motion of the odontoid process relative to the C1 anterior arch. Abnormal posterior translation (or subluxation) can cause cervical cord impingement with the potential for significant neurologic compromise and even death.

Sport Specific Biomechanics

During extremes of cervical flexion or extension, competent transverse and alar ligaments limit posterior translation of the odontoid process. Incompetent ligaments or a damaged odontoid process can allow for significant translation and potential damage in cases of cervical hyperflexion or hyperextension where axial compression is delivered to the head and cervical spine. Given the potentially serious sequelae of significant atlantoaxial dysfunction, patients with defined instability are restricted from participating in contact sports and in sports requiring significant cervical flexion or extension.

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

If asymptomatic AAI is detected on screening evaluation of an individual without recent trauma or inflammation, physical therapy may help in teaching patients proper head control and avoidance of extremes of motion or at-risk activities.

Medical Issues/Complications

Initial management of either traumatic or inflammation-induced AAI depends on the presence and progression of neurologic symptoms. An experienced neurosurgeon or spinal surgeon should be consulted in most, if not all, cases.



  • Posterior fusion of the upper cervical spine with central cord decompression is indicated in any unstable atlantoaxial joint or in the presence of significant myelopathy. The patient should remain strictly immobilized while awaiting expedient surgical referral and procedures.

    Surgery is immediately indicated only in cases of irreducible canal compromise or progressive neurologic deterioration. Otherwise, it can be schedule on a less-emergent basis.

    Posterior fusion of the upper cervical spine may also be indicated in cases of os odontoideum (non-union of previous odontoid fracture) or other forms of odontoid aplasia or hypoplasia.

  • Cases of inflammation-related subluxation may require reduction under general anesthesia with subsequent cast fixation or traction under the guidance of an experienced spinal surgeon.
  • Traumatic or inflammation-induced acute AAI involving stable lesions without any neurologic symptoms may be reduced. The patients may be placed in halo brace with vest reduction and immobilization for 3 months. Repeat radiographs are necessary after reduction has been completed; several sources warn that deformity may still be possible, even after reduction.
  • In children with confirmed radiographic evidence of transverse ligament disruption less than 3 weeks old, the likelihood of ligamentous healing increases with halo and vest management.



  • In adults, healing of the transverse and alar ligaments is unreliable. Therefore, some authorities do not consider nonoperative management in adults, while others favor nonoperative management because of the risk of common surgical complications, the often-incomplete resolution of neurologic symptoms, and the lack of long-term data supporting surgical management.

Surgical Intervention

Posterior fusion of asymptomatic individuals with AAI, such as patients with Down syndrome, remains controversial. While some authorities advocate fusion to reduce the risk of a catastrophic trauma to the spine, others do not recommend fusion if the patient remains asymptomatic. It is important to note that the incidence of serious cervical spine injury is not increased in patients with Down syndrome and AAI, as compared with other athletic populations. Posterior fusion of the upper cervical spine is mainly indicated in symptomatic individuals.

Consultations

A spinal surgeon or neurosurgeon should be consulted in all cases of acute AAI. In cases of asymptomatic AAI found on screening examination, referral is indicated to confirm the diagnosis and possible activity restrictions.

Recovery Phase

Rehabilitation Program

Physical Therapy

After prolonged immobilization, physical therapy can increase cervical range of motion and assist in regaining strength deficits due to immobilization. An experienced therapist can also emphasize the need to avoid at-risk activities and extremes of cervical flexion and/or extension.

Surgical Intervention

Posterior cervical fusion is indicated in patients who present with a deformity that has been present for longer than 3 months or with recurrence after 6 weeks of immobilization. Such fusion can also be considered in the patient with chronic AAI who develops acute symptoms or neurologic compromise.

Medication

Acute Phase

Rehabilitation Program

Physical Therapy

If asymptomatic AAI is detected on screening evaluation of an individual without recent trauma or inflammation, physical therapy may help in teaching patients proper head control and avoidance of extremes of motion or at-risk activities.

Medical Issues/Complications

Initial management of either traumatic or inflammation-induced AAI depends on the presence and progression of neurologic symptoms. An experienced neurosurgeon or spinal surgeon should be consulted in most, if not all, cases.



  • Posterior fusion of the upper cervical spine with central cord decompression is indicated in any unstable atlantoaxial joint or in the presence of significant myelopathy. The patient should remain strictly immobilized while awaiting expedient surgical referral and procedures.

    Surgery is immediately indicated only in cases of irreducible canal compromise or progressive neurologic deterioration. Otherwise, it can be schedule on a less-emergent basis.

    Posterior fusion of the upper cervical spine may also be indicated in cases of os odontoideum (non-union of previous odontoid fracture) or other forms of odontoid aplasia or hypoplasia.

  • Cases of inflammation-related subluxation may require reduction under general anesthesia with subsequent cast fixation or traction under the guidance of an experienced spinal surgeon.
  • Traumatic or inflammation-induced acute AAI involving stable lesions without any neurologic symptoms may be reduced. The patients may be placed in halo brace with vest reduction and immobilization for 3 months. Repeat radiographs are necessary after reduction has been completed; several sources warn that deformity may still be possible, even after reduction.
  • In children with confirmed radiographic evidence of transverse ligament disruption less than 3 weeks old, the likelihood of ligamentous healing increases with halo and vest management.



  • In adults, healing of the transverse and alar ligaments is unreliable. Therefore, some authorities do not consider nonoperative management in adults, while others favor nonoperative management because of the risk of common surgical complications, the often-incomplete resolution of neurologic symptoms, and the lack of long-term data supporting surgical management.

Surgical Intervention

Posterior fusion of asymptomatic individuals with AAI, such as patients with Down syndrome, remains controversial. While some authorities advocate fusion to reduce the risk of a catastrophic trauma to the spine, others do not recommend fusion if the patient remains asymptomatic. It is important to note that the incidence of serious cervical spine injury is not increased in patients with Down syndrome and AAI, as compared with other athletic populations. Posterior fusion of the upper cervical spine is mainly indicated in symptomatic individuals.

Consultations

A spinal surgeon or neurosurgeon should be consulted in all cases of acute AAI. In cases of asymptomatic AAI found on screening examination, referral is indicated to confirm the diagnosis and possible activity restrictions.

Recovery Phase

Rehabilitation Program

Physical Therapy

After prolonged immobilization, physical therapy can increase cervical range of motion and assist in regaining strength deficits due to immobilization. An experienced therapist can also emphasize the need to avoid at-risk activities and extremes of cervical flexion and/or extension.

Surgical Intervention

Posterior cervical fusion is indicated in patients who present with a deformity that has been present for longer than 3 months or with recurrence after 6 weeks of immobilization. Such fusion can also be considered in the patient with chronic AAI who develops acute symptoms or neurologic compromise.

Rabu, 05 Desember 2007

Athletic Foot Injuries

Background

Athletic foot injuries can be difficult to properly diagnose and treat. Bearing the weight of the entire body, the foot is under tremendous stress. In many sports, the foot absorbs tremendous shearing and loading forces, sometimes reaching over 20 times the person's body weight. Physicians who treat these disorders must have a good understanding of the anatomy and kinesiology of the foot.

Although foot injuries can occur from a variety of causes, the most common cause is trauma. Other etiologies include (1) rapid or improper warm-up, (2) overuse, (3) intense workouts, (4) improper footwear, and (5) playing on hard surfaces.

Physicians who evaluate and treat common foot problems should have a working knowledge of the individual sports and the injuries that are commonly associated with them. An understanding of the basic treatment approaches for these injuries also is imperative.

Frequency

United States

Estimates indicate that 15% of sports-related injuries affect the foot alone.

Functional Anatomy

Foot and ankle

The foot is composed of 26 major bones, which can be divided into 3 regions: the forefoot, midfoot, and hindfoot. The forefoot is comprised of the 5 metatarsals and the 14 phalanges. The 3 cuneiforms (ie, lateral, intermediate, medial), the cuboid, and the navicular represent the midfoot. The hindfoot is composed of the talus and the calcaneus (see Image 1).

  • The talus is oriented so as to transmit forces from the foot through the ankle to the leg.


  • The calcaneus is the largest bone in the foot. The Achilles tendon inserts on the posterior aspect of the calcaneus.


  • The navicular lies anterior to the talus and medial to the cuboid.


  • The cuboid articulates with the calcaneus proximally, with the fourth and fifth metatarsals distally, and with the lateral cuneiform medially.


  • Each of the cuneiform bones is wedge-shaped. The medial, intermediate, and lateral cuneiform bones articulate with the first 3 metatarsals distally and the navicular proximally. The cuboid articulates with the lateral cuneiform.


  • The 5 metatarsals articulate with the proximal phalanges.


  • The great toe is composed of 2 phalanges, with 3 for each lesser toe.


  • Although variation exists in the number and location of sesamoid bones, 2 constant sesamoids are present beneath the metatarsal head. The sesamoids usually are present within tendons juxtaposed to articulations.

Select tendons of the foot (see Image 2)

  • The flexor hallucis longus (FHL) tendon is one of 3 structures that lie in the tarsal tunnel. Running behind the medial malleolus, the FHL is the most posterolateral. The FHL runs anterior to insert onto the distal phalanx of the great toe. The FHL acts as a flexor of the great toe, elevates the arch, and assists with plantar flexion of the ankle.


  • The flexor digitorum longus (FDL) tendon passes between the FHL and tibialis posterior tendon. The FDL inserts onto the distal phalanges of the 4 lateral digits and acts to flex the distal phalanges.


  • The tibialis posterior tendon is the most anteromedial of the tarsal tunnel tendons. This tendon inserts on the navicular tuberosity; the 3 cuneiforms; the cuboid; and the second, third, and fourth metatarsals. The tibialis posterior muscle flexes, inverts, and adducts the foot.


  • Laterally, the peroneus longus and peroneus brevis tendons share the common peroneal tunnel running behind and around the lateral malleolus. The peroneus longus plantar flexes the first metatarsal, flexes the ankle, and abducts the foot. The peroneus brevis flexes the ankle and everts the foot.

Other important structures

  • The plantar aponeurosis or fascia is a deep span of connective tissue extending from the anteromedial tubercle of the calcaneus to the proximal phalanges of each of the toes. Medial and lateral fibrous septa originate from the medial and lateral borders to attach to the first and fifth metatarsal bones.


  • Nerve innervation of the foot runs along the medial and lateral metatarsals and phalanges in a neurovascular bundle. These nerves are vulnerable to compressive forces that, in time, can generate the painful Morton neuroma, which most commonly affects the interspace between the third and fourth metatarsals. Four nerves supply the forefoot: the sural nerve (most lateral), branches of the superficial peroneal nerve, the deep peroneal nerve, and the saphenous nerve.

Sport Specific Biomechanics

The 3 planes in which the foot and ankle function are the transverse plane, the sagittal plane, and the frontal plane. Movement is possible in all 3 planes.

  • Plantar flexion and dorsiflexion occur in the sagittal plane. Plantar flexion involves the foot moving from the anterior leg distally. Dorsiflexion is the opposite motion.

  • Inversion and eversion occur in the frontal plane of motion. Eversion occurs when the bottom of the foot turns away from the midline of the body. Inversion is the opposite action.

  • The 2 transverse plane motions are abduction and adduction. Adduction involves the foot moving toward the midline of the body, while abduction is the opposite action.
Treatment


Acute Phase

Rehabilitation Program

Physical Therapy

Physical therapy is effective in treating inversion injuries and tendonitis of the foot, particularly in athletes who are continuing competition. Most athletes with fractures rehabilitate around the injury to minimize joint restriction and to maintain fitness levels. Acute phase treatment includes relative rest, ice, electrical stimulation, phonophoresis, and iontophoresis.

  • Sesamoiditis: Treatment consists of wearing cushioned-soled shoes with total contact inserts to relieve first metatarsal head stress; taking NSAIDs; and implementing rest, ice, compression, and elevation (RICE). An orthotic device should be worn for at least 6 months.


  • Turf toe: Acute treatment consists of a period of RICE, taping, and strapping the toe in a plantar-flexed position to avoid further hyperextension. Rigid turf-toe orthotics may be helpful as well. Ambulating is well tolerated in a hard-soled shoe. Mild-to-moderate sprains may require rest from the activity from days to weeks. Severe sprains may necessitate relative rest for up to 6 weeks.


  • Sever disease: Treatment consists of implementing RICE, wearing protective heel inserts or prefabricated arch supports, performing stretching and strengthening exercises, and, occasionally, taking NSAIDs (see Image 2).


  • Posterior tibial tendonitis: Treatment depends on the degree of symptoms. Initially RICE, NSAIDs, and analgesics are used as needed. Cast immobilization may be helpful during the early stages of the disease.


  • Peroneal tendon subluxation/dislocation: If reduction is necessary, it is accomplished by directing pressure posteriorly and then casting the ankle in slight pronation and flexion.


  • Peroneal tendonitis: For acute tenosynovitis, rest or immobilization and NSAIDs are initial measures. Wearing a cast for 2-3 weeks and then implementing extensive rehabilitation is appropriate for severe symptoms. An injection of a corticosteroid should be considered for patients with resistant symptoms.


  • FHL tenosynovitis: Treatment consists of immobilization, activity restrictions, and NSAIDs.


  • Jones fracture: The management of fifth metatarsal base fractures depends on the type of fracture. Extra-articular tuberosity fractures heal well and are managed symptomatically with either a walking cast or a hard-soled shoe for 2-3 weeks. Nondisplaced diaphyseal fractures usually are treated with non–weight-bearing casting for up to 8 weeks, followed by radiographic assessment. Diaphyseal fractures of the fifth metatarsal often are complicated by nonunion, delayed union, or recurrence secondary to compromised vascular supply. Intra-articular fractures often lead to posttraumatic arthritis.


  • Morton neuroma: Initially, treatment is conservative and is designed to relieve pain while permitting the athlete to continue activity. This treatment involves rest, ice, NSAIDs, and US. The application of a felt pad under the heads of the affected metatarsals may spread the metatarsal heads and relieve pain and inflammation. Injection of a corticosteroid may be effective in reducing the diameter of the impinged nerve branch. Podiatric consultation may be considered for proper shoe fitting.


  • Metatarsal stress fractures (not fractures of the fifth metatarsal): Conservative therapy, including rest, anti-inflammatory medications, application of ice, and cessation of the offending activity, is implemented. Athletes should maintain their aerobic capacity throughout recuperation by beginning a training program that involves non–weight-bearing activity such as swimming or stationary cycling.


  • Lisfranc fracture-dislocation: Because TMT fracture-dislocations are associated with complications such as loss of arch, degenerative arthritis, chronic pain, and impaired circulation to the distal foot, it is imperative that an orthopedic surgeon determine the most appropriate course of action for the patient.

Surgical Intervention

  • Sesamoiditis: Surgical excision is a last option that is rarely indicated.
  • Turf toe: Surgical treatment may be necessary to treat sesamoid injuries and repair capsular tears.
  • Sever disease: Surgery usually is not indicated in patients with Sever disease.
  • Posterior tibial tendonitis: Severe disease may require surgical debridement or repair.
  • Peroneal tendon subluxation/dislocation: Surgery is reserved for those in whom conservative therapy has failed or for those who are high-level athletes.
  • FHL tenosynovitis: Surgical release is occasionally necessary.
  • Jones fracture: Surgery to internally fixate the fracture often is performed to speed up recovery and to minimize the length of time before the athlete can return to play.
  • Fifth metatarsal fractures: Intra-articular tuberosity fractures involving more than 30% of the articular surface may require surgical fixation; therefore; orthopedic consultation is advised. Nondisplaced diaphyseal fractures in athletes may require immediate surgical fixation. Displaced diaphyseal fractures usually are managed operatively.
  • Morton neuroma: Surgical therapy may be recommended for patients or athletes in whom conservative management techniques fail. Surgical resection of the offending neuroma can provide rapid relief from pain and inflammation. A short course of rehabilitative therapy following surgery generally is recommended.
  • Stress fractures: Surgery is considered for athletes with stress fractures if conservative therapy fails. Furthermore, surgery for stress fractures should only be considered if the fracture is in a bone in which a complete fracture would result in serious complications (ie, tarsal navicular bone, a fifth metatarsals).
  • Lisfranc fracture-dislocation: The orthopedist may elect to perform closed reduction under general anesthesia using finger traps and countertraction at the ankle. The patient may require open reduction and internal fixation for more definitive stabilization. The patient will likely require a short leg cast from 6-12 weeks following surgery. At first, the patient will have a non—weight-bearing restriction and then gradually will progress his or her weight bearing in a walking cast. A custom arch support may be used for up to 1 year.

Other Treatment

Manipulation can be used to reintroduce motion and joint play into the foot, especially after prolonged immobilization, which often occurs during the postsurgical period or during fracture care. This manipulation can speed up return to play, which is the essential issue in athletic injuries. Injections are controversial in such problems as plantar fasciitis, as corticosteroids can increase the risk of tissue failure and rupture. Never use corticosteroids in a suspected or known fracture or directly in a tendon. A steroid agent can be injected into a tendon sheath to treat recurrent inflammation, but such an agent rarely is used as a first-line treatment. A diagnostic injection with lidocaine or bupivacaine may be used only as a means of localizing pathology.

Recovery Phase

Rehabilitation Program

Physical Therapy

After the acute phase, focus moves to ROM. PROM and active range of motion (AROM) exercises are used; muscle energy can be applied to restore the muscle set points. Therapy then shifts to improving strength and proprioception. Balance exercises are vital before returning an athlete to competition to prevent further injury.

Other Treatment (Injection, manipulation, etc.)

Taping or braces may be considered when preparing to return the athlete to play. For example, an athlete with turf toe may have steel-toe inserts in his/her shoes and taping on the first MTP joint.

Maintenance Phase

Rehabilitation Program

Physical Therapy

The athlete needs to continue implementing a proprioception and strength program to maintain function. Bracing, taping, or other prophylactic measures are taken into account with each individual injury and athlete. Long-term use of braces on the foot or ankle are discouraged

Medication

NSAIDs remain the mainstays of medical therapy for athletic foot injuries. For moderate to severe pain, the addition of an opioid analgesic may be necessary as well.

Drug Category: Nonsteroidal anti-inflammatory drugs

Used to suppress manifestations of inflammation. Inhibition of cyclo-oxygenase, the enzyme responsible for biosynthesis of prostaglandins, generally is thought to be a major facet of the mechanism of action of NSAIDs.

Drug NameIbuprofen (Motrin, Ibuprin)
DescriptionClassified as a propionic acid derivative. All drugs in this class are effective inhibitors of cyclo-oxygenase, though the potency varies.
Adult Dose400-600 mg PO q6h prn
Pediatric Dose5-10 mg/kg PO q6-8h prn
ContraindicationsDocumented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
InteractionsCoadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsCategory D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Drug NameNaproxen (Naprelan, Naprosyn, Anaprox)
DescriptionClassified as a propionic acid derivative. All the drugs in this class are effective inhibitors of cyclo-oxygenase, though the potency varies.
Adult Dose250-500 mg PO q12h
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
InteractionsCoadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsCategory D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Drug Category: Cyclo-oxygenase-2 inhibitors

COX-2 inhibitors are a new class of NSAIDs. COX-2 inhibitors appear to be as effective as nonselective NSAIDs in treating pain and inflammation. Their theoretical advantage over nonselective NSAIDs involves significantly less toxicity, particularly in the GI tract. This class of drug generally is indicated for patients at risk for GI hemorrhage. These patients include those with peptic ulcer disease, patients on warfarin therapy or on concomitant steroids, and elderly persons.

There has been recent literature questioning the safety of COX-2 inhibitors. Rofecoxib (Vioxx) has been withdrawn from the worldwide market because of its association with and increased rate of cardiovascular events (including heart attack and stroke) compared to placebo. Valdecoxib (Bextra) has been recalled for similar concerns. It is not clear whether these safety concerns are specific to Valdecoxib and Vioxx. The cardiovascular issues may be a class effect of all COX-2 inhibitors. Further study should help to answer questions concerning the safety of COX-2 inhibitors.

Drug NameCelecoxib (Celebrex)
DescriptionPrimarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient. Celecoxib has the same general class labeling as conventional NSAIDs.
Adult Dose100 mg PO qd/bid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity
InteractionsCoadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsMay cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; severe heart failure and hyponatremia may occur because celecoxib may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction

Drug Category: Analgesic, Miscellaneous

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who are in pain. Opioids produce their major effects by acting as agonists on specific opioid receptors. The effects are diverse and include analgesia, drowsiness, respiratory depression, decreased GI motility, nausea, and vomiting.

Drug NameAcetaminophen (Tylenol, Feverall, Aspirin Free Anacin)
DescriptionHas analgesic and antipyretic effects that do not differ significantly from aspirin. However, acetaminophen has only weak anti-inflammatory effects. Exact mechanism of action is not clear.
Adult Dose325-650 mg PO/PR q4-6h prn
Pediatric Dose10-15 mg/kg PO q4-6h prn
ContraindicationsDocumented hypersensitivity
InteractionsCoadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsMay cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; severe heart failure and hyponatremia may occur because acetaminophen may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction

Drug NameHydrocodone and acetaminophen (Vicodin, Norcet, Lortab)
DescriptionDrug combination indicated for moderate to severe pain for pain refractory to NSAIDs.
Adult Dose1-2 tab or cap PO q4-6h prn pain
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; high-altitude cerebral edema (HACE) or elevated intracranial pressure (ICP)
InteractionsCoadministration with phenothiazines may decrease analgesic effects; toxicity increases with CNS depressants or tricyclic antidepressants
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsTablets contain metabisulfite, which may cause hypersensitivity; caution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction

Drug NameCodeine and acetaminophen (Tylenol #3)
DescriptionIndicated for the treatment of mild to moderate pain. Elixir has 12 mg of codeine combined with 120 mg of acetaminophen in 5 mL.
Adult Dose1-2 tab PO q4h prn
Pediatric Dose3-6 years: 5 mL PO q4h prn
7-12 years: 10 mL PO q4h prn
>12 years: 15 mL PO q4h
ContraindicationsDocumented hypersensitivity
InteractionsToxicity of codeine increases with administration of CNS depressants, tricyclic antidepressants, MAO inhibitors, neuromuscular blockers, CNS depressants, phenothiazines, and narcotic analgesics; rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity of acetaminophen
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsCaution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction; hepatotoxicity with acetaminophen is possible following various dose levels in those with chronic alcoholism; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses that exceed recommended maximum dose

Athletes With Disabilities

Background

Adapted sports were introduced in the mid twentieth century as a tool for rehabilitation of injuries in war veterans. Over time, adapted sports have grown in popularity. People with disabilities now can participate on the recreational level as well as the international competitive level. In many sports, such as archery, athletes who are disabled can participate side-by-side with athletes with able bodies. Adapted equipment also allows athletes with disabilities to engage in other activities.

Organized activities for individuals with disabilities date back to 1888 when the first sport club for the Deaf was established in Berlin, Germany. In 1924, the first international competition for athletes with physical disabilities, the International Silent Games, was held. Wheelchair sports were developed at the Stokes Mandeville Hospital in the mid-1940s. The first Stoke Mandeville Games for the Paralyzed, which had 16 participants in wheelchair basketball, archery, and table tennis, were held in 1948.

The First Winter Paralympic Games were held in 1976 and were hosted in Ornskoldsvik, Sweden. The events were composed of Nordic and Alpine skiing. As with the increased number of events added to the summer Paralympic Games, events such as speed skating, sit skiing, sledge racing, and sledge hockey were added to subsequent winter games. In the Lillehammer Paralympic Games, held in Norway in 1994, events for athletes with cerebral palsy were added. In 1998, events for participants with mental disabilities were added to the winter games in Nagano, Japan.

Legislation

Legislation has helped to stimulate the development of adapted sports in the United States. In 1973, the Rehabilitation Act stated that no person could be excluded from participation in any program or activity receiving federal financial assistance. This law made physical education academic programs and intramural and interscholastic sports programs at colleges and universities accessible to participants with disabilities.

The Amateur Sports Act (1978) and the Olympic and Amateur Sports Act (1998) recognized athletes with disabilities as part of the Olympic movement. As a result, 7 organizations of disability sports hold membership in the United States Olympic Committee (USOC): USA Deaf Sports Federation, Disabled Sports USA, Dwarf Athletic Association of America, Special Olympics International, US Association for Blind Athletes, US Cerebral Palsy Athletic Association, and Wheelchair Sports USA.

In 1990, the Americans with Disabilities Act (ADA) was passed into law, providing increased access for persons with disabilities to employment, transportation, public accommodations, state government, local government, and telecommunications. In general, this access facilitates the involvement of people with disabilities in athletic pursuits and the venues where they are held. For children and adolescents, the 1990 Individuals with Disabilities Education Act (IDEA) is particularly relevant. The purpose of the IDEA is to assure access to public education for children with disabilities. This law specifically requires that children with disabilities have access to adapted physical education.

MEDICAL CONSIDERATIONS OF ADAPTED SPORTS

The role of the health care provider for athletes who are disabled is to be knowledgeable of the individual's primary disability and to assist in safe participation in sports for achievement of athletic goals. Performing a preparticipation examination (PPE) and being knowledgeable about participation maintenance and disability-specific conditions are essential to the safety of the patient. The PPE and participation maintenance are discussed in this section, while disability-specific conditions are addressed in the following section.

The PPE

Prior to participating in athletics, the athlete with a disability has to have completed acute rehabilitation, must understand the disability, must set sport-specific goals, and must communicate with a health care provider familiar with the medical aspects of the disability. A PPE performed by a qualified health care provider often is required prior to participation. The specific elements required in the PPE are determined by the sport, the level of participation, the athletic organization, the clinical indications, and the athlete. This published information is obtained from the respective athletic teams, schools, and organizations and, hence, is used by the examiner to tailor the PPE accordingly. The PPE should fulfill the requirements of the particular governing organization of the sport. Moreover, it should provide information to guide the athlete, trainer, coach, and team physician toward safe participation, activity limitations, and disability-specific training.

The objectives of the examination include the following:

  • Identify conditions that 1) may require further medical evaluation before the athlete enters into training, 2) require close supervision during training, and 3) may predispose to injury.



  • Determine the athlete's general health to assess fitness level and performance



  • Counsel on health-related issues and methods for safe participation



  • Provide referral for identified conditions that require further evaluation and/or monitoring to physicians familiar with the disability and the management of the identified conditions

In general, components of the PPE include a disability and sports-specific history and physical examination. In addition to the standard components of a history, the elements of the history for an athlete with a disability also should include athletic goals of the individual, the predisability and present level of training and sports participation, information on any over-the-counter (OTC) agents taken, presence of impairments, past family cardiopulmonary history, level of functional independence for mobility and self-care, and needs for adaptive equipment.



In addition, the review of systems (ROS) permits a comprehensive overview of the examinee's general condition. For example, in addition to the standard ROS, the examiner documents the presence of external devices for bladder drainage for the genitourinary system; for the gastrointestinal system, external devices for bowel evacuation; for the musculoskeletal system, splints and bracing equipment; and for the dermatological system, wound dressings and pressure sores.

The elements of the disability and sports-specific physical examination are tailored for the individual. Sensory deficits, neurologic deficits, joint stability and ROM, muscle strength, flexibility, skin integrity, medications, and adaptive equipment needs must be assessed. For the athlete who is disabled, assess the functional limitations of his or her body in both the affected and unaffected anatomical areas. Evaluate the patient's mobility with a wheelchair or any assistive devices that will be used for sports participation. Also evaluate his or her general cognition, memory, and judgment.

During the musculoskeletal examination of an athlete who uses a wheelchair, evaluate the stability, flexibility, and strength of the commonly injured sites (eg, shoulder, hand and wrist, lower extremities) as well as the trunk. During the musculoskeletal examination of an individual who has had a lower extremity (LE) amputation, assess the stability, flexibility, and strength of the trunk, as well as the hip girdle and the unaffected and affected LE with or without the prosthesis. For individuals with upper extremity (UE) amputations, the stability, flexibility, and strength of the shoulder girdle must be assessed in the unaffected and affected extremity with and without prosthesis, in addition to a trunk and LE evaluation. For the athlete with brain injury, stroke, or multiple sclerosis (MS), it is prudent to assess the limitations of the unaffected and affected areas based on mobility and sports-specific tasks.

Cardiovascular and pulmonary examinations are vital to any PPE and can identify conditions that can cause cardiopulmonary collapse or disease progression. Suggested guidelines for cardiovascular screening of the athlete are available from the American Heart Association, American College of Cardiology, and American College of Sports Medicine. For example, in the case of detected heart murmurs, the athlete is informed and is referred to his/her primary physician for consideration of an electrocardiogram and echocardiogram before the beginning of the sports season and before entry into training.

A PPE is performed upon entry into sports and should be repeated at least every 2-3 years. An interim follow-up prior to each sport season may be necessary if the athlete's health condition changes.

Participation maintenance

The key to continued participation and recreational enjoyment is remembering that safety is integral to good training and play. Therefore, strategies to prevent injury are emphasized.

Musculoskeletal injury is the most common injury reported among athletes who are disabled. A prevailing preventive strategy for musculoskeletal injury is sports-specific conditioning, along with preexercise stretching and warm-up as well as postexercise cool-down and stretching. Musculoskeletal injuries, as well as fatigue and exhaustion, can be reduced by assuring adequate nutrition and fluid status. Instruction in the use of proper protective and adaptive equipment and clothing also is important. In addition, the location where the sporting event is to be held should be evaluated prior to each training and play for potential hazards, such as falls, and for access and maneuverability of adaptive equipment.

Training athletes who are disabled on specific fall techniques (ie, safe methods for falling and recovering from a fall) can prevent potential injuries. This part of the athlete's education can be performed by a trained physical therapist. For example, an athlete who uses a wheelchair should be taught techniques for how to protect the head and neck in the event of a fall from a wheelchair, how to prevent ejection from the wheelchair upon a fall, and how to recover to an upright position in an energy-efficient way with a locked wheelchair.

DISABILITY-RELATED MEDICAL CONDITIONS

Environment

Thermoregulatory dysregulation is a common condition for a number of neurologic disabilities such as spinal cord injury (SCI), MS, brain injury, and stroke. For these disabilities, thermoregulatory dysregulation is a condition whereby the thermoregulatory system is impaired neurologically, resulting in heightened difficulties with acclimatization to either a cold or hot environment. Hence, the play environment heavily influences the schedule for training and for the sporting event, whether the sport is played indoors or outdoors.

In individuals who are neurologically intact, body temperature is regulated by the interplay coordinated by the autonomic nervous system, thermal receptors, cardiopulmonary system, and skeletal muscle contraction. The hypothalamus is the thermoregulatory center. The afferent system to the hypothalamus is provided by peripheral and central thermal receptors; the efferent signal descends primarily through the brainstem to the thoracolumbar division of the autonomic nervous system. The efferent system coordinates adjustments in cutaneous blood flow, sweating, venous return, and skeletal muscle-generated metabolic heat. Circulating vasoactive substances and local mechanisms are known to play a role in thermoregulation in response to the ambient temperature.

For patients with SCI, thermoregulatory dysregulation is a significant aspect in participation of sports. This dysregulation has been described at the level of the afferent and efferent systems with autonomic dysfunction and sensory deficits and at the thermoregulatory center with the impaired response to the hypothalamus regulation. Individuals with a neurologic injury level of T6 and above are most vulnerable to complications related to heat or cold stress. An impaired cooling mechanism results from the loss of the sympathetic system above the lesion, which reduces the sweating capability. The autonomic dysfunction below the lesion and the limited skeletal muscle pump function associated with weak or paralyzed muscles together impair blood redistribution and decrease venous return. Adding to the equation, the increased metabolic heat generated by skeletal muscles in exercise provides added potential for complications related to thermoregulatory dysfunction.

Thermoregulation dysfunction may occur in persons with central nervous system (CNS) lesions along the thermoregulatory system, such as in the hypothalamus or brainstem, as observed in individuals with cerebral palsy or in individuals following a stroke or brain injury. Individuals with MS may have CNS and/or spinal cord lesions; therefore, impairment of the thermoregulation system also may be observed in cases of MS. In addition, among individuals with MS, the propensity of fatigability with activity increases the risk for intolerance to environmental stresses.

With advanced age, an athlete with a neurologic physical disability may experience greater intolerance to environmental stresses than an individual without the disability. This change may occur in the setting of a previous state of immobility, premorbid deconditioning, medication effects, and concomitant age-related medical problems including autonomic dysfunction, altered control in cutaneous vasodilation, impaired renal function, reduced stroke volume and cardiac output, reduced total body water, obesity, or altered vital capacity (VC). If the individual enters into recreational athletics without prior experience and is deconditioned at the onset of training, the intolerance is even more prominent. A program geared toward a gradual acclimation is advisable.

Medications may potentiate environmental intolerance. Adjustments may need to be made, depending on the intensity of the activity. For example, diuretics can increase the risk of dehydration, especially when coupled with intense exercise. Other medications include anticholinergics, neuroleptics, antihistamines, and beta-blockers.

Prevention is the key to management. Daily assessment of the training and sporting environment should guide scheduling. Clothing featuring the appropriate fit and durability is emphasized, with the selection of lightweight light-colored garments for hot climates and insulated layered garments for cold climates. Adequate nutrition and hydration is particularly important for players in competitive games and outdoor sports. An enclosed facility such as a tent provides an area for rest and protection during breaks and for first-aid administration. Comprehensive preparation would not be complete without the identification of easy access to advanced medical services, ambulance services, and a hospital. This organizational structure is essential as athletes who are neurologically disabled are at increased risk for complications related to thermoregulatory dysfunction that may require emergent advanced medical services.

Education is vital for the athlete and game officials to prevent, identify, and provide initial management of heat-related and cold-related illnesses. In addition to prevention and recognition, medical personnel should be familiar with advanced treatment of these conditions.

Heat-related illness includes a spectrum of conditions (eg, heat-induced peripheral edema, heat cramps, heat exhaustion, hypotonic fluid-induced hyponatremic collapse, heat syncope, heat stroke). Heat edema results from local peripheral vasodilation, sweating, and increased sodium and water retention leading to the development of peripheral edema. Heat edema resolves over several days during acclimatization. The differential diagnosis of distal peripheral edema in the athlete with neurologic disability is lengthy and may need further consideration if there is a high clinical suspicion of serious conditions (eg, complex regional pain syndrome, compartment syndrome, fracture, ligament sprain, myositis ossificans, heterotopic ossification, deep vein thrombosis, heart failure, hypoalbuminemia, renal failure, infection).

The term heat cramps refers to the muscular spasm associated with prolonged exercise in heat, thought to result from ongoing negative sodium balance related to endurance activities in those who are unacclimated. Although resolution is observed with minimal conservative treatment, heat cramps may portend heat exhaustion when treatment is not administered and the athlete is not monitored for the development of further signs and symptoms of heat-related illness.

Heat exhaustion is a serious condition resulting from severe dehydration and/or hyponatremia. Tachycardia, high core temperature, dry mucous membranes, and hypotension are observed. Sweating may be reduced. If not treated, this condition may progress to heat stroke. Heat syncope results from impaired CNS perfusion due to reduced cardiac output from reduced venous return associated with heat-induced peripheral vasodilation and blood pooling in the extremities. If an alternative etiology of the syncope is suggested, the differential diagnosis for syncope in the athlete with a neurologic disability should be considered, depending on the individual's medical history and clinical presentation. The etiology may be cardiovascular, pulmonary, or associated with an acute CNS event.

Heat stroke is a medical emergency and does not resolve spontaneously. This condition results from thermoregulation failure and presents with an extremely elevated core body temperature and electrolyte and metabolic derangements. Mental status changes are key clinical clues. The Table provides a summary of the heat-related illnesses.

Heat-Related Illness

Condition Heat-induced peripheral edema Heat cramps Heat exhaustion Hyponatremic collapse Heat syncope Heat stroke
SymptomsDistal UE and LE edema; transientPainful muscle group; sudden onsetFatigue, increased weakness, sweating, nonspecific symptoms, confused



Lightheadedness or fainting in the setting of end of intense activity, dehydration, or entering into a hot area from the coldMental status changes, diarrhea, vomiting, feverish, reduced sweating
Essentials to treatmentRest and evaluation of the edematous extremityRest, massage affected muscles, oral hypotonic solutionRest, cooling, hypotonic fluid and electrolyte replacement, monitor symptomsRest, cooling, measure serum electrolytes, intravenous fluidsRest in a cool area, evaluate for other etiologies of syncope, move to a reclined position, hydrationAssess ABCs, rest, cooling, immediate emergency services evaluation

Cold-related illness can be seen with swimming, during inclement weather in summer sports, or during winter sports. The predominant condition is hypothermia. Hypothermia, by definition, occurs when the core temperature is below 95°F (35°C). Assess the degree of severity of the cold-related illness. A mild condition can be treated with slow external rewarming techniques. A moderate or severe condition requires close monitoring of the condition and warrants immediate transfer for more extensive medical attention. Until emergency services are available, initial treatment is instituted, involving removal of the athlete from the cold environment and passive external rewarming techniques.

Spasticity

Spasticity is defined as the velocity-dependent increase in resistance of muscle tone believed to be due to increased motoneuronal excitability and enhanced stretch-evoked synaptic excitation of motoneurons from an upper motor neuron injury. When not controlled, the clinical result is reduced mobility and ability to perform activities of daily living (ADL). The individual may report an inability to operate a manual wheelchair, ambulate, fit clothing properly, or perform transfers and ADL. Increased risk of contractures, skin breakdown, and pain accompany spasticity. Moreover, training and sporting events may become unsafe with the potential propulsive force of involuntary muscle spasms causing, for example, falls out of the wheelchair, difficulty in ambulation with forward movement, and reduced control of balance.

Spasticity is observed in varying degrees among patients following SCI, stroke, and brain injury and among individuals with MS. Control of spasticity is preferred when play and functional ability are affected. Management is achieved through noninvasive means with pharmacologic treatment, positioning, or bracing.

Pharmacologic options depend on the patient and the severity of the tone. Administration of medications is performed best under the advisement of a physician familiar with spasticity treatment. Medication side effect profile and dosage should be reviewed, as alertness, cognition, and motor strength can be affected adversely at therapeutic dosages. The choice, route, and dose of medication should be reviewed with the choice of optimal administration to produce the fewest side effects with the greatest control.

When indicated, bracing of the affected extremities may include tone-reducing upper extremity or lower extremity braces. For athletes who use wheelchairs, wheelchair positioning and modified components can reduce triggering muscle spasms and provide increased support in case of a triggered spasm. Trials can be performed to determine the optimal wheelchair system for the athlete. Depending on the location and severity of the spasticity, these trials can be conducted with one or a combination of items, including modification of the front rigging, adjustment of footplates, adjustment of the angle of the seat with the back support, and/or addition of a lap belt or chest, thigh, knee, ankle, and/or foot straps.

Osteoporosis

In addition to the primary and secondary osteoporosis risk factors, osteoporosis in those who are neurologically disabled is observed associated with one or a combination of factors, including immobility, decreased muscular strength and weight-bearing activities, age, predisposition, and medication. In this population, varying degrees of osteoporosis commonly are encountered among athletes with a motor complete SCI and/or advanced age. The impact on the ability to play is notable because of an increased risk of fractures over osteoporotic areas.

Preventive strategies against complications are essential for the management of osteoporosis among these athletes. Pharmacologic treatment includes recommendation of calcium and vitamin D as initial agents. The addition of bisphosphonates to treat documented osteoporosis is indicated. Modifications to equipment are prudent.

For athletes who use wheelchairs, liberal chair padding provides increased protection in case of falls and reduces the stress with axial loading. Fall prevention techniques also are implemented. These techniques include assessing the play environment for potential obstruction to safe mobility and ambulation; providing advanced training in safe mobility on uneven surfaces, stairs, and sport-specific environments; and ensuring optimal treatment for sensory deficits, such as updated prescription lenses fitted for sports activity.

In addition, it is important to assess the individual athlete's needs, as well as to provide athlete and caregiver education about the routine evaluation of the integrity, functional utility, and sports-specific applicability of the athlete's equipment, including adaptive equipment, wheelchair, ambulatory equipment aids, and/or protective gear. Repairs, adjustments, and new equipment are considered to reduce risk of falls and ensure safe play.

Musculoskeletal injuries

Musculoskeletal injuries are the most frequently reported medical problem within the competitive arenas. The shoulder was the most commonly injured area of the body in the Paralympic 1996 summer games for the athletes of the Disabled Sports USA and the Wheelchair Sports USA. Overall, from 1990-1996, among US athletes with disabilities participating the Paralympics and World Championship Games, the most commonly reported musculoskeletal injuries were the thorax/spine (13.3%), the shoulder (12.8%), and the lower leg/ankle/toes (12%). For athletes with amputations and other ambulatory athletes, LE injuries were the most commonly treated condition. For athletes using wheelchairs, UE injuries were the most commonly treated condition.

Little information has been published regarding the prevalence of injury among participants in all winter sports. Depending on the sport and the nature of the athlete's disability, as well as the method of reporting, varying prevalences of anatomic sites of injury are indicated in the literature.

Preventive strategies are essential to reduce the number of musculoskeletal injuries. Elements of management were discussed previously. This section focuses on one of the elements (ie, sport-specific conditioning). This specific type of conditioning provides the athlete with an individualized program that prepares him/her for the sport's unique metabolic and biomechanical demands, injury risks, and level of fitness. The overall program goal is to improve performance and prevent injury. The conditioning program begins with the identification of the athlete's goals and choice of sport. Each program is geared to the individual's level of fitness upon entry.

With general athletic fitness as the foundation, training for the higher level of fitness needed for that given sport incorporates flexibility, muscular strength, muscle balance, aerobic endurance, speed, agility, and sports-specific skills. Conversely, for individuals with neurologic disabilities, overtraining is a major concern. These athletes are predisposed to chronic repetitive strain and overuse injuries because of the reliance on the remaining functional limb(s). For athletes with SCI using wheelchairs, chronic shoulder injuries are common occurrences that may, in large part, be due to overuse and overtraining. Hence, it is important to strike a balance between carrying out the appropriate training program and overtraining. Precautions to prevent fatigue also are presented for athletes with MS and neuromuscular disorders.

The training program is divided into phases (eg, off-season, preseason, early season, late season). The program may be gradual in intensity and of longer duration for the elite athlete, in comparison with the recreational athlete whose play season is often shorter.

Pressure sores

A pressure sore is the disruption in skin integrity due to unrelieved pressure. Unrelieved pressure can cause local ischemia and subsequent tissue damage. Interruption in skin integrity can be associated with prominent bony surfaces, which are more likely to encounter pressure forces, poor skin integrity, and friction generated by shearing forces. The skin lesion is graded upon the depth of tissue involvement. The following classifications are according to the National Pressure Ulcer Advisory Panel:


  • Grade 1 - Nonblanchable erythema



  • Grade 2 - Partial thickness breakdown through the epidermis



  • Grade 3 - Full thickness breakdown at the dermis into the subcutaneous tissue



  • Grade 4 - Deep tissue breakdown to the fascia, muscle, bone, or joint

For individuals who use a wheelchair for mobility, the commonest areas at risk for pressure sores include the sacrum and coccyx, ischial tuberosity, posterior knee, foot, and shoulder blade. For the individual who wears a prosthesis, the skin areas in contact with the prosthesis and suspension are at risk.

Athletes with sensory deficits are most at risk for the development of pressure sores related to training or play. Other risk factors include activity-related shearing; axial forces generated against the skin; and poor transfer techniques, pressure relief techniques, seating and/or prosthetic systems, skin integrity, or skin care. Athletes who use a wheelchair and athletes who have had an amputation are at risk because of a combination of these factors.

Prevention and early intervention are important to management of pressure sores. Skin checks and pressure-relieving techniques should be performed on a regular basis. For athletes who use a wheelchair, weight shifts are the predominant pressure-relieving technique taught during rehabilitation. Weight shifts from a seated position are performed by pushing up off the surface or by leaning forward or laterally. The SCI clinical practice guidelines recommend that weight shifts be performed every 15-30 minutes to reduce the effect of prolonged pressure.

Education is directed toward assuring the adequate type, condition, and fit of adaptive devices; implementing proper transfer techniques; monitoring of disrupted skin integrity areas; and treating pressure sores early to prevent progress. For athletes who use wheelchairs, alternative adjunctive preventive strategies include methods to reduce friction forces and moist skin environments. These strategies can be achieved by choosing moisture-wicking clothing, an adequate custom-fitted wheelchair cushion, and sufficient padding over potential areas of breakdown. Sitting times may need to be restricted in severe cases.

For the athlete with an amputation, adjunct strategies include a proper prosthetic fit and an adequate suspension system, as well as assessment for a silicone liner, adequate cushioning with socks and padding, and sports-specific biomechanics training with the prosthesis. Avoiding a moist skin environment over the residual limb reduces the risk of skin breakdown.

Syncope

Syncope is the complete loss of consciousness and postural tone with recovery. A near-syncopal event represents an altered level of consciousness rather than a complete loss of consciousness. Evaluation indicates the need for assessment and treatment on an emergency basis. The main categories of the differential diagnoses include vascular, cardiac, neurologic, and miscellaneous. The differential diagnosis is lengthy and beyond the scope of this article. This section only highlights several conditions.

The most worrisome etiology is cardiogenic syncope, leading to cardiac arrest from arrhythmias, myocardial ischemia, or myocardial infarction. Hence, it is important to identify accessible emergency medical services and a hospital prior to a training session or game.

Sudden cardiac death is a separate entity defined as a nontraumatic unexpected cardiac event resulting in cardiac arrest and death within 6 hours of a previously witnessed healthy state. For the pediatric population, this phenomenon has been associated with congenital cardiac anomalies, hypertrophic cardiomyopathy, increased cardiac mass, Marfan syndrome, myocarditis, long QT syndrome, severe valvular disease, use of drugs, severe bronchospasm, and coronary artery abnormalities (less commonly). For the adult population, the occurrence of sudden cardiac death is associated primarily with coronary artery disease, but it also can be associated with hypertropic cardiomyopathy, increased cardiac mass, severe valvular diseases, conduction abnormalities, severe bronchospasm, and drug use.

The most common etiology of syncope in the athlete is neurocardiogenic syncope (vasovagal or neurally mediated hypotension syncope). A specific trigger usually is identified and can be a cough, micturition, bowel evacuation, or a stressful event. Neurocardiogenic syndrome involves a reflex-mediated vascular condition. Tilt-table testing administered by a cardiologist can reproduce it. Pharmacologic intervention may be warranted.

Syncope or near-syncopal events readily reversible in the athlete include heat-related illness, hypovolemia due to dehydration, and hypoglycemia. These conditions are treated accordingly.

The differential diagnoses of syncope in athletes who are disabled include neurologic physical disability-related syncope or near-syncopal events, which may result from a number of conditions, including hypovolemia, orthostatic hypotension, seizure, transient ischemic attacks (TIAs), or stroke. These conditions are treated accordingly. For example, among athletes with SCI, orthostatic hypotension commonly can be encountered despite the patient being in a euhydrated state with neither new neurologic changes nor evidence of seizure; stroke; or cardiopulmonary, hematologic, or musculoskeletal abnormality. Theories suggest a diminished cerebral blood flow with an impaired system to autoregulate to especially positional changes. This impaired system implies an impaired autonomic system, in addition to the reduced skeletal muscle pump function by paralyzed lower extremities, leads to decreased venous return and blood volume pooling in the lower extremities.

Management involves preventive measures such as local mechanical support (the application of supportive pressure gradient stockings and abdominal binders when the patient is in an upright position). If these conservative measures fail, pharmacologic interventions are considered and include agents such as sodium chloride tablets or midodrine.

Autonomic dysreflexia

Autonomic dysreflexia (AD) is a medical emergency resulting from the massive reflex sympathetic discharge occurring in patients with SCI at or above the splanchnic outflow at T6 level or among those with brainstem lesions. The clinical picture is an unopposed sympathetic discharge below the lesion and prevailing parasympathetic outflow above the lesion. Noxious stimuli are the triggers of AD. Therefore, in the presence of a trigger, an individual with a SCI at or above T6 may present with AD.

Clinical signs of AD include sympathetically induced elevated systolic blood pressure greater than 20 mm Hg above baseline, severe peripheral vasoconstriction, and piloerection below the lesion and parasympathetic-induced profuse sweating and skin flushing due to the vasodilation. The individual commonly complains of a severe headache, nasal congestion, and feelings of apprehension. The complications of unresolved AD are the same as for other hypertensive crises: stroke, seizure, arrhythmias, myocardial infarction (MI), and death.

Triggers for AD include some form of noxious stimuli, most commonly of a genitourinary (eg, urinary tract infection, bladder distention) or gastrointestinal (eg, constipation) origin. Other etiologies that may be encountered on the field include infection, sunburn, contact with sharp objects, tight garments, an ingrown toenail, fracture, appendicitis or other abdominal pathology, malpositioning, and disrupted skin integrity from numerous etiologies.

Initial management focuses on the identification and removal of the trigger, which usually results in its resolution. Elevating the head and trunk to more than 30° is an initial maneuver to decrease the high blood pressure. Assessing for adequate bladder drainage and an aggressive bowel evacuation, loosening tight garments, adjusting the athlete's position, and performing a full skin examination are essential in identifying the cause of AD.

Blood pressure is monitored every 5-10 minutes until it normalizes to the patient's baseline. If the systolic blood pressure does not resolve spontaneously, pharmacologic intervention is warranted until the trigger is identified and treated. The initial choice is nitropaste applied to the skin, commonly on an upper extremity, chest wall, or forehead. Doses are elevated until resolution. A hypertensive urgency or emergency may develop if these conservative measures fail. In these cases, emergency medical services are required to transfer the athlete for an in-hospital evaluation.

The athlete, coach, and officials should be familiar with preventive strategies as they can address many of the potential triggers. These strategies include assuring a functioning and secure bladder drainage system, regular bowel evacuation, routine skin examination, well-fitted adaptive devices, proper clothing, sunburn protection, and proper positioning (eg, wheelchair seating system for athletes who use wheelchairs).

Boosting

Boosting is the colloquial terminology for self-induced AD identified as a performance-enhancing technique. The term boosting refers to a technique potentially employed by athletes with SCI at T6 or above. The clinical result is similar to that produced by ergogenic aids. Consequently, boosting has been prohibited because of its unethical use in competitive sports. In theory, the performance-enhancing physiologic mechanism has been attributed to increased cardiopulmonary effects, oxygen utilization, and noradrenaline release. Reported methods for boosting by some athletes include temporarily occluding one's own urinary catheter, ingesting great amounts of fluids prior to the sporting event to distend the bladder, tightening garments, and prolonged sitting, thus inducing nociceptive stimuli. The complications of a prolonged boosting trial are the same as for AD in general (eg, stroke, seizure, arrhythmias, MI, death).

Education of medical personnel, coaches, and officials about this performance-enhancing technique is essential to its detection. Discouraging the use of practices intended to induce symptoms of AD is important. Assessing the athlete's condition prior to and during sporting events can help to detect such dangerous practices.