Nerve Injuries

Nerve Injuries and Nontraumatic Disorders

The classification of nerve injuries proposed by Seddon (1943) was generally accepted but rarely used. He divided such injuries into three groups as follows:

1.Neurapraxia, designating minor contusion or compression of a peripheral nerve with preservation of the axis-cylinder but with possibly minor edema or breakdown of a localized segment of myelin sheath. Thus transmission of impulses is physiologically interrupted for a time, but recovery is complete in a few days or weeks.

2.Axonotmesis, designating more significant injury with breakdown of the axon and distal wallerian degeneration but with preservation of the Schwann cell and endoneurial tubes. Spontaneous regeneration with good functional recovery can be expected.

3.Neurotmesis, designating a more severe injury with complete anatomical severance of the nerve or extensive avulsing or crushing injury. The axon and the Schwann cell and endoneurial tubes are completely disrupted. The perineurium and epineurium also are disrupted to varying degrees. Segments of the latter two may bridge the gap if complete severance is not apparent. In this group significant spontaneous recovery cannot be expected.

A more useful classification was described by Sunderland in 1951. This classification is more readily applicable clinically, each degree of injury suggesting a greater anatomical disruption with its correspondingly altered prognosis. In this classification peripheral nerve injuries are arranged in ascending order of severity from the first to the fifth degree. Anatomically the various degrees represent injury to (1) myelin, (2) axon, (3) the endoneurial tube and its contents, (4) perineurium, and (5) the entire nerve trunk (Table 81-1).

ETIOLOGY OF PERIPHERAL NERVE INJURIES

Peripheral nerves may be injured by metabolic or collagen diseases, malignancies, endogenous or exogenous toxins, or thermal, chemical, or mechanical trauma. Only injuries caused by mechanical trauma are considered here. Every patient having injured a limb or limb girdle should be evaluated for possible musculoskeletal, vascular, and peripheral nerve damage (Table 81-5).

Primary injury of a peripheral nerve results from the same trauma that injures a bone or joint. In some instances, however, the neural injury is caused by displaced osseous fragments, by stretching, or by manipulation rather than by the initial injuring force. Secondary injury results from involvement of the nerve by infection, scar, callus, or vascular complications. These complications may be hematoma, arteriovenous fistula, ischemia, or aneurysm.

The radial nerve is the one most commonly injured. Of humeral shaft fractures, 14% are said to be complicated by injury of this nerve. Of radial nerve injuries, 33% are associated with fracture of the middle third of the humerus, 50% with fracture of the distal third of the humerus, 7% with supracondylar fracture of the humerus, and 7% with dislocation of the radial head.

The ulnar nerve is injured in about 30% of patients with combined skeletal and neural injury involving the upper extremity. This injury is most commonly associated with fractures about the medial humeral epicondyle, but it is often secondary to the formation of callus about the elbow.

The median nerve is injured in only about 15% of combined skeletal and neural injuries of the upper extremity. It is injured most commonly in dislocation of the elbow or secondarily in the carpal tunnel after injury of the wrist or distal forearm.

Axillary nerve stretch injuries occur in approximately 5% of shoulder dislocations.

The peroneal nerve is injured most commonly at the fibular neck in fracture of the tibia and fibula or dislocation of the knee.

Branches of the lumbosacral plexus are injured in less than 3% of pelvic fractures; it is reportedly injured in 10% to 13% of posterior dislocations of the hip. The tibial nerve may be injured in fractures of the proximal tibia and injuries about the ankle.

Peripheral nerve injuries should be carefully excluded in every patient with an acute extremity injury. Equal diligence should be applied in evaluation after surgery, manipulation, casting, and recovery from skeletal injury to detect secondary neural injury.

CLINICAL DIAGNOSIS OF NERVE INJURIES

Immediately after a severe injury to an extremity, recognition of a peripheral nerve injury is not always easy. Pain often is so severe that cooperation by the patient is limited at best. Here the preservation of life and limb is always the first objective. However, when possible, some simple tests should be made to detect injuries of major nerves of the extremity. In the upper extremity, for instance, loss of pain perception in the tip of the little finger indicates ulnar nerve injury. Loss of pain perception in the tip of the index finger indicates median nerve injury, and inability to extend the thumb in the hitchhiker’s sign usually indicates radial nerve injury though the extensor tendons may be severed and render this test invalid. Similarly, in the lower extremity loss of pain perception in the sole of the foot usually indicates sciatic or tibial nerve injury, whereas inability to extend the great toe or the foot indicates peroneal or sciatic nerve injury. As with the radial nerve, injury to the tendons or muscle bellies may render these tests useless. However, they may be carried out quickly and usually serve as effective screening procedures.

In evaluating peripheral nerve lesions, a precise knowledge of the course of the nerve, of the level of origin of its motor branches, and of the muscles that these branches supply is essential. Knowledge of the more common anatomical variations in nerve supply is extremely helpful. Furthermore, one must be familiar with the various zones of sensation, as well as with the areas in which sweating may be diminished or absent and in which skin resistance may be increased. Evaluation of motor loss is highly important. This can be accurate only if one can palpate or see the tendon or muscle belly under consideration. If one relies on analysis of movement alone as an indication of intact nerve supply, errors will be made because of substitution and trick movement

DIAGNOSTIC TESTS

Electromyography. Immediately after section of a peripheral nerve the electromyogram will demonstrate normal insertion activity (Figure 81-9). There will be no muscle response after stimulation of the nerve proximal to the site of injury. During the interval between 5 and 10 days after section, early denervation changes may be seen. Within 5 to 14 days positive sharp waves consistent with denervation are seen (Figure 81-10). Within 12 days denervation fibrillation potentials may be seen. No motor unit potentials are evident during attempted volitional contraction of the muscle, confirming the clinical finding of paralysis involving the muscle being

tested. Electromyography immediately after injury is valuable to demonstrate residual innervation or retained motor unit potentials during attempted volitional contraction that could be so minimal as to be undetected clinically. Retained motor unit potentials found under these circumstances suggest that complete interruption of the supplying nerve did not result from the injury. In such a situation anomalous innervation must be excluded.

Nerve conduction studies. Stimulation of a peripheral nerve by an electrode placed on the skin overlying the nerve will readily evoke a response from the muscle or muscles innervated by that nerve. This response can be seen, palpated, or measured electromyographically.

The techniques of both peripheral nerve stimulation studies and electromyography are exceedingly useful in separating hysterical or functional problems and malingering from organic illness that they might mimic.

Tinel sign. The Tinel sign is elicited by gentle percussion by a finger or percussion hammer along the course of an injured nerve. A transient tingling sensation should be experienced by the patient in the distribution of the injured nerve rather than at the area percussed, and the sensation should persist for several seconds after stimulation. It should be tested for in a distal to proximal direction. A positive Tinel sign is presumptive evidence that regenerating axonal sprouts that have not obtained complete myelinization are progressing along the endoneurial tube. With progressive regeneration, the positive response fades proximally, presumably because of progressive myelinization along the more proximal part of the regenerated segment. Distal progression of the response along the course of the nerve in question can be measured, and the rate of this progression has been used by some to establish prognosis or suggest the need for exploration.

Sweat test. Sympathetic fibers within a peripheral nerve are among the most resistant to mechanical trauma. The presence of sweating within the autonomous zone of an injured peripheral nerve reassures the examiner to a degree, suggesting that complete interruption of the nerve has not occurred. Preservation of sweating can be determined very simply, as pointed out by Kahn, by observing beads of sweat through the +20 lens of an ophthalmoscope. The time-honored sweat test (iodine starch test) consists of dusting the extremity with quinizarin powder. Sweating is induced by various means. The powder remains dry and light gray throughout the denervated area and assumes a deep purple color throughout the area of normal sweating. The triketohydrindene hydrate (Ninhydrin) print test as recommended by Aschan and Moberg is another method of assessing sweat patterns in the hand.

Skin resistance test. The skin resistance test is another method of evaluating autonomic interruption; in it a Richter dermometer is used. The autonomous zone with absence of sweating demonstrates an increased resistance to the passage of electric current. The adjacent innervated areas have a normal resistance, and further decreased resistance in these areas can be elicited by high external temperatures that will not affect the denervated area. The area outlined by the Richter dermometer roughly approximates the autonomous zone of the nerve in question.

Electrical stimulation. Electrical stimulation through the intact skin has been used in one form or another by many investigators and clinicians for a long time. Faradic stimulation often is of little value because normally innervated muscles may fail to respond to this current. Additionally, if response to faradic stimulation is still present after 3 weeks, then the muscles in most instances are capable of voluntary contraction and no additional information is obtained by the study. Galvanic stimulation is useful in determining chronaxy and the strength-duration curve. These determinations frequently give early evidence of denervation after nerve injury and are useful in following the evolution of reinnervation, which is less readily assessed by other methods.

GENERAL CONSIDERATIONS OF TREATMENT

As in any other injury, initial management of the patient with peripheral nerve damage should begin with careful assessment of the vital functions. When indicated, appropriate actions to prevent cardiopulmonary failure and shock should be taken and systemic antibiotics and tetanus prophylaxis should be provided. Once the extent of any injury to the major viscera has been determined and appropriate resuscitative measures have been started, the injury to the peripheral nerve should be evaluated and the specific nerve deficit should be carefully assessed.

An open wound in which a peripheral nerve has been injured should be thoroughly cleansed and debrided of any foreign material and necrotic tissue, using local, regional, or general anesthesia. If the wound is clean and sharply incised, if the condition of the patient is satisfactory, and if a repair can be carried out in a quiet and unhurried setting with adequate personnel and equipment, immediate primary repair of the nerve is preferred. On the other hand, if the general medical condition of the patient does not permit adequate repair or if circumstances otherwise cause an undue delay, we prefer to perform the neurorrhaphy during the first 3 to 7 days after injury; in this instance the wound first is covered with a sterile dressing and is observed for evidence of sepsis.

When open wounds are caused by blasting, abrading, or crushing agents and when contamination with foreign material is severe, the wound is thoroughly cleansed and debrided and a sterile dressing is applied. If the ends of the nerve can be identified, they are marked with sutures such as those of stainless steel that can be easily identified later. In the absence of a significant nerve gap, loose end-to-end apposition prevents retraction of the nerve segments and makes later repair easier. In the presence of a segmental gap in the nerve, suturing the ends to the soft tissues prevents their retraction. Soft tissue coverage of the wound consistent with the management of the injured part is carried out, and the nerve is repaired at a later date when the soft tissues have healed, usually between 3 and 6 weeks after injury.

A closed injury in which a peripheral nerve has been damaged requires careful assessment of residual function and documentation of discrete deficits. After the initial pain has subsided, and the wound has healed, early active motion of all joints of the involved extremity should be started. When necessary, gentle passive exercises that avoid disrupting nerves and tendons may be instituted. All joints of the extremity must be kept supple, and soft tissue contractures must be avoided. Exercises help keep the soft tissues of the extremity in a better physiological state so that when the nerve has regenerated, rehabilitation is easier. The specific effects of electrical stimulation of muscles remain unclear. Regardless of the details of the treatment program the patient must become actively involved in it to prevent contractures and to strengthen muscles with intact innervation. Similarly an extremity with a peripheral nerve injury should not be immobilized indefinitely. Dynamic and static splinting to support joints and to prevent contractures should be used intermittently.

When closed fractures are complicated by peripheral nerve deficits, to await reinnervation seems reasonable, and early surgical exploration usually is avoided. Then the progress of return of function in the injured extremity is evaluated with periodic electromyograms, nerve conduction velocities, and frequent clinical evaluation. Conversely, if the nerve deficit follows manipulation or casting of a closed fracture in the absence of a prior nerve deficit, early exploration of the nerve is favored.

FACTORS THAT INFLUENCE REGENERATION AFTER NEURORRHAPHY

Several important factors that seem to influence nerve regeneration are (1) the age of the patient, (2) the gap between the nerve ends, (3) the delay between the time of injury and repair, (4) the level of injury, (5) the condition of the nerve ends, and (6) the experience and techniques of the surgeon. The first five of these are discussed here.

GENERAL CONSIDERATIONS FOR SURGERY

Indications. In the presence of a traumatic peripheral nerve deficit exploration of the nerve is indicated as follows:

   1.When a sharp injury has obviously divided a nerve, early exploration is indicated for diagnostic, therapeutic, and prognostic purposes. Neurorrhaphy may be carried out at the time of exploration or may be delayed.

   2.When abrading, avulsing, or blasting wounds have rendered the condition of the nerve unknown, exploration is required for identification of the nerve injury and for marking the ends of the nerve with sutures for later repair.

   3.When a nerve deficit follows blunt or closed trauma and no clinical or electrical evidence of regeneration has occurred after an appropriate time, exploration of the nerve is indicated. This is also true when a nerve deficit complicates a closed fracture. In this instance it has been our practice to observe the patient for evidence of nerve regeneration for an appropriate time,      depending on the nerve and its level of muscle innervation. Then if regeneration has not occurred, we favor exploration. In situations in which a nerve has been intact before closed reduction and casting of a fracture but a significant deficit is found immediately after, we explore the nerve as soon as feasible.

   4.When a nerve deficit follows a penetrating wound such as that caused by a low-velocity gunshot, the part is observed for evidence of nerve regeneration for an appropriate time. If there is no evidence of regeneration, exploration is indicated.

Conversely, delay in exploration of a nerve injury is indicated if progressive regeneration is evidenced by improvement in sensation, motor power, and electrodiagnostic tests and by progression of the Tinel sign.

Time of surgery. It has been the time-honored policy to advise primary suture when possible. This is logical when one considers what happens to the distal end of the nerve, motor end plates, sensory nerve endings, muscles, joints, and other tissues of the denervated extremity. The controversy concerning whether primary or secondary nerve repair is better remains unsolved. Primary repair carried out in the first 6 to 8 hours or delayed primary repair carried out in the first 7 to 18 days is appropriate when the injury is caused by a sharp object, the wound is clean, and there are no other major complicating injuries. Ideally such repairs should be performed by an experienced surgeon in an institution where adequate equipment and personnel are available. The development of magnification devices, new instruments, and new techniques and the modification of a variety of small instruments for use in nerve surgery have improved the technique of early repair. Primary repair should shorten the time of denervation of the end organs, and fascicular alignment should be improved because minimal excision of the nerve ends is required.

BRACHIAL PLEXUS

The brachial plexus is formed by the union of the anterior rami of C5, C6, C7, C8, and T1.

Upper plexus injury (Erb) involves the segments innervated by the C5 and C6 nerve roots with or without dysfunction of the C7 root. Typically the limb is extended at the elbow, flaccid at the side of the trunk, and adducted and internally rotated. Abduction is impossible because of paralysis of the deltoid and supraspinatus muscles, and external rotation is impossible because of paralysis of the infraspinatus and teres minor muscles. Active flexion of the elbow is impossible because of paralysis of the biceps, brachialis, and brachioradialis muscles. Paralysis of the supinator muscle causes pronation deformity of the forearm and inability to supinate the forearm. Sensation is absent over the deltoid muscle and the lateral aspect of the forearm and hand.

Lower plexus injury (Klumpke) can be diagnosed by finding segmental sensory and motor deficits involving C8 and T1 with or without C7 dysfunction. Associated Horner syndrome should alert the examiner to the possibility of an avulsing injury of the lower plexus, and myelography and electromyographic studies may be necessary to exclude such an injury. In addition to penetrating wounds, many lower plexus injuries are caused by difficult births, falling on the outstretched arm, or trauma from crutches. The primary dysfunction is apparent in the intrinsic musculature of the hand along with paralysis of the wrist and finger flexors. The sensory deficit is along the medial aspect of the arm, forearm, and hand.

RADIAL NERVE

The radial nerve, a continuation of the posterior cord of the brachial plexus, consists of fibers from C6, C7, and C8 and sometimes T1. It is primarily a motor nerve that innervates the triceps, the supinators of the forearm, and the extensors of the wrist, fingers, and thumb. This nerve is injured most often by fractures of the humeral shaft. Gunshot wounds are the second most common cause of radial nerve injury.

After repair of the radial nerve the prognosis for regeneration is more favorable than for any other major nerve in the upper extremity, primarily because it is predominantly a motor nerve and secondarily because the muscles innervated by it are not involved in the finer movements of the fingers and hand.

The following muscles supplied by the radial nerve can be tested accurately because their bellies or tendons or both can be palpated: the triceps brachii, brachioradialis, extensors carpi radialis, extensor digitorum communis, extensor carpi ulnaris, abductor pollicis longus, and extensor pollicis longus. Injury to this nerve results in inability to extend the elbow or supinate the forearm and in a typical wristdrop. The inexperienced examiner, however, often may be misled by the patient’s ability to extend the wrist merely by flexing the fingers. The examiner therefore should be discriminating because analysis of movements may often result in error in evaluating the function of a nerve. The triceps is not seriously affected by injuries of the nerve at the level of the middle of the humerus or distally. In injuries of the nerve at its bifurcation into the deep and superficial branches the brachioradialis and the extensor carpi radialis longus continue to function; thus the arm can be supinated and the wrist can be extended.

Sensory examination is relatively unimportant, even when the nerve is divided in the axilla, because usually there is no autonomous zone. When present, the autonomous zone usually is over the first dorsal interosseus muscle, between the first and second metacarpals.

ULNAR NERVE

The ulnar nerve is composed of fibers from C8 and T1 coming from the medial cord of the brachial plexus. It may be divided at any point along its course by missile wounds or lacerations. When it is injured in the upper arm, other nerves or the brachial artery because of their proximity also may be injured. In the middle of the arm the ulnar nerve is relatively protected, but in the distal arm and at the elbow it often is injured by dislocations of the elbow and supracondylar and condylar fractures. An ulnar nerve deficit complicating a fracture or dislocation may be caused by the initial trauma, by repeated manipulations of the osseous injury, or by scar formation developing sometime after injury. The nerve is injured most commonly in the distal forearm and wrist

Interrupting the ulnar nerve proximal to the elbow is followed by paralysis of the flexor carpi ulnaris, the flexor profundus to the little and ring fingers, the lumbricals of the same fingers, all of the interossei, the adductor of the thumb, and all of the short muscles of the little finger. Occasionally when a nerve is completely divided at this level, the intrinsic muscles of the hand function normally because of anomalous innervation of these muscles by the median nerve. In these instances the fibers that supply the intrinsic muscles may be incorporated in the median nerve down to the middle of the forearm where they leave the median nerve to join the ulnar nerve (Martin-Gruber anastomosis). Complete division of the ulnar nerve at the wrist usually causes paralysis of all ulnar-innervated intrinsic muscles unless an anatomical variation connects the median and ulnar nerves in the palm (Riche-Cannieu anastomosis). Usually when the nerve is divided at the wrist, only the opponens pollicis, the lateral or superficial head of the flexor pollicis brevis, and the lateral two lumbricals remain functional.

The sensory examination usually is straightforward, although anatomical variations may cause confusing sensory findings. One need examine only the middle and distal phalanges of the little finger, which make up the autonomous zone of the ulnar nerve (Figure 81-26). Complete anesthesia to pinpricks in this area strongly suggests total division of the nerve. If one is in doubt about the sensory examination, skin resistance studies or an iodine starch test will be useful.

In patients suspected of having cubital tunnel syndrome, a positive percussion test over the ulnar nerve at the level of the medial epicondyle and a positive elbow flexion test are strongly suggestive of a significant compressive neuropathy. With the elbow fully flexed, the patient will complain of numbness and tingling in the small and ring fingers, often within 1 minute. Nerve conduction studies are helpful and should demonstrate slowing in the ulnar nerve velocities across the elbow, although normal velocities may be maintained during early involvement. Electromyography may demonstrate fibrillations in the ulnar innervated intrinsic muscles.

MEDIAN NERVE

The median nerve, formed by the junction of the lateral and medial cords of the brachial plexus in the axilla, is composed of fibers from C6, C7, C8, and T1

Median nerve injuries often are caused by lacerations, usually in the forearm or wrist.

The muscles of the forearm and hand supplied by the median nerve that can be tested with relative accuracy are the pronator teres, flexor carpi radialis, flexor digitorum profundus (index), flexor pollicis longus, flexor digitorum sublimis, and abductor pollicis brevis. Substitution movements caused by action of intact muscles may cause confusion during the examination. The works of Sunderland provide an excellent review of these movements and the methods of recognizing and preventing them. Usually if the forearm can be actively maintained in pronation against resistance, the pronator teres is intact. If the wrist can be actively maintained in flexion and a contracting flexor carpi radialis is palpated, this muscle is intact. Similarly if the interphalangeal joint of the thumb can be maintained in flexion against resistance with the wrist in the neutral position and the thumb adducted, the flexor pollicis longus is functioning. The flexor digitorum sublimis to each finger is examined separately while the remaining fingers are held in full passive extension.

Variations in the sensory supply of the median nerve also may be confusing, but usually the volar surface of the thumb, of the index and middle fingers, and of the radial half of the ring finger and the dorsal surfaces of the distal phalanges of the index and middle fingers are supplied by the median nerve. The smallest autonomous zone of the median nerve covers the dorsal and volar surfaces of the distal phalanges of the index and middle fingers (Figure 81-32). The iodine-starch test or triketohydrindene hydrate print test may be helpful in diagnosis. Autonomic changes such as anhydrosis, atrophy of the skin, and narrowing of the digits because of atrophy of the pulp also are valuable signs of sensory deficit

SCIATIC NERVE

Of the muscles innervated by the sciatic nerve that can be tested accurately, those supplied by the tibial component include the hamstrings, the gastrocsoleus, the tibialis posterior, and the long flexors of the toes; those supplied by the peroneal component include the tibialis anterior and the long extensors of the toes (deep peroneal nerve) and the peroneus longus and the peroneus brevis (superficial peroneal nerve). Testing of the intrinsic muscles of the foot, except the extensor digitorum brevis, is impractical. An extremity in which the sciatic nerve has been divided may develop an equinus deformity of the foot, clawing of the toes, and atrophy of the muscles innervated by the nerve, depending on the level of the injury. Profound weakness of flexion of the knee, inability to dorsiflex the foot or extend the toes, inability to plantar flex and evert the foot, and inability to flex the toes may be seen. When the peroneal part is involved, the sensory loss is primarily over the lateral aspect of the leg and dorsum of the foot. When the tibial nerve is involved, the sensory deficit is primarily over the plantar aspect of the foot. Anesthesia on the plantar surface may result in chronic ulceration. Autonomic disturbances and chronic pain may follow an injury to the sciatic or tibial nerve. The sciatic nerve is difficult to stimulate in situ because it is so deeply located. Stimulation is significant only when it causes contraction or pain. Electromyography is of considerable help in evaluating this nerve

The autonomous zone of the sciatic nerve (Figure 81-36), includes the area over the metatarsal heads and over the heel, the lateral and posterior aspects of the sole of the foot, and the dorsum of the foot as far medially as the second metatarsal, as well as a narrow strip up the lateral aspect of the leg.

TIBIAL NERVE

The tibial nerve, composed of fibers from L4, L5, S1, S2, and S3.

The muscles supplied by this nerve that may be accurately examined were described in the discussion of the sciatic nerve. The autonomous zone of the tibial nerve (including the medial sural cutaneous branch) varies but generally includes the sole of the foot (except the medial border of the instep), the lateral surface of the heel, and the plantar surface of the toes. Because the nerve is deep in the popliteal fossa, stimulating the nerve in this area is not always dependable, and consequently electromyography is indicated. The tibialis posterior, flexor digitorum longus, and flexor hallucis longus are supplied by branches of the tibial nerve after the nerve passes deep to the arch of the soleus muscle. The flexor digitorum longus and flexor hallucis longus may be difficult to test, but the tendon of the flexor hallucis longus may be palpated posterior to the medial malleolus as it passes to cross the medial aspect of the plantar arch. Atrophy of the intrinsic muscles of the foot may allow palpation of the flexor digitorum longus tendons; otherwise this muscle may not be palpable for testing. The autonomous zone of the tibial nerve as it passes deep to the soleus muscle is smaller than that of the nerve as it passes through the popliteal fossa because the sural nerve is excluded. Although electromyography may be necessary for evaluating injury to the tibial nerve beneath the soleus, the nerve may be stimulated with relative ease at the posterior aspect of the medial malleolus.

TENDINITIS AND BURSITIS

In the evaluation of patients with tendinitis of the lower extremity, a careful history of work conditions and exercise routines is necessary. Overuse (repetitive activity) or overload (sudden increase in activity) often accentuates tendinitis. Tendinitis from these causes usually responds to relative rest, ice, the use of a Neoprene sleeve, antiinflammatory medications, and alterations in work or exercise habits. Mechanical abnormalities, leg length inequality, leg malalignment, or foot abnormalities (such as excessive supination or pronation) may respond to the use of properly fitted orthotics. Muscle imbalance should be treated with appropriate flexibility and strengthening exercise programs.

Bursae are sacs lined with a membrane similar to synovium; they are usually located about joints or where skin, tendon, or muscle moves over a bony prominence, and they may or may not communicate with a joint. Their function is to reduce friction and to protect delicate structures from pressure. Bursae are similar to tendon sheaths and the synovial membranes of joints and are subject to the same disturbances: (1) acute or chronic trauma, (2) acute or chronic pyogenic infection, and (3) low-grade inflammatory conditions such as gout, syphilis, tuberculosis, or rheumatoid arthritis. There are two types of bursae: those normally present (as over the patella and olecranon) and adventitious ones (such as develop over a bunion, an osteochondroma, or kyphosis of the spine).

Adventitious bursae are produced by repeated trauma or constant friction or pressure. Kuhns showed that adventitious bursae lack a true endothelial or synovial lining and that the same pathological changes can be found in adventitious bursae as in normal ones: infection, tumors, enlargements, and fibrosis.

Treatment is determined primarily by the cause of the bursitis and only secondarily by the pathological change in the bursa. Surgery is not required in most instances. Systemic causes, such as gout or syphilis, and local trauma or irritants should be eliminated, and, when necessary, the patient’s occupation or posture should be changed. One or more of the following local measures usually are helpful: rest, hot, wet packs, elevation, and, when necessary, immobilization of the affected part. Surgical procedures useful in treating bursitis are (1) aspiration and injection of an appropriate drug, (2) incision and drainage when an acute suppurative bursitis fails to respond to nonsurgical treatment, (3) excision of chronically infected and thickened bursae, and (4) removal of an underlying bony prominence.

The usual principles of treating infections are employed in treating those of bursae. The responsible organisms should be identified when feasible, and the infection should be treated with appropriate systemic antibiotics. Aspiration of the bursa and injection of the appropriate antibiotic may be indicated in addition to the supportive measures just described; a compression dressing should be applied after aspiration. Occasionally surgical drainage is necessary.

Traumatic bursitis often will respond favorably to aspiration and injection of an appropriate steroid preparation and the usual nonoperative treatment.

Adventitious bursae that develop as a result of repeated trauma usually have a much thicker fibrous wall than do normal bursae and are more susceptible to inflammatory changes. This type of bursa is treated by removing the cause, for example, excising an osteochondroma or correcting a bunion; at the time of operation the bursal sac usually is excised. Only those bursae that most often require surgical drainage or excision will be described.

Prepatellar bursitis.

Tibial collateral ligament fibrositis and bursitis

Fibular collateral ligament bursitis

Infrapatellar bursitis.

Popliteal cyst (Baker cyst)

Medial gastrocnemius bursitis.

Bursitis associated with gluteus maximus muscle

Subgluteal bursitis.

Trochanteric bursitis.

Ischiogluteal bursitis

ELBOW INJURIES: ELBOW TENOPATHIES

Tennis elbow, a familiar term used to described a myriad of symptoms about the lateral aspect of the elbow, occurs more frequently in nonathletes than athletes, with a peak incidence in the early fifth decade and a nearly equal gender incidence.

The diagnosis of tennis elbow is made by localizing discomfort to the origin of the extensor carpi radialis brevis. In actuality, the origin is covered by the adjacent extensor carpi radialis longus and extensor communis origin and usually is found just distal to the midpoint of the lateral epicondyle. Pinching with the wrist in extension usually reproduces pain at this site.

OSTEOCHONDROSIS OR EPIPHYSITIS

The terms osteochondrosis and epiphysitis designate disorders of actively growing epiphyses. The disorder may be localized to a single epiphysis, or occasionally may involve two or more epiphyses simultaneously or successively. The cause generally is unknown, but evidence indicates a lack of vascularity that may be secondary to trauma, infection, or congenital malformation.

EPIPHYSITIS OF TIBIAL TUBEROSITY (OSGOOD-SCHLATTER DISEASE)

Surgery rarely is indicated for Osgood-Schlatter disease; the disorder usually becomes asymptomatic without treatment or with simple conservative measures such as the restriction of activities or cast immobilization for 3 to 6 weeks. Krause, Williams, and Catterall, in a review of the natural history of untreated Osgood-Schlatter disease in 69 knees in 50 patients, found that 76% of patients believed they had no limitation of activity, although only 60% could kneel without discomfort. Two distinct groups were identified: (1) those who before treatment had roentgenographic fragmentation and who had either separated ossicles or abnormally ossified tuberosities at follow-up and (2) those who before treatment had soft tissue swelling without roentgenographic fragmentation and who were asymptomatic at follow-up. Krause et al. concluded that symptoms of Osgood-Schlatter disease resolve spontaneously in most patients and that those who continue to have symptoms are likely to have distorted tibial tuberosities associated with fragmentation of the apophysis on initial roentgenograms. Lynch and Walsh described premature fusion of the anterior part of the upper tibial physis in two patients with Osgood-Schlatter disease who were treated nonoperatively, and they recommend screening for this rare complication.

LEGG-CALVÉ-PERTHES DISEASE

Irritable hip syndrome occurs only twice as frequently in boys as in girls, whereas Legg-Calvé-Perthes disease occurs three times more frequently in boys than in girls. The average age of patients with irritable hips is 3 years, and the average age of those with Legg-Calvé-Perthes disease is 7 years. Children with irritable hips have an average duration of symptoms of 6 days, whereas those with Legg-Calvé-Perthes disease have symptoms present for an average of 6 weeks.

Once the diagnosis is established, the primary aim of treatment of Legg-Calvé-Perthes disease is containment of the femoral head within the acetabulum. If this is achieved, the femoral head can reform in a concentric manner by what Salter has termed ‘‘biological plasticity.’’ Containment in most patients who continued weight-bearing has been satisfactorily achieved by abduction and internal rotation devices such as the Newington or Toronto brace and Petrie casts, and by abduction alone in the Scottish Rite brace. Because the prognosis cannot be established accurately, all children with total head involvement, regardless of age, should be treated actively.

Lloyd-Roberts, Catterall, and Salamon classified patients with this disease into groups according to the amount of involvement of the capital femoral epiphysis: group I has partial head or less than half head involvement, groups II and III have more than half head involvement and sequestrum formation, and group IV has involvement of the entire epiphysis. Furthermore, they noted that, especially in group II, III, and IV patients, certain roentgenographic signs described as ‘‘head at risk’’ correlated positively with poor results. These head-at-risk signs include (1) lateral subluxation of the femoral head from the acetabulum, (2) speckled calcification lateral to the capital epiphysis, (3) diffuse metaphyseal reaction (metaphyseal cysts), (4) a horizontal physis, and (5) Gage sign, a radiolucent V-shaped defect in the lateral epiphysis and adjacent metaphysis. They recommend containment by femoral varus derotational osteotomy for older children in groups II, III, and IV with head-at-risk signs. Contraindications include an already malformed femoral head and delay of treatment of more than 8 months from onset of symptoms. Surgery is not recommended for any group I children or any child without the head-at-risk signs.

We have used the Scottish Rite brace, popularized by Purvis and others because of its ability to place the legs in abduction and slight flexion (Figure 24-19). We realize that this brace does not provide maximum containment because it does not internally rotate. In fact, roentgenograms made with the brace on actually show some external rotation; however, the brace does allow some activities of daily living and psychosocially is more acceptable to the child and his parents than some other devices.

Contraindications to bracing include (1) a noncompliant patient, (2) parents or patient to whom the brace is psychosocially unacceptable, and (3) bilateral involvement at different time intervals, requiring prolonged brace wear. In any of these circumstances surgery may be indicated.

Frozen Shoulder

In 1945, Neviaser introduced the term adhesive capsulitis and described pathologic changes in the synovium and subsynovium. Till now unknown etiology.

Etiology: Recent reports suggest that adhesive capsulitis may be caused by biochemical changes in the joint capsule resulting in progressive fibrosis and motion loss.

Several factors have been associated with it: female gender, age greater than 40 years, trauma, diabetes, prolonged immobilization, thyroid disease, cerebral or cardiac infarction, and the presence of autoimmune disease.

The enhancement resulted from increased blood flow in and around the synovial tissue-recently reported MRI visualization of thickening of the joint capsule and synovium.

Diagnosis: It is defined as a painful and stiff developed in an otherwise healthy person 40 to 70 years of age. A duration of more than 1 month prior to examination

TREATMENT

The treatment is dependent on the stage of the disease and the symptoms.

Treatment protocols vary from benign neglect to supervised physical therapy, intra-articular corticosteroid administration, and early surgical intervention.

Traditional manipulative treatment of patients with joint contracture relies on forces applied with a long lever arm, risking fracture, especially in osteoporotic patients.

Intra-articular corticosteroids

The literature support the hypothesis that adhesive capsulitis is an inflammatory and fibrotic condition.

In the early stages, a hypervascular synovial hyperplasia is present that results in eventual fibrosis of the subsynovium and capsule.

Early treatment with it may provide a chemical ablation of the synovitis, thus limiting the subsequent development of fibrosis and shortening the natural history of the disease.

Non-steroidal anti-inflammatory drugs NAIDS

They have some effect in diminishing inflammation and oedema, in the past, ibrufen and diclofenac are used commonly for arthritis.

NAIDS has been shown to be effective both as an analgesic and as an antiinflammatory drug but also has side effects, especially on the gastrointestinal system, and should be used with caution and for a limited period in most cases.

Steroids such as hydrocortisone and prednisone are sometimes used in local injection to avoiding the severe  general side effects.

New techniques for manipulation promise to lessen the risk of fracture, and the development of improvements in post-manipulation pain control, such as catheters for continuous local anesthesia, may improve patient outcome.

The treatment remains varied

The positive improvement in patient function noted with home-based physical therapy;

The intra-articular corticosteroid.

There remain significant gaps in our understanding of the etiology of frozen shoulder, which must be answered to best provide appropriate and efficacious treatment for these patients.

Carpal tunnel syndrome

Carpal tunnel syndrome results from narrowing of the carpal tunnel. This narrowing may be secondary to a previous fracture, osteoarthritis or synovial thickening in pregnancy or conditions such as rheumatoid arthritis.

The patient complains of an aching wrist, often worse at night when the arm is warm, together with variable numbness in the radial three and a half fingers and weakness and wasting of the thenar muscles.

TREATMENT: Rest with a simple detachable splint and anti-inflammatory drugs may give some relief but division of the flexor retinaculum of the wrist is often necessary.