Basic Factors Leading to
Physical Conditioning Factors Contributing to Malnutrition
Stages of Malnutrition
Malnutrition in the Physically
Although bone proper is insensitive to pain,
orthopedic pain originates from the periosteum, joint capsules,
surrounding connective tissues, or irritated or inflamed bursa.
Receptors are summarized in Table 5. A fractured bone produces
pain from the periosteal rupture and pressure of soft-tissue
hemorrhage. Arthritis is painful because of capsule inflammation.
A history of a recent injection of antitoxin or the
administration of a new drug may suggest joint symptoms having an
Table 5. Joints
Outer layers of joint capsule,
grape-like clusters (33/4 8)
Sparsely found in deep layers of
joint capsule and in fat pads, grape-like clusters (2-4)
Myelinated and unmyelinated;
variable size (923/4 200 m
Signals static position of joint,
speed and direction of joint movement. Constant firing aids in
regulating posture and muscle tone during joint
Signals only rapid changes in
movement: acceleration, deceleration; helps to initiate
Signals direction of movement;
guards against excessive joint movement by regulating muscle tone (braking
Signal noxious changes:
mechanical or chemical
*Adapted from data of Kessler/Hertling and Wyke.
Sharp pain occurring only when the joint is moved a certain way
and that's usually relieved by rest or immobilization points to
joint dysfunction, not joint disease. In degenerative joint
disease of the weekend athlete, the pain that occurs on motion
and is relieved by rest is the result of joint dysfunction rather
than the arthrosis itself.
Onset. The onset of pain in several joints
simultaneously points to joint disease unless several joints have
been immobilized such as in multiple fractures or involved in
severe trauma with multiple bruises. Gradually developing pain is
often associated with chronic nonspecific arthritis. A rapid
onset is seen in acute rheumatic conditions and gout. Both
primary joint dysfunction and joint disease may present sudden
pain following trauma or an episode of stress; however, joint
swelling is uncharacteristic of joint dysfunction but is of joint
Joint disease may have an insidious onset that is unusual in
joint dysfunction. An exception to this would be intrinsic trauma
causing joint dysfunction occurring during sleep or
unconsciousness. Typical causes of pain near a single joint are
listed in Table 6.
Roentgenography is helpful in differentiating the various
arthritides. Table 7 lists the major roentgenographic features
that differentiate rheumatoid arthritis from osteoarthritis.
Roentgenographic features of gout versus atypical osteoarthritis
are shown in Table 8.
Table 6. Typical Causes of Pain Near a Single Joint
Subacute or chronic pain
Other inflammatory synovitis
Table 7. Roentgen Features: Rheumatoid Arthritis vs Osteoarthritis
Involvement of many peripheral
joints, especially metacarpophalangeal and proximal
interphalangeal joint of hands, and first interphalangeal foot
Knees and hips especially. First
carpometacarpal and acromioclavicular joints are often involved
Early synovitis, characterized by
fusiform soft-tissue swelling.
No signs of soft-tissue
Diffuse loss of joint space.
Asymmetric loss of joint
Involved bones are osteoporotic.
Development of subchondral
Little reactive new bone
Reactive bony sclerosis;
formation of osteophytes.
Eventual fibrous ankylosis.
Possible late bony
Table 8. Roentgen Features of Gout vs Atypical Osteoarthritis
May involve any joint but most
commonly attacks first metatarsophalangeal joint of the foot.
Joint space is preserved in spite of eroded bones of the foot,
other foot joints, and carpometatarsals.
Commonly involves hips, knees,
metacarpophalangeal, midcarpal, and patellofemoral joints.
Asymmetric joint-space narrowing, sclerosis, bone enlargement,
Erosions caused by tophi in
cartilage, often with a spicule of surrounding bone; asymmetric
soft-tissue swelling caused by urate deposits.
Formation of subchondral cysts;
collapse of bony surface.
Timing. Pain from a herniated disc gets progressively
worse as the day goes on. A dull ache during rest that's
aggravated by motion suggests inflammatory arthritis. Pain
lasting for several weeks or longer is common in chronic
arthritis. In acute rheumatic fever and often in gonococcal
arthritis, joint pain lasts for several hours, disappears, then
reappears in other joints. Pain worse in the morning after rest
that is relieved after mild exercise but worsens in the evening
points to joint disease. Deep, aching, throbbing, dull or sharp
pain that may be either constant or spasmodic is typical of joint
Unusual Absence. Neuropathy is suspect when there is no
pain but obvious joint disease. In such cases, diabetes mellitus
is the usual fault. When pain fibers are destroyed or deadened in
joint disease, injury is not safeguarded against and traumatic
osteoarthritis advances rapidly. In history of a nonmedicated
painless limp, muscle disease is the first suspicion, but a
metabolic bone disease or an endocrine dysfunction may be
involved in children.
Pain, tenderness, and heat in, near, or at a distance from the
hard (probably bony), boggy (probably infiltration), thickening
of capsule and periarticular structures, or fluctuating (probably
fluid) in the joint. Enlargement is generally unmistakable; but
when there is much muscular atrophy between the joints. The
joints may seem enlarged by contrast when they are not. Fluid or
semifluid exudates in joints may fill and smooth the natural
depressions around the joint, or, if the exudate is large, may
bulge the joint pockets. In the knee joint, four eminences may
replace natural depressions: two above and two below the
of contour: osteophytes or lipping (attached to bone); gouty
tophi (not attached to bone); constriction line opposite the
articulation; or protrusion of joint pockets in large effusions,
filling natural depressions. Irregularities of contour are easily
recognized, providing the normal contour is
motion. This is due to pain and effusion, muscular spasm,
thickening or adhesions the capsule and periarticular structures,
obstruction by bony overgrowths or gouty tophi or
as in extremity subluxation. This is recognized simply by
contrast with the limits furnished us by our knowledge of anatomy
and physiology of joint motion at different ages. When the bone
and cartilage seem normal or are not grossly injured, the
excessive motility of the joint is called a subluxation, but
excessive motility may also be due to destruction of bone and
other essential of the joint (eg, as in Charcot
creaking. These are detected simply by resting one hand on the
suspected joint, with the other hand putting the joint through
its normal range of motions while the patient remains
Free bodies in
the joint. These are not palpable externally and are recognized
only by their symptoms, roentgenography, or invasive
over or near a joint (cold, sweaty, mottled, cyanosed, white or
glossy skin, muscular atrophy).
the sinus leading to necrosed bone, gouty tophi, or an abscess in
or near the joint.
malposition due to contractures in muscles near the joint, to
necrosis, to exudation, or to subluxation.
the joint with shortening (limb, toe, finger, or trunk).
Shortening of a limb as evidence of joint lesion is tested by
careful measurements. The vast majority of such measurements are
made with reference to the hip joint. One method is to mark the
tip of each ASIS with a skin pencil and likewise the tip of each
inner malleolus. Then, with the patient lying prone on a flat
table, the distance from the ASIS to the inner malleolus is
measured bilaterally on each side with a tape.
"springy" block exhibiting some rebound at the end of an arc
usually indicates contracture or a deranged cartilage; motion may
be normal in one direction and completely absent in another. In
most cases of chronic extremity subluxations, resistance will be
felt before passive motion induces pain.
If the extent of joint limitation depends on the position of
another joint, it can generally be assured that the cause is
extra-articular; ie, the cause is within a structure spanning the
two joints. Hip flexion, for example, may be limited with the
knee extended but not with the knee flexed, indicating shortened
hamstrings. Another example can be seen in Volkmann's ischemic
contractures in which the fingers cannot be extended unless the
wrist is first flexed. When a sudden protective spasm occurs at
some point during motion (felt as a firm resistance), an active
localized lesion should be suspected.
Neuritis associated with joint stiffness causes pain on active
motion but a full passive range of movement exists. Pain induced
by passive motion in one direction and active motion in the
opposite direction signifies a lesion of a muscle or its tendon;
ie, the muscle becomes painful when passively stretched by
manipulation or contraction of its antagonists.
To distinguish muscle spasm from bony outgrowth as a cause of
limited joint motion, remember that bony outgrowths allow free
motion to a certain point and then motion is arrested suddenly
and without pain. Muscle spasm, on the contrary, checks motion
somewhat from the onset. Resistance and pain gradually increase
until the examiner's efforts are arrested at some point that
feels like a "thick rubber" block. When passive motion causes
sharp pain far before the end of motion has occurred and little
internal resistance is felt on further motion, an acute
inflammatory process, a mass, or a psychosomatic disorder should
Contractures typically exhibit limited motion in one direction
and painless motion in all other possible directions. A
"snapping" sound results when a tendon abruptly slips over a bony
prominence or fibrotic soft tissue. This is often seen in tendon
displacements, osteoma, lax joints, and trigger fingers.
Tenosynovitis exhibits pain during both stretch and relaxation
as the roughened tendon slides within its inflamed sheath. A
mushy "boggy" sensation at the end point is the typical feature
of chronic joint effusion in which synovitis is minimal. A firm
"leathery" arrest occurring before the end of normal motion in
some directions but not others suggests restraining fibrotic
ligaments, adhesions, or capsule thickening as often seen in
Motion limited by capsular thickening and adhesions are not,
as a rule, as painful after the first limbering-up process is
over. There is no sudden arrest after a space of free mobility,
but motion is limited very early and usually in all directions
even if the muscles around the joint are not rigid. The
possibility of limbering-out after active exercise (or passive
motion) distinguishes this type of limitation. Restricted
mobility from capsule restriction usually follows inadequately
treated acute traumatic arthritis, degenerative joint disease, or
Joint trauma is often profiled by a cool periarticular
swelling that is extremely tender. Direct trauma or secondary
inflammation can result in hemorrhage or effusion. Painless bony
lumps and asymptomatic joint swelling can often be traced back to
forgotten trauma, especially when associated with sport injuries.
In degenerative joint diseases, the trauma may be only normal
activity sufficient to elicit effusion.
Joint swelling can originate from edema arising in the joint
proper, edema originating in the extra-articular tissues around
the joint, and/or edema derived from the bones forming the joint.
The key features of joint swelling are its variable character,
shape, effect on motion restriction, and effect on joint
positioning, and its visibility.
Character. Swelling around a joint that is warm and
painful is characteristic of gout and rheumatic arthritis.
Synovial inflammation is characteristic of the nonspecific
arthritides, rheumatic fever, septic arthritis, gout, and various
collagen-vascular diseases. A gonococcal wrist or ankle joint
will usually be associated with nearby tenosynovitis.
Swelling about a joint can be caused by edema from fluid
overload or venous insufficiency. When this occurs, pain and
tenderness will be absent. Infiltration, effusion, or
inflammation can cause direct joint swelling. Localized
infiltration is seen in leukemia, myeloma, and amyloid disorders.
The major differentiating signs of hemarthrosis and synovitis are
shown in Table 10.
Table 10. Differentiation of Posttraumatic Joint Swelling
Slow onset, may not occur for
Small periarticular swelling
Hot, painful joint
Shape. The shape of a swollen joint corresponds to that of
the synovial membrane distended in toto. When a subcrural pouch
becomes dilated, for instance, swelling of the knee joint may
extend as much as 7 inches above the joint line. Another example
is that distention of the tabular process of endothelium about
the long head of the biceps in the shoulder may exhibit
enlargement over the surgical neck of the humerus.
Location. A swollen joint is often the result of
thickening synovial membrane or excessive fluid in the joint
cavity. This swelling is often obscured by bones, muscles, and
tendons overlying the joint cavity or its pouches; however, it is
noticeable over thinly covered areas of the joint. For instance,
swelling in the hip joint is almost impossible to detect.
Swelling in the elbow is observed only at the posterior aspect
on the sides of the olecranon process because the anterior
surface of the elbow joint is thickly covered with muscles and
the lateral aspects by strong collateral ligaments that prevent
protrusion. For the same reasons, a wrist swelling is least
noticeable when viewed from the front and radial side and a knee
swelling is least noticeable when viewed from the medial or
Positioning. Because of the relative position of
various bones and associated relaxation of the muscles around
joints, every joint has one position in which the synovial cavity
attains the greatest dimensions. When tension increases in the
synovial cavity because of effusion, the patient will adopt a
specific position that gives the greatest relief.
Motion Restriction. In general, joint motion becomes
restricted from either pain or mechanical disability. Intra-articular swelling impairs both active and passive movements,
while extra-articular swellings impair only one type of movement
or none. Foreign bodies or fragments within a joint resulting in
effusion are associated with intermittent motion restriction.
arthritis presents with signs of pain, possible ecchymosis, and
soft-tissue swelling of periarticular tissue that may be limited
to effusion within the capsule or obliterate bony prominences.
This depends on the severity of the trauma. As the process
develops, spurs and lipping at fibrous tissue attachments,
fibrocystic degeneration of articular surfaces, and possibly
posttraumatic deformity in bone tissue are typical. In soft
tissues, fibrous and fatty degeneration may be noted. Motion is
usually limited because of pain, and there will be joint
instability if the injury is sufficient to tear a tendon or joint
capsule. Intra-articular fractures and fragments may be
Second only to polyosteoarthritis, the most common cause of
bone/joint degenerative disease is the result of posttraumatic
degenerative arthritis from severe injury or chronic stress. The
phases of chronic peripheral joint degeneration are shown in
Table 11. Any joint may be involved, but the most common sites
are the hip, knee, first metacarpophalangeal joint, first
metatarsophalangeal joint, and apophyseal joints of the spine.
Table 11. Phases of Chronic Peripheral Joint Degeneration
Strain/sprain with likely history
of previous injury.
Chronic episodes of
Signs and symptoms
Periarticular muscle spasm, pain
aggravated by certain movements (eg, "catches"), tenderness,
motion restriction, slight swelling at times.
Like features of dysfunction,
except tendency toward collapse and feelings of weakness are
usually reported, a periodic segmental shift may be seen during
Pain, area stiffness,
incapacitating attacks after minor trauma, muscle weakness.
Tension or compressive overstress
leading to subluxation.
Hypermobile joint motion with
frequent subluxation, cartilages likely malpositioned.
Small cartilage fissures,
possible disc displacement, synovitis leading to fixation by
intra-articular adhesions and/or articular cartilage
degeneration, likely subluxation.
Lax capsule, coalesced probable
subluxation. disc tears, possible nipping of
Fibrosis, cartilage bodies,
severe joint space thinning, marginal osteophytes leading to
Whenever joint trauma is the chief factor, an acute arthritis
is likely to be induced. As with all trauma, the extent of the
local reaction is relative to the severity of the injury and the
resistance of the tissues. Arthritis resulting from a single
severe injury, especially if improperly treated, may be
indefinitely prolonged and result in chronic symptoms and
permanent disability. Repeated injuries from excessive joint
stress can cause pathologic reactions or derangement within the
It was once thought that this common disorder was the result
of joint trauma and overwork, but evidence collected during
recent years shows that degenerative bone disease is just as
common in the sedentary individual as it is in the manual laborer
or professional athlete. Thus, the explanation of prolonged
overstress can no longer be held valid as a general assumption.
While the cause of osteoarthritis is still unknown, it is
possible that it will be found within investigations of the
nutrition of articular cartilage. We do know that fibrocartilage
and hyaline cartilage is nourished essentially by a pump-like
action in which nutrients are pulled or sucked inward and
metabolic products are exuded or expelled outward during
reciprocatively opposite joint motions. If an articular fixation
(motion restriction) exists, it is likely that this pump-like
mechanism will not be effective.
If any tissue is not properly nourished, its power and
reserves to withstand normal stress are diminished and lead to
inflammation initially and degeneration when prolonged and tissue
defenses are depleted. When degeneration is advanced, the
structural design of the segment will not allow normal function
and normal proprioceptive input to the CNS is severely
muscle strain damages the periosteum, and if severe enough to
detach periosteum, a degree of hematoma develops. The bruised
area is swollen, extremely tender, and movements are restricted.
Physical examination makes one suspicious of fracture, but early
roentgenographic findings are negative. Later, ossification of
the hematoma is exhibited by induration of the swelling and new
bone formation. New bone formation occurs from many causes
whenever the outer periosteal membrane of bone is irritated
(osteoblastic reaction). The formation of new bone may appear on
film as either a solid or an interrupted mass, which can be an
aid in differentiation.
fluid-filled pads designed to aid motion between contiguous
tissues. Bursitis is an inflammatory reaction of thickened
synovium in which there is excessive secretion of fibrin-rich
synovial fluid that may lead to an abscess if secondary infection
occurs from local or systemic sources.
The microscopic picture of bursitis and tenosynovitis is
almost identical, but prolonged friction is the most common cause
of bursitis. The size of an inflamed bursa may increase many fold
if not protected from further injury. The bursa located near the
patella, olecranon, and hip are commonly involved.
Synovitic vs Mechanical Lesions
and periarticular disorders present with one or more of three
basic clinical patterns: (1) joint inflammation or synovitis, (2)
mechanical or cartilaginous lesions, and/or (3) nonarticular
rheumatism that mimics arthritis. Bursitis and tendinitis also
express themselves on periarticular structures, but signs of
internal joint involvement are absent. Weakness of proximal
muscles is a major finding in myositis, not swelling or
tenderness about involved joints. Refer to Table 1.
Synovitic Lesions. Synovitic lesions may involve any
synovial joint. In contrast, mechanical lesions primarily attack
only the weight-bearing synovial joints. Thus, deformities of
non-weight-bearing joints such as the elbows, wrists, and fingers
generally indicate the effects of synovitis. Synovitic disorders
are characterized by persistent symptoms during use and at rest
that are helped by anti-inflammation therapy. There is prolonged
morning stiffness, and the course fluctuates with exacerbations
lasting from weeks to months.
Mechanical Lesions. Mechanical disorders are
characterized by symptoms arising chiefly with use that respond
poorly to anti-inflammatory therapy. Morning stiffness is minimal
and short-lived after loosening movements. Damaged cartilage has
little ability to repair itself. Thus, once mechanical lesions
are produced, they tend to progress in severity with time and
use. Asymptomatic intervals do not occur as they do with
Possibly Associated Nonarticular Rheumatism Involving
Some types of periarticular inflammation or
rheumatism may mimic rheumatoid or degenerative joint lesions or
be superimposed on them. Fibrositis, polymyalgia rheumatica,
palmar fascitis, reflex sympathetic dystrophy syndrome, and
psychogenic rheumatism follow an intermittently or gradually
worsening course and are thus likely to be mistaken for
rheumatoid or degenerative joint disease. Hypertrophic
osteoarthropathy should also be differentiated.
tear is usually the results of an unexpected joint force, often
occurring in an abnormal plane of motion. The torn tissues
produce hemorrhage and local tenderness. Damage to the synovial
membrane is commonly associated, resulting in effusion and
possible hemarthrosis. Unless joint instability is severe,
capsule injuries improve well with conservative care. Early
treatment is not remarkable. It should consider cold, pressure,
rest, and a graduated muscle education and exercise regimen.
After acute symptoms subside, contrast baths, deep heat, and more
active movement can begin.
joint stress, often rotational, may cause some soft tissue to be
pinched within articular structures. This is most frequently seen
in the knee where infrapatellar fat is nipped, resulting in
effusion and possibly hemorrhage. Management is the same as that
for strain/sprain, but movement is delayed for several days
because injured fat is slow to heal.
adhesions, pain arises from most cartilaginous tissues only when
they are displaced or swollen and stretch or pressure is applied
on adjacent pain-sensitive receptors. The periphery of most
fibrocartilages (eg, IVDs, menisci of the knee and jaw) contains
some nociceptors, but the degree that they are involved in a
patient's report of pain is difficult to determine. A
cartilaginous loose body will certainly produce pain if it is
caught between two apposing pain-sensitive articular surfaces.
Cartilaginous thickening and even chondrophytes at articular
sites have been shown to be impregnated with sensory fibers;
thus, pain can arise when they are compressed. If adjacent
tissues are inflamed, then both compression and tensile forces
will give rise to pain.
fibrocartilage is usually associated with the spine and knee but
is occasionally related to the temporomandibular,
sternoclavicular, and distal radioulnar joints. Moderate cases
can usually be managed by adjustments, rest, physical therapy,
and muscle reeducation, but crippling cases may require surgery.
When injured, cartilaginous and disc substances progressively
undergo degenerative change with possible dehydration and
fragmentation. IVD damage results from repeated vertebral
subluxation and the strain of mechanical and postural
incompetence that tend to weaken the annulus, and, in the
cervical and lumbar spine areas especially, at the posterolateral
aspects with possible bulging into the intervertebral foramen.
Some DCs believe that there may also be a visceral reflex causing
a slight vasospasm leading to degeneration.
dislocation (luxation) is defined as the displacement of the
normal relationship of the articular surfaces of the bones that
comprise a movable joint. It places considerable stress on the
ligaments that normally maintain the involved joint's position.
There may be injury to these ligaments, the capsule they form
around some joints, articular cartilage, synovial membrane, and
other related soft tissues, as well as hemorrhage into or around
the joint. Gross dislocations require x-ray analysis before
reduction by a specialist.
A dislocation may result in a complete luxation or a
subluxation. If articular surfaces lose contact during the
disruption of trauma and lock in this position, a dislocation is
formed. If articular surfaces lose contact but return to a
position where the articular surfaces are in contact, an
orthopedic subluxation is formed. Regardless, the finding of a
dislocation or an orthopedic subluxation implies a sprain has
Following reduction of acute dislocation or mobilization of a
fixated subluxation, the injury is treated as any severe sprain
(acute or chronic). The fact that articular surfaces present in a
dislocated or subluxated position or remain so for 30 seconds or
30 days gives no indication of the extent of ligament damage
(grade of sprain). Thus, although static x-ray films may
eliminate suspicions of fracture, they are no help in determining
whether a mild sprain exists or a severe rupture has occurred
requiring surgical repair.
In the extremities, a subluxation may be the effect of a
spontaneously reduced dislocation and associated with
considerable capsule and ligament damage. Pain, swelling, and
deformity are centered about the joint. There usually is loss of
motion. Related ligaments are frequently torn and may require
Emergency Care and Related Considerations. A
dislocation is immobilized in the same way as a fracture: close
to the joint. Cold compresses may be applied to the joint to
relieve pain and reduce swelling, but the patient's temperature
must not be lowered to a point inviting shock.
Postreduction immobilization usually requires 6 weeks in the
lower extremity and 3 weeks in the upper extremity. These
durations should be reduced whenever possible to reduce the ill
effects of immobilization. Inadequate care, especially in ankle,
shoulder, and spinal dislocations/subluxations leads to chronic
weakness, movement restrictions, instability, and recurrent
dislocation in which subsequent surgery or conservative care has
a poor prognosis in restoring preinjury status.
plates in the young are highly susceptible to severe stress
because of their vascularity.
Epiphyseal Displacements. Malpositions are often seen
in the young and are almost always associated with trauma. They
may occur spontaneously, especially in the hip where they are
often associated with unexplained or misdiagnosed knee pain. The
growth plate is weakest at the site of cell degeneration and
provisional calcification, especially in children undergoing a
rapid spurt in growth or who are overweight in proportion to
their skeletal maturity. A common pitfall in orthopedics is to
confuse an epiphyseal slip for a ligament injury; eg, at the knee
joint. Epiphyseal slips should be treated as fractures, for
fractures are what they are rather than a disease process.
Osteochondritis. Traumatic intrajoint changes as the
result of overstress are featured by displacement, bony
fragments, distortion or collapse, and irregular ossification
during the late stages. Osteochondritis may occur at almost any
epiphyseal plate, and it is often named after a descriptive
author. For example:
Vertebral plates -- Scheuermann's disease
Femoral head -- Perthe's disease
Tibial tubercle -- Osgood-Schlatter's disease
Tarsal navicular --Kohler's disease
Heel -- Sever's apophysitis
Metatarsal heads -- Freiberg's disease
Such terminology is confusing as the condition is not a
disease, and this should be explained to the afflicted.
Osteochondritis Dissecans. This disorder features
inflammation of subchondral bone and articular cartilage that
results in split pieces of cartilage within an affected joint.
The cause is not completely understood, but the damage is
inevitably at a point where compression occurs in a jarring
injury. The clinical picture reflects avascular necrosis where
flakes or loose bodies of bone and/or cartilage are extruded into
the joint. The knee, ankle, and elbow are most often
Posttraumatic paralysis may be immediate as the result of a
severed nerve or a nerve block (eg, fracture) or slowly
progressive because of the growth of a mass (eg, hematoma, scar
tissue). Unless caused by a penetrating wound, few cases require
surgical joining. Most cases recover completely and relatively
rapidly, unless axons degenerate, with conservative therapy to
the involved nerve and the musculature it supplies. However, any
nerve injury requires careful monitoring. If necessary, surgical
exploration should only be delayed for a reasonable time (30--60
Three Classes of Peripheral Nerve Trauma
Contusion (Neurapraxia). Contusion may be
the result of either a single blow or through persistent
compression. Fractures and blunt trauma are often associated with
nerve contusion and crush. Peripheral nerve contusions exhibit
early symptoms when produced by falls or blows. Late symptoms
arise from pressure by callus, scars, or supports. Mild cases
produce pain, tingling, and numbness, with some degree of
paresthesia. Moderate cases manifest these same symptoms with
some degree of motor-sensory paralysis and atrophy. Recovery is
usually achieved within 6 weeks.
Crush (Axonotmesis). Recovery rate is about an inch per
month between the site of trauma and the next innervated muscle.
If innervation is delayed from this schedule or if the distance
is more than a few inches, early referral for surgical correction
should be considered.
Laceration (Neurotmesis). Laceration follows sharp or
penetrating wounds and is less frequently seen associated with
tears from a fractured bone's fragments. Surgery is usually
required. A traction injury typically features several sites of
laceration along the nerve. Stretching injury is usually but not
always limited to the brachial plexus.
Nerve Pinch or Stretch Injuries
syndromes are less common than nerve stretch syndromes, but they
are usually more serious. A nerve stretch syndrome is commonly
associated with sprains, fractures, dislocations, or severe
lateral cervical flexion with shoulder depression. Nerve fibers
may be pulled, partially torn, or ruptured most anywhere in the
nervous system -from the cord to peripheral nerve terminals.
Nerve "pinch" or "stretch" syndromes are common in sports, but
they are also seen after falls and industrial accidents. The
syndromes can appear in the face, spine, pelvis, and extremities.
Hardly any peripheral nerve is exempt. A nerve pinch syndrome may
be due to direct trauma (contusion and swelling), subluxation,
dislocation, an expanding mass (eg, hematoma), or fracture
(callus formation and associated posttraumatic adhesions). Any
telescoping, hyperflexion, hyperextension, or hyperrotational
blow or force to a limb may result in a nerve pinch syndrome
where pain may be local or extending distally.
Nerve Entrapment Syndromes
peripheral nerve entrapment syndrome is a distinct type of
neuropathy in which a single nerve is compressed at a specific
site (eg, within fibrous tissue, a fibrous-osseous tunnel, or a
muscle), either by external forces or surrounding tissues in an
abnormal state. Peripheral entrapment syndromes are often related
to congenital defects, overuse, and scar-tissue development
following trauma or surgery. A locally impaired blood supply may
further damage the entrapped nerve if associated vessels become
stretched, kinked, or compressed, or if blood flow is obstructed
in some way.
So the patient may avoid unnecessary pain and disability, it
is important to identify a peripheral entrapment syndrome rapidly
through examination and appropriate diagnostic studies such as
electromyography, nerve conduction evaluations, and
roentgenography. Severe impairment of nerve function is usually
only reversible in its early stages.
Vulnerability to Trauma
nerves of the body were placed end to end, they would span an
average distance of 45 miles. Fortunately, most large nerves of
the body lie deep where they are protected by muscle and bone. In
only a few areas are major peripheral nerves particularly exposed
to direct contusion from a blow:
The axillary nerve in the shoulder
The radial nerve in the midarm
The ulna nerve at the elbow
The peroneal nerve behind the head of the fibula.
General Neuromuscular Mechanisms
muscle is characterized by active contraction in response to the
reaction of the nervous system to the environment. This readiness
to act results in firing of motor units as stimuli from the
environment impose upon the nervous system; it is expressed as
muscle tone. Muscles losing their tone through lack of activity,
primary muscle disease, or nerve damage become flaccid.
The tone of musculature is due to the constant steady
contraction and relaxation of different fibers in individual
muscles that help to maintain the "chemical engine" of the muscle
cells. Even minor exercise helps to maintain tone by renewing
blood supply to muscle cells.
trauma can be superimposed on a subclinical peripheral nerve
disease, which will often offer a confusing clinical picture. The
primary causes of peripheral neuropathy are shown in Table
Table 13. Causes of Peripheral Nerve Disease
Collagen vascular disease
Peroneal muscular atrophy
Acute intermittent porphyria
Pathologic peripheral nerve disorders are characterized by
paresthesias (eg, numbness, pins and needles), dysesthesias (eg,
hypesthesia, hyperesthesia, anesthesia), weakness, cramping with
rapid fatigue, and muscle atrophy. The causative lesion, which
may or may not have trauma in its history, can be in a root
(radiculopathy), plexus (plexopathy), individual nerve
(mononeuropathy), or several nerves (polyneuropathy). As the
peripheral nervous system is a direct extension of and two-way
communicator with the central nervous system, the concept of a
pure peripheral disorder is theoretical.
Besides trauma, peripheral neuropathy may be associated with a
large number of diseases. Diabetes, cancer, liver or kidney
failure, immunologic impairments, and endocrine or metabolic
disturbances are the most frequent agents. Folic acid, niacin,
pyridoxine, thiamin, and vitamin B12 deficiencies have also been
linked to peripheral neuropathy.
Various medications, industrial solvents, commercial poisons
and pesticides, and exposure to heavy metals are also common
causes of diffuse peripheral neuropathy. Any of these conditions
may be underlying or superimposed on what first appears to be a
simple joint disorder. Differential diagnosis can be a complex
When peripheral neuropathy is suspected, the physical work-up
should include evaluation of reflexes, muscle strength, pain,
temperature (hot and cold), joint position, and vibration.
Appropriate blood tests include sedimentation rate, hematocrit,
CBC and differential, glucose tolerance, blood culture, serum
electrolytes, serum calcium, serum acid and alkaline phosphatase,
and drug screens. Urine should be examined for heavy metals. In
many chiropractic offices, electrodiagnostic evaluations are
considered a standard part of the neurologic examination rather
than a laboratory procedure. Electromyographic recordings should
be taken if the equipment is available.