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.
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