The Evaluation of Joint Trauma
From R. C. Schafer, DC, PhD, FICC's best-selling book:
“Basic Principles of Chiropractic Neuroscience”
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Introduction Common Signs and Symptoms History of Joint Pain Standard Procedures Inspection Palpation and Percussion Temperature and Pulse Thermography Reflexes Limb Length, Circumference, and Width Measurements Goniometry: The Measurement of Joint Motion Joint Motion Evaluation Resisted Joint Motion Testing Limb-Muscle Strength Electromyography Electrodiagnosis Laboratory Procedures Basic Considerations in Diagnostic Imagery Connective-Tissue Trauma
Chapter 1: The Evaluation of Joint Trauma
Profiling disorders of the musculoskeletal system begins with a complete history and physical examination. A detailed history that covers the patient's present ailment, clinical history, birth circumstances, and family background are inevitably significant.
The physical examination of a distressed joint generally includes inspection, bony palpation, soft-tissue palpation, determining the passive and active range of motion, testing muscle integrity and strength, testing superficial and deep reflexes, and investigating associated areas. Other investigative procedures are employed as necessary for the clinical picture at hand.
One function of joints is to transmit stress when stabilized by musculature. This stabilization is necessary so that muscles can achieve their maximum leverage for motion. Joints are usually overstressed from a direct blow leading to connective-tissue contusion and possible intra-articular fracture.
A slipped growth plate may occur in the young. The blow is often an unexpected one where protective mechanisms have not been put in force, or it may be so excessive that protective mechanisms fail. This is because the stability of synovial joints is primarily established by action of surrounding musculature.
Common Signs and Symptoms
The typical overt changes that are commonly discovered in disorders of the musculoskeletal system include:
(1) color changes such as ecchymosis and redness,
(2) local heat,
(3) soft-tissue swelling from synovial thickening, periarticular swelling, or nodules,
(4) swelling from bony enlargement,
(5) deformity from abnormal bone angulation or subluxation,
(6) wasting from atrophy or dystrophy,
(7) tenderness on palpation,
(8) pain on motion,
(9) limitation of motion,
(10) joint instability, and
(11) carriage and gait abnormalities.
Fracture pain is severe, throbbing, and acutely aggravated by movement of the part. Pain from degenerative arthritis and muscular disorders is an aching type that is relieved by rest, aggravated by certain motions, and often accompanied by muscle splinting and paresthesias.
A sharp severe pain (associated with muscle changes and sensory disturbances) radiating along the distribution of a nerve is characteristic of acute nerve compression. Bone pain resulting from tumor or aneurysm is usually deep, constant, boring, more intense at night, and rarely relieved by rest or a change in position.
Referred pain is often associated with musculoskeletal disorders, as are somatosomatic, somatovisceral, viscerosomatic, somatopsychic, and psychosomatic reflexes. Because the body is a whole, a pure somatic or visceral disorder is highly unlikely.
History of Joint Pain
Probing into the history of joint pain and its onset, character, and duration can offer significant clues (Table 1.1). For example, gradually developing pain is often associated with chronic nonspecific arthritis. A rapid onset is seen in acute rheumatic conditions such as rheumatic fever, septic arthritis, and gout. A history of a recent injection of antitoxin or the administration of a new drug may suggest joint symptoms having an allergic basis. Severe throbbing pain is characteristic of gout and septic arthritis. A dull ache during rest that is aggravated by motion suggests inflammatory arthritis. Meniscal injury is always suspect when the patient's history indicates knee "locking."
Table 1.1. Typical Questions Asked During the Investigation of Joint PainWhat seems to be the matter? What do you think caused it? Where exactly does it hurt? Does it always hurt there? Does the pain feel sharp, dull, burning, tingling, boring, or what? Does it feel deep inside or near the surface? Does its quality or intensity ever change? Is it constant or does it come and go? Does the pain seem to start at one place and spread to another? Do you notice other things at the time the pain is severe? When did the pain first arise? Did it first occur gradually or rapidly? Was an injury or some unusual activity involved? At what time of day is the pain worse? At what time of day is the pain better? How long have you suffered with this condition? Have you ever had this condition before and it appeared to go away? If so, what did you do for it? Does anything seem to participate an attack? What aggravates the pain? What relieves the pain? What home remedies have you tried and what were their effects? How has this problem affected your work, activities, or sleep? How is your health otherwise? Are you presently being treated for any other condition? Are you taking any drugs or medications? What illnesses have you had in the past? What injuries have you had in the past? Has anybody else in your family had a condition similar to this? Do you have any opinion on what might have caused this problem? Is there anything else you would like to add?Note: Many of these questions would be pertinent to a complaint other than pain.
Symptoms of a musculoskeletal nature that cannot be linked to trauma are suspect of a chronic degenerative or organic process. Unfortunately, a history of stress or strain may not be remembered. Even severe trauma is easily put out of the mind during sports when emotions are high or forgotten once the pain and swelling have left. Whether pain is present or not, the history must be investigated to determine if the dysfunction is the result of bone, the joint, or the motor apparatus involved in the joint motion.
The Origin of Joint Pain. Although bone proper is insensitive to pain, orthopedic pain originates from the periosteum, joint capsules, surrounding connective tissues, or irritated or inflamed bursa. Arthritis is painful because of the joint capsule irritation. A fractured bone produces pain because of the periosteal rupture and soft-tissue hemorrhage pressure. A bone tumor yields pain due to the pressure upon and/or stretching of the periosteum. In degenerative joint disease, pain occurs on motion and is relieved by rest. In acute rheumatic fever and often in gonococcal arthritis, pain lasts for several hours, disappears, then reappears in other joints. Severe and persistent pain in one joint that begins to spread to adjacent joints is characteristic of inflammatory arthritis that is chronic and nonspecific in nature. Pain lasting for several weeks or longer is common in chronic arthritis.
The Nature of Joint Pain. Sharp pain occurring only when the joint is moved a certain way and which is usually relieved by rest or immobilization points to joint dysfunction. Joint pain worse in the morning after rest that is relieved after mild exercise but worsens in the evening points to joint disease. Severe bone disease and tumors are characterized by severe night pain that awakens the patient. Deep, aching, throbbing, and dull or sharp pain that may be either constant or spasmodic is typical of joint disease. Local or referred pain originating from a herniated intervertebral disc is relieved by rest and gets progressively worse as the day goes on.
The Onset of Joint Pain. Both primary joint dysfunction and joint disease may present with sudden pain following trauma or an episode of stress; however, joint swelling is uncharacteristic of uncomplicated joint dysfunction but is typical of joint disease. Joint disease may also 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. The onset of pain in several joints simultaneously points to joint disease unless several joints have been immobilized (eg, multiple fractures) or involved in a severe trauma (eg, multiple bruises).
The Absence of Joint Pain. Neuropathy should be suspected when there is no pain but obvious joint disease. In such cases, diabetes mellitus is the usual fault but tabes dorsalis, Charcot's joint, and syringomyelia are not rare causes. When pain fibers are destroyed in joint disease, injury is not safeguarded against properly and traumatic osteoarthritis advances rapidly. With a history of a painless limp, muscle disease is the first suspect but a metabolic bone disease or an endocrine dysfunction resulting in abnormal bone growth may be involved in children.
Associated Circumstances of Joint Pain. Pain triggered by heavy eating or drinking suggests gout. A history of trauma to the joint points toward joint dysfunction or traumatic or possibly gouty arthritis. Pain following exercise or strain is characteristic of traumatic arthritis, sprain, or joint strain. Joint pain occurring after a sore throat suggests rheumatic fever. Gonococcal arthritis or Reiter's syndrome usually has pain associated with urethritis. A history of childhood heart disease, St. Vitus dance, or chorea suggests joint pain resulting from acute rheumatic fever. Allergic conditions point to a diagnosis of nonspecific intermittent hydrarthosis. Joint pain associated with a history of joint aspiration or intra-articular medication injections suggests pyarthosis. Joint pain may be associated with a history of either old or new venereal disease, especially in gonococcal arthritis or syphilis bony changes. Tuberculosis or brucellosis is often associated with a history of raw milk consumption, weight loss, heavy sweating, unexplained fever, a chronic cough, and joint pain.
Unusual Factors. A genetic influence may be at hand that requires investigation. Ankylosing spondylitis, gout resulting from an enzyme defect or glycogen storage disease, and several types of familial amyloidoses have been associated with hereditary factors. Joint pain resulting from ochronosis or hemophilia is not usually difficult to differentiate from joint dysfunction. If the history indicates recent travel abroad, the symptomatic picture may represent problems not usually seen in this country. For example, joint pain may be the result of hydatid disease, amebiasis and other parasitic infestations, fungal infections, or of some tropical diseases that may express themselves in joints during their acute or chronic course.
Suggested procedures in joint examination are shown in Table 1.2. A common procedure is to first seek gross abnormalities. Next, observe gait, and note any awkwardness in rhythm, weight shifting, or imbalance. Note any bone distortion or limp. When a specific joint is involved, observe any gross deformity or swelling from either:
(1) fluid, where a wave can be demonstrated or
(2) thickened synovial tissue, where there is no wave but boggy tissue can be palpated.
Inflammation associated with a red and swollen area suggests an acute synovitis. Inspect muscles for hypertrophy and atrophy, and note areas of old ecchymoses which point to previous trauma. Sinus formation is rarely seen. When present, the sinus leads to necrotic bone, to gouty tophi, or to abscess in or near the joint.
Irregularities of contour may be the result of osteophytes or lipping (attached to the bone); gouty tophi (not attached to the bone); constriction line opposite the articulation; or protrusion of joint pockets in large effusions filling natural depressions. Irregularities of contour are easily recognized provided the normal contour of different body types is familiar. Signs should be sought for distortion or malposition due to muscle contractures near the joint, necrosis, exudation, or subluxation.
Table 1.2. General Points of Significance During Joint Examination
Direct Inspection and Palpation
Pain, tenderness, and heat in, near, or at a distance from the joint.
Enlargement: 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 in fact 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 out the joint pockets. In the knee joint, four eminences may take the place of the natural depressions, two above and two below the patella.
Irregularities of contour: osteophytes or lipping (attached to the bone);gouty tophi (not attached to the bone); constriction line opposite the articulation; or protrusion of joint pockets in large effusions, filling of natural depressions. Irregularities of contour are easily recognized, provided the normal contour is familiar.
Limitation of motion. This is due to pain and effusion, muscular spasm, thickening or adhesions in the capsule and periarticular structures, obstruction by bony overgrowths or gouty tophi, or ankylosis.
Excessive motion 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 appear normal or are not grossly injured, we call the excessive motility of the joint a subluxation, but excessive motility may also be due (eg, as in Charcot's joints) to destruction of bone and other essentials of the joint.
Crepitus and 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 passive.
Free bodies in the joint. These are not palpable externally and are recognized only by their symptoms, by roentgenography, and by operation.
Trophic lesions over or near a joint (cold, sweaty, mottled, cyanosed, white, or glossy skin; muscular atrophy).
Sinus formation; the sinus leading to necrosed bone, to gouty tophi, or abscess in or near the joint.
Distortion or malposition due to contractures in the muscles near the joint, to necrosis, to exudation, or to subluxation.
Telescoping of 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 of 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 with a tape on each side.
General constitutional symptoms, their presence or absence. These include fever, chills, leukocytosis, glandular enlargement, albuminuria, and emaciation.
Blood analyses such as tuberculin and Wassermann reactions, bacterial presence or absence.
Disease of other organs, their presence or absence; ie, syphilis; tuberculosis; tabes and other chronic spinal-cord lesions; endocarditis; hemophilia; various acute infections such as gonorrhea, influenza, scarlatina, septicemia; and skin lesions such as psoriasis, purpura, hives, and herpes.
The course of the disease and the results of treatment.
Palpation and Percussion
An involved joint should be palpated for masses and points of tenderness that may indicate osteoarthritis, synovitis, a torn ligament or meniscus. Palpation should be conducted for tenderness, masses, muscle tone, fasciculations, and spasm. A suggestion of bone inflammation is enhanced when the bone is percussed at a site distant from the point of tenderness and pain is felt at the site of tenderness rather than at the site of percussion.
Static Bony Palpation
The major purpose of static bony palpation is to assess bony relationships to determine if structural malalignment is present and/or to note hypertrophic changes. The palpation should be conducted in the various planes of reference of one bony structure to another and compared bilaterally. When structural abnormalities are suspected (eg, dislocation, fracture, osteophytes), they should be confirmed by roentgenography.
Dynamic Bony Palpation
Healthy articulations can be moved through their planes of normal motion actively and passively without causing pain; ie, until they reach their anatomical limit. A general rule of thumb holds that pain emanating from compressed tissues will be relieved by traction and aggravated by compression. Conversely, pain arising from tensile lesions will be relieved by compression and aggravated by traction.
Some joint movements are accompanied by compression, others by distraction, and others by compression and distraction depending upon the range and angle of motion. The term closed-packed position refers to a specific joint position where the articular surfaces are at their maximum point of congruency. Opposing articular surfaces may be either in a state of:
(1) approximation (compression) such as when moving toward the closed-packed position or
(2) separation (distraction) such as when moving away from the closed-packed position. Alternating compression and distraction within a joint has a distinct influence on articular surface nutrition and lubrication. Such alternating motions also comprise the basis of proprioceptive neuromuscular facilitation techniques.
The closed-packed positions for many joints are shown in Table 1.3. Knowledge of the closed-packed position of each joint, which movements involve compression and which involve distraction can be determined. Most subluxations, dislocations, and fractures occur when a joint is in the closed-packed position. In contrast, most sprains occur when the joint is in a loose-packed position because the force is imposed more on the supporting periarticular structures of the joint than on the intra-articular structures.
Table 1.3. Closed-Packed Joint Positions*
Joint Closed-Packed Position Temporomandibular When the heads of the condyles are at their most retruded position. Glenohumeral When horizontal adduction, abduction, and external rotation are fully achieved. Acromioclavicular During elevation and horizontal adduction of the arm; combining upward scapular rotation and narrowing of the scapula-clavicle angle (as seen from above). Elbow Full extension. Wrist (as a whole) Full dorsiflexion and radial deviation. Trapeziometacarpal Opposition. Metacarpophalangeal Full flexion. Interphalangeal Full Extension. Hip Full internal rotation, extension, and abduction. Knee Full extension and lateral rotation. Ankle mortise Full dorsiflexion. Subtalar Full eversion. Forefoot (as a whole) Wide weight-bearing position, where the forefoot is supinated relative to the heel and the longitudinal arch flattens.
*Modified from Kessler/Hartling.
Most long-bone joints are in the ovoid class in which the cross-sectional surface curves so that it has a smoothly changing radius. As an opposing articular surface moves along an ovoid surface, the apposing surfaces will not closely fit (impure swing) except at one particular point, which every joint has, where congruency is relatively close (the closed-packed position). It is at this point that movement stops.
An impure swing during joint motion requires conjugate rotation. This type of rotation produces a twisting action upon the capsule and major ligaments of the joint that, in turn, causes the joint surfaces to approximate until the closed-packed position is reached.
Falls upon an outstretched hand, for example, throw almost every joint of the upper extremity into a closed-packed position. Two exceptions are the metacarpophalangeal and acromioclavicular joints. If the force exceeds structural strength, either a joint must dislocate or a bone fracture.
There is a small but precise accessory movement within synovial joints called "joint play" that cannot be influenced except passively. Although joint play is necessary for normal joint function, it is not influenced by a patient's volition. Thus, joint play can be defined as that degree of end movement allowed passively that cannot be achieved through voluntary effort. In other words, total joint motion is the sum of the voluntary range of movement plus or minus the joint play exhibited.
Joint play occurs because normal joint surfaces do not appose tightly. There are small spaces created by articular incongruence necessary for hydrodynamic lubrication. In addition, because joint surfaces are of varying radii, movement cannot occur about a rigid axis. The capsule must allow some play for full motion to occur. Besides translatory joint play, a degree of distraction normally exists. If this is impaired for some reason, the articular surfaces become closely packed and motion will be restricted.
Although joint play cannot be produced by phasic muscle contraction, voluntary action is greatly influenced by normal joint play. This is because the loss of joint play results in a painful joint that becomes involuntarily protected by secondary muscle spasm. Thus, motion palpation to detect restricted joint play is an important part of the biomechanical examination of any painful and spastic axial or appendicular joint. Pain and spasm result when a joint is forced (actively or passively) in the direction in which normal joint end-play is lacking. Once normal joint play is restored, the associated pain and spasm subside.
Joint play should exist in all ranges of motion that are normal for a particular joint. That is, if a joint functions in flexion, extension, abduction, and adduction, the integrity of joint play in all these directions should be evaluated. It is typical, not unusual, in joint disorders that joint play is restricted in some planes but not others.
The importance of freeing articular fixations (eg, by chiropractic adjustments, mobilization) is brought out in several points made by Mennell. Normal muscle function depends on normal joint function. If joint motion is not free, the involved muscles that move it cannot function and cannot be restored to normal. Thus, impaired muscle functions leads to impaired joint function, and impaired joint function leads to impaired muscle function. In this cycle, muscle and joint function cannot be functionally separated from the other.
The Motion Barrier
When a joint is passively tested for range of motion, the examiner will note increasing resistance to motion referred to as a "bind" or the physiologic motion barrier. If a joint is carried past this point, the added motion becomes uncomfortable to the patient. This point is referred to as the anatomical motion barrier. In evaluating the degrees of passive motion, joints should be moved up to but not through the anatomical motion barrier. Thus, joint motion is evaluated by passively carrying the joint(s) through a range of motion until the motion barrier is encountered. The degrees of movement allowed should be recorded.
Bony outgrowths may be obvious (as in Heberden's nodes), but if they are near the periphery of a joint, they may be recognized only by the sudden arrest of an otherwise free joint motion. In true ankylosis, there is no mobility whatever and adjacent joints are often hypermobile. In most cases, roentgenography is necessary for diagnosis.
Bony outgrowths within a joint are sometimes only recognized by the sudden arrest of an otherwise free joint motion at a certain point. That is, an abrupt halt in motion usually signifies bone-to-bone contact, signifying that further movement should not be conducted. Such an approximation will be felt before the end of normal motion when hypertrophic bone growth (eg, an osteophyte, a malunited fracture, or myositis ossificans) has developed. If force is continued beyond the point of a bony block is painless, a neuropathic arthropathy is likely.
Muscular spasm is distinguished from bony outgrowth as a cause of limited joint motion by several features. Bony outgrowths allow perfectly free motion up to a certain point, after which motion is arrested suddenly, completely, and without great pain. Muscular spasm, on the contrary, checks motion slightly from the onset. Resistance and pain gradually increase until the examiner's efforts are arrested at some point.
Free bodies in a joint are not palpable externally and are recognized only by their symptoms, roentgenography, or exploratory surgery. They are the result of trauma, degeneration, or an inflammatory process and may be singular or multiple, free or attached, and of bony, cartilaginous, or synovial origin. Deranged cartilages and loose fragments occur commonly in the temporomandibular joint, knee, and spine. They occur far less frequently in the elbow, hip, and ankle joints.
Loose-body formation is the outstanding symptom of osteochondritis dissecans and osteochondromatosis. However, there are other conditions in which loose bodies occur as a complication of a pathologic process such as breaking loose of new bone processes and cartilage in certain degenerative joint disorders (eg, osteoarthritis), the organization of clots of fibrin forming rice bodies and melon-seed bodies, and intra-articular fractures, especially compression fractures.
Calcareous bodies are abnormal calcifications within a joint of such an age as to show advanced signs of ossification in roentgenography. They normally are not true free bodies but developments within tissue attached to the joint capsule. Free bodies are demonstrated by a change in position in subsequent roentgenography. Fragments of a fractured cartilage are rarely visible on films unless a degree of calcification has taken place.
The importance of atmospheric pressure and surface tension of synovial fluid in joint stability is readily exhibited during the action of knuckle cracking or the audible click accompanying a chiropractic dynamic adjustment. A relaxed loosely packed joint may be moved several degrees to demonstrate that its collateral ligaments are relaxed. When the joint is distracted to the degree that a sound is heard, it is at this point that the articular surfaces suddenly separate, and a bubble of gas forms within the joint cavity which can often be demonstrated by roentgenography.
A distraction force applied transversely in the joint is resisted by both synovial surface tension and atmospheric pressure. The adhesiveness of synovial fluid attempts to maintain articular juxtaposition; but, once it is overcome, the intra-articular pressure is suddenly reduced to a level below atmospheric pressure so that gas is audibly released from the fluid. The larger the joint, the greater the force necessary for distraction. This is not only because of the proportionately greater contributions of surface tension and atmospheric pressure but because of the stronger stabilizing muscles and ligaments.
There are several types of crepitation that characterize a specific type of lesion: bone crepitus, joint crepitus, tenosynovitis crepitations, and traumatic pulmonary emphysematous crepitus. Bone fractures produce an audible grating when the ends of broken fragments rub against each other during movement. The crepitation from an epiphyseal separation resembles that of a broken bone but is softer in character than the crepitus from a fracture.
Joint crepitus can be felt by placing a hand over the joint while passively moving the joint with the other hand. Fine crepitus signifies slight roughening of apposing surfaces; coarse crepitus, extensive roughening. When coarse crepitations are transmitted to the palm of the palpating hand, osteoarthritis, chronic rheumatoid arthritis, or tubercular tenosynovitis is usually involved. Intermittent crepitus of bone against bone signifies that the articular cartilage is extensively worn. Other acute or chronic lesions present fine crepitations. To amplify the crepitations involved, it is often helpful to apply a stethoscope to the joint during passive motions.
Crepitus may be felt over an effused joint following inflammation of the tendon sheath. In traumatic tenosynovitis of the extensor tendon sheaths of the forearm, for example, test by grasping the arm above the wrist while instructing the patient to clench his fist and open his hand with rapid motion several times. The presence of effusion will result in a transmissible or audible crepitation.
A fractured rib in which a fragment of bone has pierced a lung allows air from the lung to escape into the subcutaneous tissues. Crepitus may be felt when the fingers are placed with mild pressure over the affected area.
Soft-Tissue Restrictions and Stiffness
If a patient affirms that joint stiffness is common, its distribution and duration should be explored. Inquiry should also be directed to related activities and circumstances that relieve or aggravate the stiffness.
Joint stiffness is often produced by edema or structural changes. Edema around the joint capsule is found in inflammatory disorders. Edema within the capsule secondary to inflammation is characterized by being worse after rest; eg, in the morning or arising after sitting for a long period. Stiffness that lasts for more than a half hour points toward one of the inflammatory arthritides in which it may last for several hours.
Stiffness resulting from structural changes can usually be traced to cartilage degeneration or capsule tears. Previous trauma or inflammation may have resulted in adhesion formation. Stiffness resulting from degenerative diseases becomes pronounced when area muscle compensation fails to protect thinning cartilage. Here also the stiffness is more pronounced after rest, but it is quickly relieved by mild exercise.
Evaluating Joint Stiffness
In most cases of chronic extremity subluxations, resistance will be felt before passive motion induces pain. A tough "springy" block that exhibits some rebound at the end of motion usually indicates contracture or a deranged cartilage. Motion may be normal in one direction and completely absent in another.
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 that spans 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.
If a sudden protective spasm occurs at some point during the arc of motion (felt as a firm resistance), an active localized lesion should be suspected. To distinguish muscular spasm from bony outgrowth as a cause of limited joint motion, remember that bony outgrowths allow free motion up to a certain point and then motion is arrested suddenly and without pain. Muscular spasm, on the contrary, checks motion a little from the onset, the 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 to further motion, an acute inflammatory process, a mass (eg, a neoplasm), or a psychosomatic disorder should be suspected. Tenosynovitis will exhibit 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 that occurs before the end of normal motion in some directions but not others suggests fibrotic ligamentous restraint, adhesions, or capsule thickening as is often seen in subacute arthritis. Motions 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 from the first 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 degenerative joint disease, acute trauma, arthritis, or prolonged immobilization.
Nerve irritation is characterized by pain on active motion but a full passive range of movement is present. 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. Contractures are characterized by 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.
It has been estimated that from 50% to 60% of the pains and discomforts that the average ambulatory patient has are the direct or indirect result of involuntary muscle contraction. Thus, the physician is compelled to consider the relationship of muscle contraction to pain symptoms in both diagnosis and therapy.
Spasticity. The primary function of muscle is to contract. When contraction occurs involuntarily, the cause can usually be traced to neuropathology or a protective reflex (splinting). This splinting reaction to inhibit movement is not always beneficial, especially when the disorder becomes chronic. When muscles become acutely spastic or chronically indurated, normal movement is impaired and foci for referred pain can be established.
Both spastic and indurated muscles are characterized by circulatory stasis that is essentially the effect of compressed vessels, which leads to the poor nutrition and the accumulation of metabolic debris. Palpation will often reveal tender areas that feel taut, gristly, ropy, or nodular. An area of chronically indurated muscle tissue is often located adjacent to an area of muscle that has entered into a state of fatty degeneration. When found through palpation, this area should be differentiated from that of a site of a common lipoma.
Stretch Reflex Effects in Spasticity. A spastic resistance is essentially a stretch reflex activity whose receptors are the muscle spindles that are scattered in parallel with the muscle fibers. In common spasticity disorders, spastic muscles relax when the part is comfortably rested with support and become spastic with volitional movements, tendon tapping, vibration, or even startling noises. Three hypotheses have been put forward by DeBacher to explain the hyperactive stretch reflexes that occur in spasticity:
Loss of corticospinal inhibition leaves the alpha motor neurons with a lower firing threshold so that they readily fire in response to any impinging sensory input, including that from stretch receptors.
A hyperactive gamma efferent system puts muscle spindles in a contracted state so that there is an abnormal response to stretch stimuli.
Spinal motor neurons normally exert a primarily inhibiting presynaptic modulating influence on afferent connections just proximal of the alpha motor neurons and damage to or dysfunction of the corticospinal pathways weaken this influence so that afferent impulses from stretch or other sensory receptors are more likely to increase the firing rate of alpha motor neurons even if the muscle spindles are not contracted.
Tenderness. Pain produced by external pressure commonly results from trigger points, traumatic lesions of sensitive subdermal tissue, or the development of a toxic accumulation or deep-seated inflammatory irritation. Mild cases of joint involvement invariably have points of maximum tenderness that correspond to those endothelial regions that are most superficial. For example, they are elicited:
(1) in the ankle at the anterior surface of the joint,
(2) in the knee on both sides of the patella,
(3) in the wrist over the anatomical snuffbox, and
(4) in the elbow over the radiohumeral joint.
Local Hyperthermia. In cases of inflammation, the presence of local heat is a valuable sign. This may be noted by passing the outstretched hand rapidly over the affected part to an unaffected part and back again. Any difference in warmth from the affected area to the unaffected area signifies an increase in local temperature.
Pitting on Pressure. Pitting is a sign of liquid infiltration into the underlying tissues. Tenderness associated with pitting indicates inflammatory edema. While edema gives rise to soft pitting, a degree of induration can be felt if pus is present. A suspicion of edema may be confirmed by applying thumb pressure over the area in cases of massive infiltration and index-finger pressure in cases of localized swelling. This pressure should be maintained for at least 10 seconds. A positive sign of edema is indicated by a depression in the area after the action thumb or finger is removed. The depression is often palpable with the fingertips even if it is not visible.
Fluctuation. All swellings should be tested for fluctuation in two planes at right angles to each other if the swelling is more than an inch in diameter. If a mass fluctuates in one plane but not in another, it is negative for swelling because a swelling fluctuates in both planes. Fat and muscle also transmit an impulse, but they do so in a less perfect manner than fluid.
Moderate swellings are tested for fluctuation by pressure exerted with the tip of one forefinger midway between the center and outer border of the swelling while the tip of the other forefinger is placed at an equal distance on the opposite side but remains stationary. The stationary finger moves passively from the pressure exerted by the action finger on the other side. Then the procedure is reversed, with the originally passive finger becoming the active finger and vice versa. If displacement takes place in two planes at right angles to each other, there is little doubt that the swelling contains fluid. When examining small swellings, it is often best to use two fingers of each hand. A swelling less than an inch is difficult to test for fluctuation. In such a case, Paget's test can be used, which consists of pressing the mass with a fingertip. A solid swelling is hardest in the center, while a cyst is softest in its center.
Myoedema. Myoedema technically refers to an edematous muscle or group of muscles. The term is often restricted to a contractual "lumping" or "mounding" within a wasted muscle after it is sharply struck. This fatigable "knot" is usually located at the margin of percussion. The cause is unknown, and the phenomenon is always symmetric. It is a common occurrence in atrophied pectoral muscles overlying a tubercular cavity in a lung. Other wasting disorders that feature myoedema are acute infections, chronic alcoholism, gastritis, malnutrition, malignant cachexia, myxedema, peripheral neuropathy, and sprue.
Muscle Tone. The typical feeling of a normal muscle upon palpation is one of resilience. An increased perception of tone by the examiner denotes a hypertonic muscle; decreased tone, a hypotonic muscle.
Muscle Mass. Palpation and mensuration are used to determine extremity muscle volume. Upon palpation, there should be a mass that is symmetrical bilaterally. If not, a measurement should be made with a flexible tape from a bony prominence to the belly of a suspected muscle and the point marked with a skin pencil. The circumference of the part should then be measured at that point and then compared with a contralateral measurement. The two sides should be approximately the same circumference unless there is a large degree of unilateral occupational activity. A decrease in size (eg, midcalf or thigh) indicates atrophy and is usually associated with some degree of hypotonicity.
Joint swellings originate from:
(1) swellings arising in the joint proper,
(2) swellings derived from the bones forming the joint, or
(3) swellings originating in the extra-articular tissues around the joint. In diagnosis, the key features of any swelling will be elicited by noting its character, effect on motion restriction, effect on joint positioning, and its shape.
Joint trauma is often profiled by a cool periarticular swelling that is extremely tender. Trauma or inflammation may result in hemorrhage or effusion. Painless bony lumps and asymptomatic joint swelling can often be traced back to forgotten trauma, especially when associated with sports injuries. In degenerative joint diseases, the trauma may be only normal activity that is sufficient to elicit effusion.
A swollen joint is often the result of thickening of the synovial membrane or of excess fluid in the joint cavity. Such swelling is often obscured by bones, muscles, and tendons that overlie 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 posterior aspect.
During the evaluation of a swollen joint, its shape, character, associated motion restriction, and position of the part should be noted.
Shape. The shape of a swollen joint corresponds to that of the synovial membrane distended in toto. For instance, when a subcrural pouch becomes dilated, 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.
Character. Swelling around a joint can be caused by edema from fluid overload or venous insufficiency. If 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. 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.
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.
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 position that gives the greatest relief.
Temperature and Pulse
The taking of oral temperature and comparing various extremity pulses should be routine in any musculoskeletal examination. Traumatic joint injuries are no exception.
Thermography is sometimes used to measure the slightest variations in temperature of soft tissue in the body using infrared heat sensors. The area to be tested is usually placed on a heat-detection device or rapid-scan equipment is utilized to record specific temperatures, either by color changes or a direct display of temperatures. The technique can be used to detect peripheral inflammation most anywhere on the body as inflammation usually raises local temperature. It can often detect vascular disorders that feature inhibited circulation.
Evaluation of pertinent superficial and deep tendon reflexes should be conducted as a standard procedure. Upper-limb reflexes are supplied essentially by C5–T1 segments of the cord; lower-limb reflexes, L2–S3 segments. See Table 1.4.
Table 1.4. Summary of Normal Reflexes
Afferent Nerve Center Efferent Nerve Superficial reflex Anal Pudendal S3–S5 Pudendal Consensual Optic Midbrain Oculomotor Corneal Trigeminal Pons Facial Cremasteric Femoral L1 Genitofemoral Lower abdominal T10–T12 Cord level T10–T12 Nasal (sneeze) Trigeminal Brain stem, Cranial V, VII, IX, X, upper cord and spinal nerves of respiration Plantar Tibial S1–S2 Tibial Upper abdominal T7—T10 Cord level T7–T10 Uvular Glossopharyngeal Medulla Vagus Tendon or periosteal reflex Achilles Tibial S1–S2 Tibial Biceps Musculocutaneous C5–C6 Musculocutaneous Jaw jerk Trigeminal Pons Trigeminal Patellar Femoral L2–L4 Femoral Radial Radial C6–C8 Radial Triceps Radial C6–C7 Radial Visceral reflex Accommodation Optic Occipital Oculomotor Bulbocavernous Pudendal S2–S4 Pudendal Carotid sinus Glossopharyngeal Medulla Vagus Ciliospinal Sensory nerve T1–T2 Cervical sympathetics Light Optic Midbrain Oculomotor Oculocardiac Trigeminal Medulla Vagus
Limb Length, Circumference, and Width Measurements
A suspicion of limb shortening as the result of structural telescoping or shortening can be enhanced by axial measurements. Measurements of anatomical lengths should be taken between well defined, stable (eg, bony) reference points.
Measurements for extremity length and circumference should be made when the part is relaxed in a normal position. Circumference measurements should be taken bilaterally at equal points above and below the involved joints and compared. When the measurement of width is indicated (eg, extremity joint, pelvis, skull), measuring calipers can be used. Such measurements are helpful in determining the existence of local swelling or atrophy.
Goniometry: The Measurement of Joint Motion
The measurement of joint motion is an important evaluative procedure in physical examination of the joints for it offers an accurate record of joint motion and extent of disability as part of a patient's permanent record. The most common methods of measurement employ the goniometer, either the 180 system or the 360 system. Both systems depend on the fact that a long bone is like a lever rotating around a fulcrum; and when it moves, it describes the arc of a circle. It is this arc that is used in determining the amount of joint motion, and the goniometer is used to measure the angle produced between two bony segments when the maximum motion in a particular plane has been made.
Debrunner points out that goniometry will yield correct measurements if:
(1) the axis around which the joint moves is accurately determined;
(2) the fulcrum of the goniometer lies on the axis of rotation of the joint, and
(3) the plane in which the motion takes place has been clearly defined (eg, the sagittal, frontal, or transverse plane).
Joint Motion Evaluation
A patient suffering musculoskeletal pain will typically refer to one or more particular joints as the source of their affliction. The basic decision that must be made by the physician is whether the lesion is:
(1) within the joint (articular),
(2) periarticular (around the joint; involving muscles, ligaments, or bursae), or
(3) the target of referred pain. Most but not all articular disorders manifest pain on movement in all directions. Most but not all periarticular disorders exhibit pain on movement in some but not all directions. Relatively pain-free passive motion suggests a referred pain syndrome. Tenderness helps in differentiation, but tenderness can be referred.
The examination of the musculoskeletal system must be greatly adapted in examining an acutely injured patient from that of a patient presenting nontraumatic complaints. For instance, it is a safe procedure not to conduct active and passive ranges of motion until after roentgenograms have demonstrated the mechanical integrity of the joint. If contraindications are not found, active ranges of motion should be evaluated. The joint should then be simultaneously palpated during passive motions to determine the presence of restrictions and crepitation. Bone integrity is determined by its ability to resist a deforming force.
Joint motion limitation may be the result of:
(1) pain associated with movement,
(2) bone or joint instability (eg, muscle weakness, fracture, torn ligament), or
(3) restricted joint movement by subluxation, effusion, muscular spasm, thickening or adhesions in the capsule and periarticular structures, and obstruction by bony overgrowths or gouty tophi. Excessive motion found unilaterally such as with joint tears is recognized simply by its contrast with the limits furnished us by our knowledge of anatomy and physiology of joint motion at different ages. Excessive motility may be due to destruction of bone and other essentials of the joint.
Resisted Joint Motion
The purpose of passive resistance to active motion is to reveal and isolate pain, weakness, hypermobility, hypomobility, and associated patient reactions. During such a test, it is important that the joint be held near mid-range, the resistance must be strong enough to avoid joint motion, and, when possible, specific muscles should be isolated. The general interpretations of responses to resisted motion are shown in Table 1.5.
If resisted motion in opposite or incompatible directions induces pain, a muscle lesion is highly unlikely; rather, a nonmuscle lesion should be suspected near the site of attachments of the involved muscle. For example, resisted motion will exhibit pain in periosteal tears, fractures, bursitis, or when a tender structure (eg, an abscess, neuroma) is compressed by a muscle.
Table 1.5. General Interpretation of Resisted Motion Signs
Response Probable Cause Strong with excessive range of motion Capsule laxity, ligamentous instability. Strong and painful in a specific direction Minor musculotendinous lesion. Strong and painful in all directions Neurosis. Strong with pain on repetitive Arterial flow deficit. resisted movements. Strong and unchanged pain in all Referred pain syndrome. directions. Strong, painful, and hypomobile Guarded joint for some reason. Strong, painless, and hypomobile Contracture, adhesion. Weak and sharply painful Fracture, dislocation, rupture, gross pathology. Weak without aggravation of pain (painless or unchanged constant pain) Neurogenic disorder, muscle or tendon rupture. Weak and painless in all directions Nonmusculotendinous deficit, probable neurogenic lesion. Pain only at specific point of arc Functional entrapment, lax joint, dislocated tendon, loose body. Pain at one range extreme Subluxation, tissue entrapment, eroded cartilage. Painful with gross hypermobility Severe sprain. Painless with gross hypermobility Ruptured tissues with interrupted sensory path.
Testing Limb-Muscle Strength
Muscle power should be judged when there is:
(1) a complaint or sign of weakness or incoordination or
(2) a need for an aid in subluxation analysis and in evaluating correction. Note that muscles often test differently in various positions (eg, from prone or supine to upright weight-bearing positions).
An attempt should be made to evaluate one muscle at a time, thus the patient should be requested not to recruit allied muscles during resistance. Caution should be used during resistance to avoid creating cramps, stretch injuries, or excessive fatigue.
In testing muscle strength, the patient is asked to perform various muscular actions against the examiner's resistance. For example, the patient should press the thumb and middle finger of the same hand tightly together, and the examiner should try to pry the fingers apart with the patient resisting. Normally, it would be difficult for the examiner to do so. Another example would be to have the patient flex or extend an arm or leg against the examiner's resistance. The strength of an involved joint should be tested, compared bilaterally, and the results noted.
Factors Affecting Normal Muscle Contraction
A study by MacDonald/Stanish showed that the mechanical factors governing muscle contraction are:
(1) the angle of pull,
(2) the length of the muscle, and
(3) the velocity of muscle shortening. The optimum angle of pull is at a 45 joint angle, and a muscle fiber's contractile force is greatest during extension. Obviously, a long muscle fiber can shorten more than a short fiber. Parallel to this is that a suddenly prestretched muscle has an increased contractile capacity.
Besides these mechanical factors, temperature and flexibility should be considered. Hill's studies showed that a muscle's speed of contraction can be increased 20% by raising body temperature 5*F, thus the benefit of adequate warm-up before athletic participation is underscored. Reducing muscle temperature appears to increase the threshold of irritability, which causes weakened and more sluggish contractions. Improved flexibility through static stretching exercises, which do not activate the stretch reflex, appears to reduce soft-tissue restrictions and enhance antagonist relaxation.
A dynamometer offers the examiner four data:
(1) muscle strength,
(2) fatigue rate,
(3) recovery rate, and
(4) a comparison between ipsilateral and contralateral muscles. Three readings are usually taken in sequence to show strength, fatigue, and recovery rates. While initial readings are helpful in diagnosis, subsequent readings are helpful in determining the patient's rate of recovery. Some clinicians use a dynamometer to also measure the response strength of tendon reflexes.
The major problem with manual methods is that evaluation rests a great deal upon the subjective skill of the examiner. Thus, it is important that the same examiner records initial and follow-up evaluations of the degree of muscle "resistance." The criteria shown in Table 1.6 are commonly used in recording muscle strength.
Table 1.6. Grade of Muscle Strength
Extent Rating Findings Grade 5 100% Normal Full range of motion against gravity with full resistance. Grade 4 75% Good Full range of motion against gravity with some resistance. Grade 3 50% Fair Full range of motion against gravity. Grade 2 25% Poor Full range of motion with gravity eliminated. Grade 1 10% Trace Evidence of slight contractility, but no joint motion. Grade 0 0% Zero No evidence of contractility.
In recent years, several companies have developed more objective but relatively expensive equipment designed to measure resistive forces and display the value on a dial or digital readout display. The Digital Myograph, Cybex, Biodex, Kin-Com are typical examples.
An accurate, inexpensive adaptation (invented by Dr. John Palo) to a Jamar dynamometer has proved quite useful in measuring the strength of most muscles. A 1/4-inch-thick 3 X 8-inch leather strap with a 3/4-inch diameter hole at each end is used. The dynamometer prongs are inserted into the holes of the leather strap. Tension applied to the strap from the muscle being tested (as the doctor holds the dynamometer) registers the strength of the muscle or group of muscles being tested.
Palo suggests that, "Until standards of dynamometer placement and normal ranges of readings can be ascertained, we would be wise to follow the advice of Hippocrates; ie, compare the relative strength of the abnormal muscle against that of the normal muscle tested in the same manner. In evaluating the upper extremities, allow for the individual's handedness."
Electromyography (EMG) allows the recording of oscillations in potential variations of skeletal muscles at rest and during activity. Basically, it offers a tracing of electrical activity transmitted from muscle to an electrode and then to an oscilloscope. This neurologic test studies the potential of muscle at rest, the reaction of muscle to contraction, and the response of muscle to external stimulation.
Such tracings aid in determining whether a patient's illness is directly affecting the spinal cord, muscles, or peripheral nerves. EMG recordings help to establish the scientific basis for both diagnostic conclusions and to monitor the effectiveness of therapy. Accurate analysis, however, requires specialized training.
The use of EMG can be placed in several broad categories. EMG is frequently used to evaluate the amount of muscle activity occurring in specific muscles, and it can be used to study kinesiologic function of muscle. The general rule is that there will be less EMG activity in eccentric contractions as compared to concentric contractions. It can be used in pathologies to determine the nature, scope, and prognosis of diseases involving neuromuscular function. It can be used to differentiate between neurogenic and myogenic paralysis and differentiate between organic paralysis and psychogenic reactions. Thus, if muscle weakness is exhibited, an EMG will determine whether the loss of power is caused by a deficit in impulse transmission (eg, myasthenia), myopathy, or neuropathy.
EMG is valuable in localizing a disorder within the peripheral motor neuron and differentiating between lesions of first-order and second-order neurons. It has also been shown to be effective in differentiating between pyramidal and extrapyramidal hypertonicity, in the analysis of tremor, in assessing myotonic and myasthenic disorders, in evaluating the success of therapy, and in arriving at a prognosis in traumatic and neuritic lesions. In its most common application, EMG provides objective evidence of partial muscle denervation.
Electrodiagnosis is used to test the integrity of muscles and nerves. As a common adjunct to the physical examination of the motor system, it has become a valuable tool in evaluating if partial degeneration of a nerve or muscle fibers is suspected. Such tests:
(1) help to determine if disease of the upper or lower motor neuron is being dealt with,
(2) help to determine if the nerve is interrupted, and
(3) help to determine if the muscles are undergoing degeneration.
Low voltage currents are used in the process, and the degree of reaction gives the practitioner an idea of the extent of disability present. Innervated muscles normally react to electrical stimulation; however, several situations exist in which normal responses are not seen.
Blood, urine, and other analyses should be used whenever the clinical picture of the joint disorder warrants it. The most commonly utilized profiles are:
- Blood sugar
- Platelet count
- Blood uric acid
- R-A test
- CBC and differential
- Sedimentation rate
- Coagulation profile
- Febrile agglutins
- VD serology.
- Hemoglobin level
Urine and blood cultures, vaginal smear, EMG, ECG, and thermography are often added to the above list. Serum calcium, phosphorus, alkaline and acid phosphatase, and serum protein electrophoresis are useful tests in determining the cause of bone lesions. If suppuration within a joint is suspected, referral for aspiration and its analysis may be necessary.
BASIC CONSIDERATIONS IN DIAGNOSTIC IMAGERY
Joint abnormalities exhibit significant alterations in structure, symmetry, continuity, positional relations, length and breadth, cartilaginous joint space, and density. Calcareous density is much greater than muscle density, fat density is much less than muscle density, and gas density is far less than that of fat density.
Radiographic findings should be used to confirm or dispose of suspicions arising during the history and physical examination, and not to be the sole basis of the diagnosis. Once relevant features have been found to classify an abnormality, a search should then be made for those details which enable it to be distinguished from others in the same class. This takes careful evaluation of frequently subtle soft-tissue changes that confirm osseous alterations. The examiner must be well acquainted with the nature of all substances visible on a film.
Along with roentgenography of distressed joint(s), spinal and chest films are usually included if the possibilities of referred pain or systemic symptoms are involved.
The area between adjacent articular cartilages may be wide, thin, or unbalanced. Function has a major effect on joint cartilage thickness. The frequent movements and increased motions of athletes tend to thicken cartilage, while a lack of motion tends to decrease thickness by atrophy or underdevelopment. Joint imbalance in the extremities is commonly seen in the knee, indicating a derangement of the meniscus on the thin side, especially if there is no other feature except effusion. The medial side may appear thin, while the lateral side will be abnormally wide or vice versa.
Increased joint space in the extremities is characteristic of capsule distention from massive effusion, overdevelopment of cartilage, a delayed conversion of cartilage into osseous tissue, or a mass or tumor-like development.
The area may be reduced by atrophy, cartilage underdevelopment, excessive conversion of cartilage to bone, fibrous degeneration, or destructive disease processes.
Fat Pad Alterations
Fat pads help to outline the contour of and view the thickness and smoothness of adjacent articular cartilage. Clear visualization of some tendons (eg, patella, calcaneal) is made possible on lateral films by adjacent fat pads, helping in the evaluation of stenosing tenosynovitis. Most normal soft-tissue structures show little difference in film shadows except fat, which shows as a radiolucency. Warts and sebaceous cysts can produce opacities that can be confusing. Although calcification of a fat pad is rare, it most commonly occurs around a joint after trauma, presenting a picture of minute and multiple amorphous calcifications resembling thin rods in the early stage. Later, they appear more nodular and can sometimes be confused with a tumor.
Masses and Swellings
Soft-tissue enlargements generally tend to have a spherical outline and a definite limit that differentiates them from healthy tissue. Swellings, on the other hand, tend to be elongated rather than spherical and blend into unswollen tissues without a sharp demarcation. Effusion is suggested when a joint capsule becomes visibly distended by accumulated material that has the density near that of muscle tissue. If a joint is well supplied with fat pads (eg, patellar, calcaneal), distention is usually quite clear.
Inert swelling has features that differentiate it from reactive swelling. Unless its density is extremely close to that of near tissue, inert swelling tends to present a peripheral limit. Poor demarcation of its sides is characteristic of a reactive swelling. This is the result of increased vascularity that fades peripherally in adjacent tissues and the reaction to infectious irritation. The poor demarcation is especially prominent if fat is near the edge of the swollen tissue. The normally invisible deep, abundant, minute vessels become visible and exhibit faint perpendicular striations deep within the tissue.
Ossification vs Calcification
Ossification is the result of accumulated material of bone density that exhibits osseous structure when it is laid down. It has rounded smooth corners, internal reticulation, and a line of continuous calcareous density at the periphery representing the cortex. Common calcareous densities within soft tissues include the ossification seen in sesamoid bones, sesamoidomas, and accessory bones. Calcification, on the other hand, is the result of accumulated material of bone density that is initially amorphous. During calcification, bone structure develops slowly and indirectly, thus some areas at the periphery will most likely still be amorphous. Distinction between ossification and calcification is beneficial in identifying many roentgenographic features relevant to sports injuries.
Calcification in soft tissue has a marked relative increased density, usually homogenous in character. Two forms are seen:
(1) The most common form is dystrophic calcification. It is associated with local tissue degeneration and reduced blood supply causing low tissue vitality from disease or old age. Dystrophic calcification is usually found in costal and laryngeal cartilages, lymph glands, pericardium, pleura, adrenals, thyroid, uterine fibroid, hypernephroma, dermoid cysts, tuberculous foci, and intracranial calcifications.
(2) Less commonly, metabolic calcification occurs in previously normal tissues. It occurs in hyperparathyroidism and some cases of chronic renal insufficiency.
The difference between calcification and ossification is difficult to recognize and is only possible when definite bony trabeculation can be visualized. Bony spurs are often found at tendinous and ligamentous insertions. The most common sites are the os calcis, olecranon, patella, and external occipital protuberance. They are usually produced by repeated minor trauma but seldom are of clinical importance.
Most soft-tissue calcareous densities are abnormal. Typical examples include arteriosclerosis, phleboliths, calcareous loose bodies, chondromatosis, posttraumatic calcifications, and postinfection calcifications.
The possibility of traumatic or pathologic fracture must be eliminated before adjustive therapy. Pathologic fractures of bone may accompany a vast list of disorders that produce bone weakness or brittleness.
The earlier and the more accurately a fracture is reduced, the sooner function will be restored and the smaller the callus result. Dislocations often involve severe joint impaction and fragmentation. They usually produce great instability and require operative repair. If a recent fracture is found, referral to an orthopedist is the general rule. The two common exceptions to this are simple fatigue fractures and joint comminutions. Obviously, the decision to treat even these types of fractures will be determined by the state legislated chiropractic scope of practice and the practitioner's expertise in treating the situation at hand.
Intra-articular fractures involve the articular surfaces of joints and the associated articular cartilage. Osteoarthrosis results if reduction is not accurate. However, a displaced fragment need not be removed if it does not interfere with function by impingement.
When fractures involve joints, the prognosis should always be guarded because it is difficult if not impossible to accurately judge the damage to soft tissues or what effect their repair will have on function strictly through roentgenography. Synovial lining is slightly phagocytic, is regenerative if damaged, and secretes synovial fluid, which is a nutritive lubricant that has bacteriostatic and anticoagulant characteristics. This anticoagulant effect may result in poor callus formation in a situation of intra-articular fracture where the fracture line is exposed to synovial fluid.
Physical Features of Fractures and Dislocations
An initial working diagnosis of fracture or dislocation may be based on any one of several physical features. Additional assistance in diagnosis may be obtained from the history and roentgenography. A history of falling, receiving a blow, or of having felt or heard a deep snap may help in the discovery of more evidence such as:
Tenderness over the site of injury. Tenderness or pain upon slight pressure on the injured part may indicate a fracture or dislocation.
Swelling and discoloration. These signs at the site of injury increase with time and may indicate bone fracture or displacement. The swelling is due to the accumulation of tissue fluid and blood. When blood collects near the surface of the skin, a bluish discoloration may be seen.
Abnormalities with movement. Deep, sharp pain upon an attempt to move the bone is presumptive evidence of fracture or dislocation. Grating of bone ends against each other indicates fracture. Movement, however, should rarely be attempted to see if crepitation is present as it causes further damage to the surrounding tissues and promotes shock.
Deformity of the part. Unnatural depression or abnormal flexion may indicate fracture.
An obvious fracture is noted on film by the lack of normal contour, continuity, organizational structure, and the spiculated surfaces of the fragments; however, difficulty occurs when the division takes place within a cartilage line whether it be a normal or accessory line or one in an unexpected place.
In traumatic cartilage fracture, the line normally tends to exhibit even width throughout its length with fairly straight and smooth abutting bone surfaces. At the ends of the line, the bone does not tend to be angular, but rounded. In contrast, a bony fracture line tends to be wider at one end than the other with sharply irregular bone surfaces on the line. At the ends of the line, the bone is definitely angular rather than rounded. With reparative change and sclerosis, an old fracture line may be smooth with rounded margins.
Long Bone Fractures
Long bone fractures exhibit typical evidence such as a fracture line, a break in outline, and sometimes deformity. One exception to this picture is that of the "torus" fracture seen in children where buckling of the cortex occurs and there is no visible fracture line or it is seen as a line of increased density. As healing occurs within a torus fracture, a variable amount of callus formation may be seen.
Fractures within long bones may result without direct trauma strictly via muscle exertion if the bone has been previously weakened by the presence of cysts, malignancy, or constitutional disease. With the exception of underlying bone cancer, these fractures tend to heal well.
Bone-fatigue fractures may be the effect of an improper relation between overstress and adaptability of bone. The most common example of this is the so called "march foot" of infantrymen and new track recruits. It is the result of subjects being overstressed in running practice (or forced marching) without adequate preliminary conditioning.
Hairline fractures, where a true fracture line is not clear, may develop in weight-bearing bones after trauma. These will usually not be evident in films taken immediately after injury. Often 7–10 days must elapse before they can be visualized. On occasion, they are seen only by overlying periosteal elevation, callus formation, and not by a readily detected fracture line. If symptoms persist without change for 7–10 days after trauma despite negative films taken immediately after the injury, new films should be taken to rule out fracture.
Dislocations may occur at any joint, but they are more common in the shoulder, elbow, wrist, and hips. Except for posterior shoulder dislocations, most are obvious in radiographs.
Dislocation places considerable stress on soft tissues that normally maintain joint position. There may be injury to muscles, tendons, ligaments and the capsule they form around some joints, articular cartilage, synovial membrane, as well as hemorrhage into or around the joint. A misplacement may result in a complete luxation that spontaneously reduces into a subluxation and be associated with considerable capsule and ligament damage. Pain, swelling, and deformity are centered about the joint. There is usually a loss of function.
Emergency Immobilization (Splints)
To prevent further damage during referral, a fractured bone must be immobilized by immediately splinting the joints above and below the fracture, as movement of these joints would move the bone segments. All splints should be well padded to protect the skin from injury, loss of circulation, inflammation, and infection.
Bandages used to secure a splint must not be applied so tightly that they impair circulation even for a few minutes. A bluish discoloration of the nailbeds or skin of the affected limb indicates that one or more bandages are too taut. Security bandages should never be tied directly across a wound or bruise.
In limb fracture, the pneumatic inflatable splint is especially useful as it offers both immobilization and compression to minimize hemorrhage. It must be applied only tight enough to support the fragments without inhibiting circulation. To immobilize a fractured bone in the thigh or hip, an improvised splint must extend from the groin and the armpit to several inches below the foot. Padding should extend over the ends of the splint at the groin and the armpit.
A dislocation is immobilized during referral in the same way as a fracture: close to the joint. Related ligaments are frequently torn and require surgical repair. Cold compresses may be applied to the joint to relieve pain and reduce swelling, but the patient's temperature must not be lowered to invite shock.
Postreduction immobilization of a dislocation usually requires 6 weeks in the lower extremity and 3 weeks in the upper extremity. Inadequate care, especially in ankle and shoulder dislocations, leads to chronic weakness, movement restrictions, instability, and recurrent dislocation wherein subsequent surgery has a poor prognosis in restoring preinjury status. Except for recurring dislocations, almost all dislocations require anesthesia before reduction.
Bones break or dislocate from either direct blows or indirectly such as a fall on an outstretched hand resulting in an injury of the wrist, forearm, elbow, shoulder, or clavicle. It is thus imperative that the injured person be examined as a whole. For example, even if a fall on the outstretched hand does not result in fracture, dislocation, strain, or sprain, a rib or spinal subluxation may result. The inexperienced doctor may overlook a slipped femoral capital epiphysis in a patient whose complaints are restricted to the knee. The list can go on and on.
Soft-tissue damage is usually more painful and can be more serious than bone injury. Bone heals with calcium, whereas soft tissue heals with fibrous or scar tissue. The latter is different from the original soft tissue and lacks the elasticity or viability of the original tissue. Soft tissue also takes longer to heal than bone tissue. Bone tissue may actually be stronger after the healing process has taken effect, whereas soft tissue is usually weaker after repair.
Muscular contusion is a disturbance of muscle tissue in the nature of a bruise resulting from a direct force over the muscle. Usually, there is no or little accompanying disturbance to the skin or subcutaneous tissues. The thigh and upper arm are most commonly involved. After contusion, there are local swelling, tenderness, pain on motion, and often ecchymosis (which does not appear until hours after the injury occurred). Unlike strains and muscle ruptures, there is little or no disturbance of function.
Following repeated intermittent trauma to a muscle, the normal resolution is interrupted, fibrous scarring occurs in the hemorrhagic area, and this is frequently followed by calcification (myositis ossificans).
Myalgia and Related Conditions
Any type of excessive motor fiber stimulation results in pathologic, involuntary, and painful muscle spasm. Keep in mind that severe spasm must place considerable tension on highly sensitive periosteum via its tendon attachment.
It is one thing to find muscle spasm present and another to determine if it is protective, compensatory, hysterical, or a causative factor. Careful analysis of the dynamic motion of the involved joint is an important method of gaining differential clues. Limitations of motion due to spasm are seen with special frequency in joint pathology and subluxation syndromes, but they may occur in almost any form of joint trouble, particularly in the larger joints.
Spasm may be due to irritation, stretching, or pressure upon a nerve trunk or plexus; irritation or pressure upon peripheral nerve branches; muscle spasm secondary to trauma of an adjacent structure; primary muscle spasm from direct irritation or trauma; toxic irritation of the anterior horn cells; or psychogenic muscle spasm.
Peripheral spasm may be the result of encroachment irritation of a nerve root. It is for this reason that chiropractic spinal adjustments have corrected many cases of chronic shoulder, arm, and knee pain that have been previously treated medically or surgically only at the site of pain.
Muscle pain has its peculiar characteristics. The pain that arises from an injury to muscle tissue may be elicited by making the muscle contract against resistance without allowing it to shorten; ie, preventing movement of adjacent joints.
This test, although it may be of help in differentiating myalgia from the pain of other etiologies, is not absolute because it is not always possible, even with great care, to avoid some indirect pressure or tension on adjacent structures. An additional feature is that pain arising from a chronic contraction of the involved muscle is not increased by contracting the muscle further.
The myotatic stretch reflex uses a single sensory neuron and is initiated by stretching the muscle spindle's annulospiral receptors. The effect is a protective contraction, designed to protect against further stretch so that the muscle may maintain a constant length. This reflex action is several times more severe if initiated by a sudden stretch (eg, jerk, dynamic thrust) than by a slow stretch. In addition, inhibitory impulses are transmitted to the motor neurons of the antagonists (reciprocal inhibition) and facilitating impulses are transmitted to the synergists both of which enhance the response. The stretch reflex is not normally initiated by voluntary contraction.
Striated muscles, especially the erectors, become painfully splinted (intrinsically immobilized) by spasm, active or involuntary, when they are fatigued. In time, trophic changes occur and tone is lost. Splinting differs from ordinary spasm in that relaxation of the affected muscles occurs at rest.
Prolonged pain from bone, muscle, tendon, and joint lesions with resultant long-term splinting or pseudoparalysis may lead to eventual osteoporosis in involved and possibly adjacent bones. Joint contractures may also develop. This is an example, similar to a psychic conversion symptom, where a sensory symptom may lead to definite structural changes.
If there is spasm present after trauma, the irritating focus can usually be attributed to irritating ischemia initially and blood debris later. For some unknown reason, prolonged states often establish a self-sustaining reflex spasm that continues after the initial cause has been erased.
Musculoskeletal disorders are frequently associated with muscle cramps. These are powerful involuntary muscular contractions shortening the flexor muscles that result in extreme, often incapacitating, pains stimulated by ischemia and hypoxia of muscle tissue. There are two types of extremity muscle cramps:
(1) cramps associated with prolonged exercise and
(2) nocturnal cramps. The exact cause in either case is unknown.
A large number of localized tender sites, widely dispersed and symmetrical, suggests fibrositis. In contrast to fibrositis, a few points clustered in a single region and unassociated with diffuse aching stiffness and fatigue suggest a referred pain syndrome. Smythe describes 14 sites commonly found in fibrositis. They are listed in Table 1.7. He urges that they be tested within the routine of every standard clinical examination.
Table 1.7. Common Sites of Fibrositis
Name Bilateral Locations Low cervical Anterior surface of intertransverse spaces C5–C7 Trapezius Center of upper fold Costochondral Just lateral and cephalad to 2nd costochondral junction Supraspinatus Near the scapula's medial border, above the scapular spine Lateral elbow About 1-1/2 inches distal to the lateral epicondyle, in the lateral intermuscular space ("tennis elbow" point) Low lumbar L4–S1 interspinous ligaments Gluteus medius Superior-lateral aspect of buttocks (deep) Medial fat pad Over superomedial knee ligaments, cephalad to joint line
Although skeletal muscle tissue lacks an intrinsic lymph supply, a muscle's connective-tissue sheath and tendons are richly endowed with lymphatic vessels. During the normal physiologic exchange of fluids through capillary walls, the quantity of fluid leaving the capillary is usually greater than that entering the venule. The related lymphatic network takes up the excess and eventually delivers it to the venous system. It is this process that allows a continuous exchange of tissue fluids and maintains a constant pressure of interstitial fluid.
Lymph flow is increased during activity as is capillary circulation, but the flow can be impeded by excessive pressure exerted by a constantly hypertonic or phasic contracted muscle. De Sterno shows that inhibited lymph drainage contributes to muscular pain during prolonged activity by:
(1) causing a buildup of interstitial fluids that increases hydrostatic pressure and
(2) encouraging the accumulation of metabolic waste products that would normally be drained by the lymphatics and venules.
Pain may arise from any joint tissue containing nociceptors such as ligaments, tendon insertions, periosteum, fibrocartilages (slightly), capsules, and vascular walls. Authorities differ in whether synovium contains nociceptors; most believe that it does not.
Hemarthrosis vs Traumatic Synovitis
The correct differentiation of joint swelling between hemarthrosis and synovitis is an important part of any joint examination following trauma. This differentiation is important because joint aspiration is usually contraindicated in simple synovitis but early aspiration is almost mandatory in hemarthrosis. See Table 1.8.
Blood within a joint is an irritant, easily becomes a site of infection, and may resolve into iron deposits, fibroblastic proliferation, and severely restricting adhesions. Synovial fluid is normal within a joint, and excessive amounts will be readily absorbed with rest and applications of elevation, cold, and pressure unless the cause of the swelling remains (eg, repeated trauma).
Table 1.8. Differentiation of Posttraumatic Joint Swelling
Hemarthrosis Synovitis Rapid onset Slow onset, may not occur for 24 hours Small periarticular swelling Large periarticular swelling Hot, painful joint Warm, aching joint
Irritated ligaments become painful by stretching and deep pressure. Periarticular ligaments, and even deeper ones, can be stretched by passive movements of the related joint to the limit of their range of motion. When accessible to palpation, an irritated ligament will be tender; and if it can be squeezed, pain will be evoked.
Ligament pain develops when a joint is under extremely prolonged tension, and a hypomobile joint should be the first suspicion in such cases. Generally, chronic pain arising from ligaments comes on slowly after assuming some posture in which the involved joint(s) are held at a limit of motion. The ache arises from the stimulation of intraligamentous and periosteal receptors.
Pain from damaged tendons usually arises when the attached muscle is contracted. The torn tendon fibers will usually not cause pain when the muscle is relaxed; but, with the least muscle shortening, pain arises. The pain of true tendinitis is often superficial, resulting from a tenosynovitis. It is evoked by passively moving the tendon to and fro within its sheath.
Adhesions in themselves do not contain nociceptors. During movement, however, pain may arise when they stretch or occlude adhering, connecting, or congruent pain-sensitive tissues (eg, periosteum, vascular walls, joint or visceral capsules). The cause may be from direct compression or tensile forces or be the product of ensuing stasis, ischemia, or distention. The pain is immediate in onset and not delayed as when the ligaments are relaxed. Another diagnostic clue is that there is a pronounced structural hypomobility when adhesions are present.
A most common situation encountered is the painful adhesions that develop after surgery or major trauma. However, adhesions may develop naturally as the result of adhesive capsulitis, rheumatoid arthritis, and septic arthritis. The pain originating in capsules tightened by adhesions occurs immediately when the capsule is stretched. If the adhesions are stretched further, a sharp pain may ensue, leaving the surrounding muscles flaccid. The intensity of such a pain varies with the site and size of the adhesions. For the most part, pain arising from adhesions is only momentary because motion is quickly halted as soon as the sharp pain is felt.
As with adhesions, pain arises from most cartilaginous tissues only when they are displaced or swollen and stretch or pressure is applied upon adjacent pain-sensitive receptors. The peripheries of most fibrocartilages (eg, IVDs, menisci of the knee and jaw) contain 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 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.
When considering bone-originating pain, we must recall whether the structure involved is compact or cancellous and if any increased pressure is involved. Compact bone is, for the most part, insensitive to painful stimuli. Most of the pain sensitive fibers within the medullary portion of bone are those few located within vascular walls. The periosteum, however, is richly supplied with nociceptors.
Neurogenic pain manifests within the involved nerve's distribution, on the surface or deep, and it usually radiates. There is an excessive response to stimulation. It is difficult for the patient to describe its character as it is unlike any other type of pain and usually is a combination of painful sensations. It is provoked by any peripheral stimulation in the involved zone, and stimulated trigger points cause spontaneous paroxysms. The patient vigilantly guards the involved part and shows great apprehension.
Pain that is accentuated by heat points to neuritis or congestion. In contrast, pain that is relieved by heat suggests something producing abnormal myotonia. Pain of intrinsic neurologic origin is generally accompanied by paresthesias and root signs. When throbbing pain is present, vascular congestion, crush syndrome, a vasomotor disturbance, or possibly Paget's disease should be the first suspicions.
Pain in the extremities may originate from muscle, skin, bone, ligaments, joints, arteries, veins, and lesions of the nervous system. Muscle etiologies commonly include trauma, systemic infection, altered circulation, inflammation, and neoplasms. Pain from lesions of the nervous system may originate from:
(1) CNS lesions,
(2) spinal root and plexus lesions (eg, nerve root lesions, lesions of the brachial or lumbosacral plexuses), or
(3) peripheral nerve disease from trauma, entrapment neuropathies, reflex sympathetic dystrophy, or peripheral neuritis. Thus, limb pain may be the result of almost any structural disorder of the extremities or a disturbance elsewhere where the sensory phenomena are referred to the limbs.
A thorough history will frequently reveal the point of origin of extremity pain by its peculiar location and quality. The cause may be of mechanical, chemical, thermal, toxic, nutritional, metabolic, or circulatory origin, or a combination of several of these factors, depending upon the nature of the pathologic process involved. The most important clues toward determining cause —type of pain, its distribution, and its associated symptoms— are the result of a detailed case history.
Peripheral nerve disease will sometimes indicate a history of an entrapment neuropathy. Nutritional disorders may result in a polyneuropathy because of unfavorable metabolic activities within the neural apparatus. When an inflammatory process (eg, neuritis) involves sensory fibers, pain (neuralgia) is frequently perceived along the total course of the nerve.
Pain may be referred along a somatic dermatome because of visceral inflammation, ischemia, or a tumor (eg, the shoulder-arm pain associated with myocardial infarction or angina). Such pains have two major features in common:
(1) their distribution is limited to an anatomical dermatomal pattern, and
(2) interruption of the nerve's function by any means will alleviate the symptoms (at least temporarily).
Key muscle, skin sensation, and reflexes utilized in routine examinations are shown in Table 1.9.
Table 1.9. Common Myotome Tests, Dermatome Tests, and Reflexes
Segment Key Motions to Test Key Sensory Areas to Test Reflex C4 Shoulder shrug, diaphragm action C5 Shoulder abduction, external rotation Biceps C6 Wrist extension, elbow flexion Thumb, index finger, radial edge of hand Biceps, triceps C7 Wrist flexion, elbow extension Middle fingers Radial, triceps C8 Ulnar deviation of wrist, thumb abduction Ring and small finger, ulnar edge of hand Radial T1–2 Finger approximation Ciliospinal T7–9 Upper abdominal T10–12 Lower abdominal L1 Cremasteric L2 Hip flexion Medial thigh Patella L3 Knee extension, hip flexion Anteromedial and distal thigh Patella L4 Knee extension, ankle dorsiflexion Medial surface of large toe Patella L5 Ankle eversion, large toe dorsiflexion Web space between large toe and 2nd toe S1 Plantar flexion, ankle eversion, knee flexion Beneath lateral maleolus Plantar, Achilles S2 Plantar flexion, knee flexion Back of knee Plantar, Achilles, bulbocavernous S3–4 Saddle region Anal, bulbo-cavernous
Neuralgia is a general term that refers to any sharp, severe, stabbing, paroxysmal, remittent pain with temporary abatement in severity that travels along the course of one or more nerves. The pain is usually associated with tenderness along the course of the nerve and violent episodic spasms in the muscles innervated. Although the term neuralgia is nondiagnostic, it is often used in situations where the exact etiology and pathology involved are idiopathic.
Neuralgia rarely subsides spontaneously. It is often so severe that the victim becomes totally incapacitated and frequently addicted to narcotics. Depression is often associated, and suicidal tendencies are not infrequently seen. Usually, morphologic changes cannot be detected early in a pure neuralgia or neurodynia. The term neurodynia is sometimes used to describe a similar pain that is less severe, ie, a deep ache.
Hyperalgesia literally means an excessive sensitivity to pain. A painful tenderness produced by external pressure frequently results from trigger points, traumatic lesions of sensitive subdermal tissue, the development of a toxic accumulation, or a deep-seated inflammatory irritation. An extremely "ticklish" person is one whose superficial reflexes (skin and muscles) are very lively, thus a low pain and temperature threshold can be anticipated.
Pottenger pointed out that hyperalgesia of soft tissues is not uncommon in the areas that have been the seat of reflex sensory pain. For example, subcutaneous soreness within the shoulder and upper arm muscles is often associated with inflammatory diseases of the lungs. He also reported that cutaneous hyperalgesia is a common finding in visceral disease.
Hyperalgesic skin frequently overlies an area of pleurisy, a tubercular cavity, a peptic ulcer, or an inflamed ovary. Zones of hyperalgesia (often associated with precapillary vasoconstriction and hypermyotonia) are more commonly associated with acute and subacute visceral disease than with chronic disorders.
The term causalgia refers to an agonizing burning pain, usually associated with severe trauma, that is essentially a reflex vasomotor dystrophy. It consists chiefly of sympathetic phenomena. It is often followed by organic changes such as bone atrophy and mottling, resulting from persistently recurring nutrient artery spasms as well as skin and muscle dystrophy and atrophy.
The ischemia from the vasospasm produces an excruciating, diffuse burning pain that may involve either or both the lower or upper extremities. Joint immobility with or without pain, scleroderma, and contractures may occur. Emotional disturbances are often associated. Any slight thermal, tactile, sensory, or even psychic stimulus may produce an explosive attack.
Vigorous muscle activity can lead to three common clinical problems:
(1) muscle soreness,
(2) exercise cramps, and
(3) various degrees of strains. In strain, both intrinsic or extrinsic muscle overstress produces partially or completely torn muscle fibers, connective tissues, and vessels within a muscle belly or at its points of origin or insertion. Muscles that cross two joints (eg, hamstrings, deep spinal muscles) seem to be the most vulnerable to strain.
A strain cannot affect a muscle and not the tendon or vice versa; if it affects one part of the unit, it affects the other. Thus, the musculotendinous unit must be considered as a whole in cases of strain.
Muscle and Tendon Dysfunction
A muscle's strength is much less than its resistance to tearing. Some tissues can resist a tearing force of 175 psi, whereas the strength of the most powerful muscles seldom exceeds 85 psi. This factor of safety prevents a muscle from injuring itself during forceful contractions. Muscles are usually torn by a combination of the forces of antagonistic muscles, the force of momentum, and the force of external objects.
Symptoms of Acute Strain. The onset is acute with searing pain that rapidly fades into a dull ache. Pain is increased on movement, especially against gravity. Weakness is not commonly associated. Examination reveals a locally spastic and tender muscle with swelling. If rupture is severe, a gap may be palpated. A bulge in the long axis (eg, thigh) on vigorous contraction points to hernia. Contraction against resistance and passive stretching produces pain. In the late stage, extensive skin discoloration is common and often appears some distance from the site of injury. Subacute and/or chronic strains may result in a myofascitis and/or myofibrositis.
Chronic Strain. Chronic strain is the result of prolonged overuse that produces an inflammation at the tendinous attachment, musculotendinous junction, or within the tendon itself. As activity continues, the inflammatory reaction progresses to calcification at the muscle origin or tendon insertion with possible spur development. Tendons with sheaths are more likely to become inflamed, with the inflammation spreading between the tendon proper and the sheath. Intramuscular hemorrhage is not uncommon in conditions of acute strain, and smaller hemorrhages can occur in chronic strains.
Fascial hernias develop as a result of contusion or small puncture wounds that produce a rent in the fascial sheath that envelops all muscles. They may also develop in weakened aponeuroses in patients with chronic compartment syndromes as the result of the increased compartment pressure. In addition, they are sometimes found where a muscle's nerves emerge from its fascia. Palpation should reveal a tumor-like mass when the muscle is relaxed, which may disappear when the muscle is activated.
A muscle action not balanced by reciprocal inhibition of the antagonistic muscle (eg, blow, unexpected force) may result in its rupture by sudden contraction or a less common injury to its antagonist by overstretching. Muscles previously weakened by fatigue or disease are more apt to rupture.
Complete muscle rupture is rare, but a split in a muscle sheath due to weakness or a break may allow the muscle tissue to herniate during contraction. It may follow injury or be a surgical complication. The sheath opening may be large or small. A soft mass is noted at the site of the opening during palpation that disappears when the muscle is contracted and reappears on relaxation. Weakness may be a complaint. Permanent correction can only be made by surgery.
Rupture is characterized by knife-like pain, followed by a sensation of extreme local weakness. If a complete tear occurs, the lesion is usually at the tendinous attachment to the muscle belly. Normal continuity is broken and quite obvious on palpation until obliterated by hemorrhage and swelling. Function is lost in proportion to the degree of tear.
Direct evidence is gained by testing function with gravity eliminated. The asymptomatic ripple-pattern (ladder muscle) seen in some athletes on passive stretch is not of traumatic origin but considered an effect of banding of the overlying fascia.
Muscle ruptures associated with nonpenetrating wounds are seen in both the young and old. In youth, they occur when a muscle is suddenly stressed beyond its tensile strength and the muscle fails at the musculotendinous junction. Such rupture is characterized by painful voluntary contraction, ecchymosis at an area of local tenderness, swelling, edema, and hemorrhage. Palpation will often reveal the defect.
After the acute stage, persistent weakness remains and there is an increase in muscle bulk proximal to the rupture site upon contraction. In the elderly, muscle rupture occurs under minimal loads as a result of degeneration within the muscle's tendon. These ruptures are featured by considerably less pain, swelling, tenderness, and ecchymosis; however, they do present with the later persistent weakness and increased bulk upon contraction.
Interstitial hematomas are usually the result of contusion, while intramuscular hematomas are the result of intrinsic tears. Both contractile and noncontractile elements are damaged during muscle strain, but the greatest injury is suffered by the capillary network between skeletal muscle fibers. The effect is seepage of blood and tissue fluid into interstitial and extracellular muscle spaces that are already congested by activity hyperemia. A degree of hematoma is the result, and it may protrude within the potential space between muscles. When extrinsic stress is severe, bleeding may also result within the deep and subcutaneous connective tissues to compound the problem.
When intramuscular tension returns after injury, intramuscular bleeding points tend to become compressed. Clotting occurs within a few hours, but slight trauma (eg, massage) may cause further hemorrhage even after 2–3 days. Resolution follows with a degree of absorption and fibrosis.
Classification of Strains
Strains are classified by either severity or by area. When classified by area, specific muscles are used such as gluteal, intercostal, abdominal, and paravertebral. If the muscles involved are of a nonspecific multiple nature surrounding a joint, the general area may be used as a descriptor such as a right iliofemoral strain, left knee strain, or right thoracocostal strain of T6–T11. When classified by severity as well, the terms first degree (mild), second degree (moderate), and third degree (severe) are generally applied.
First-Degree Strain. This is a mild muscle pull caused by trauma to a part of the musculoskeletal unit from forceful stretch that results in a low-grade inflammation and some muscle-tendon disruption. Hemorrhage, disability, and strength or function loss are mild. It is characterized by local pain aggravated by movement or muscle tension. Physical signs include local tenderness, swelling, mild spasm, ecchymosis, and minor strength and function loss. The common complications in recurring strain are tendinitis and periostitis at the site of attachment.
Second-Degree Strain. This is a moderately pulled muscle caused by trauma to the musculoskeletal unit from excessive stretch or violent contraction that results in torn fibers without complete disruption. It is characterized by increased first-degree strain symptoms. There is moderate hemorrhage and swelling. Muscle spasm and function loss are especially greater. The complications are similar to those seen in first-degree strain.
Third-Degree Strain. This is a severely strained muscle. The trauma results in a ruptured muscle or torn tendon that may be represented as a muscle-muscle, muscle-tendon, or tendon-bone separation. A palpable defect is often present. It is characterized by severe pain, tenderness, swelling, spasm, disability, ecchymosis, hematoma, and muscle function loss. Prolonged disability is the major complication. After the acute stage, x-ray films exhibit soft tissue swelling and an avulsion fracture at the tendinous attachment. Surgical joining is usually necessary.
A sprain can be defined as a joint injury in which the ligaments, capsule, and surrounding tissues are partially torn or severely stretched. The cause is primarily from forcing a range of motion beyond the power of a ligament to withstand the stress. The extent of damage depends upon the amount and duration of the force and tissue strength.
Ligaments are generally much stronger than necessary to resist normal forces. However, if overstress is chronic or occurs at an unguarded moment, the ligaments are so stretched as to allow the articulating bones to slide (subluxate) out of their normal positions.
Ligaments play a much greater part in supporting loads than are generally thought. Electromyographic studies in situations involving fatigue from forces acting across a joint prove that muscles play only a secondary role. Such fatigue is essentially a form of pain originating in the ligaments rather than the muscles. Thus, some researchers feel that if the muscles involved in a problem are weak to begin with, there is a more immediate ligamentous strain that produces the characteristic fatigue syndrome.
In chronic conditions, the relatively rapid stretching of fibrous bands under continuous overtension is due partly to fiber elongation. However, the majority of the stretching is a product of proliferative fibroblastic activity where more collagenous tissue is produced to increase the length of the structure.
This phenomenon is often seen in subluxations of postural or occupational origin where unilateral stress results in stretching and laxity of some supporting and check ligaments. It is for this reason, among others, that chronic subluxations are often difficult to hold in normal alignment. The site must be periodically adjusted and supported until ligament laxity is corrected. Just as unnecessary bone is resorbed, a ligament will not retain an unnecessary lengthened state. This process is demonstrated in acquired flatfoot where weight is constantly applied on the medial aspect of the foot, which leads to stretching of supporting ligaments and a flattening of the arch.
Effects of Acute Sprain Added to Chronic Sprain
When connective tissue is subjected to continuous pull, it becomes chronically inflamed and invaded by collagen substance and mineral salts. This results in sclerosing and varying degrees of calcification. In addition, when these tissues are subjected to acute traumatic stress, some of the constituent fasciculi rupture. This is attended by minute hemorrhages.
Further attempts at repair result in collagen tissue deposition and mineral invasion that also produce sclerosing and calcification. If the involved ligament possessed elastic fibers, there will be a definite shortening.
Capsule and Fibrocartilage Damage
A capsule tear usually results from an unexpected joint force and often occurs 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.
Injured fibrocartilage is usually associated with the spine and knee but are occasionally related to the temporomandibular, sternoclavicular, and distal radioulnar joints. When injured, cartilaginous and disc substance progressively undergoes degenerative change with possible dehydration and fragmentation. Disc damage results from repeated subluxations and the strain of mechanical and postural incompetence that tend to weaken tissue fibers.
Classification of Sprains
Sprains are classified by severity, stage, or the area of involvement. In differentiating sprain and strain, keep in mind that sprain involves the ligaments of a joint and strain involves the muscular and tendinous structures. Sprain usually elicits pain on passive movement of the affected joint when the joint's muscles are relaxed; strain elicits pain on active motion even without joint motion (eg, resisted movement).
First-Degree Sprain. In a mild sprain, there is a small amount of internal bleeding in a localized area of the ligament with only a few fibers separated. No actual loss of function or reduced strength is present. Generally, the ligament requires no protection and is not weakened. Mild sprain is characterized by tenderness over the ligament that is not marked at the bony insertion by swelling or other symptoms of mild local inflammation. Joint instability is negligible.
Second-Degree Sprain. This is a moderate sprain with a partial ligamentous tear, characterized by increased severity of first-degree symptoms. A tendency toward recurrence is a complication, as is the possibility of traumatic arthritis and permanent instability. A moderate sprain results from severe tearing of the ligaments, although at least half of the fibers remain undamaged. This type of sprain shows some loss of function in the injured area even if the torn ligaments are not widely separated. They will rejoin during the natural healing process unless the damage is great. If damage is great, considerable scar tissue may form, and a permanent weakness of this section of the ligament may result. Moderate sprain is characterized by a greater degree of symptoms than presented in a mild sprain, lack of normal ligamentous resistance on digital pressure, and increased joint movement on tension from movement or manipulation.
Third-Degree Sprain. This is a severe sprain with a complete ligamentous tear, characterized by severe swelling, hemorrhage, tenderness, complete loss of function, abnormal motion, and possible deformity. When a sprain is termed severe, it denotes a complete loss of function of the ligament caused by a force sufficient to pull it completely apart or tear it loose from the surrounding tissues. A severe sprain has a greater degree of symptoms than presented by a moderate sprain plus marked excessive joint motion indicating definite separation on tension or motion. Severe pain may or may not be present. Abnormal motion may be exhibited with bilateral stress roentgenograms. Persistent instability and traumatic arthritis are common complications. If seen soon after injury before swelling occurs, a palpable gap may be felt at the site of tear. Surgical joining is usually necessary.
Complications to Strains and Sprains
The spine and extremity joints commonly suffer strains that may be uncomplicated or complicated. For example, a complicated strain is accompanied by mild autonomic disturbances and may be associated with pre-existing arthropathy, cartilage changes, congenital deformities, systemic diseases, secondary infection, or myofascitis.
Tendons repair slowly and handle infection poorly because of their relative avascularity. Sheath trauma or infection can block nutrition, especially in those tendons that extend via long tunnels and are served with a long axis blood supply.
A complicated sprain is accompanied by pre-existing pathology or injury to a synovial joint's contents. Typically, complications result from sprains in which the tissues are abnormal or the general system is physiologically deficient at the time of injury because the lowered vitality of the locally damaged cells and the accumulation of exudate may provide fertile soil for the production of inflammatory processes and delayed repair.
An individual's joint structure at a particular point in time represents the quality and quantity of the chemical components of bone and associated tissues to cope with the action of external and internal forces. Bones, being essentially unyielding structures, are damaged when excessive force is applied directly or indirectly.
With intrinsic forces, the nature of the damage depends on the direction of the applied force, its momentum, and on the manner in which these bones are attached to other structures. With extrinsic forces, the shape (eg, sharp, pointed, blunt) of the inflicting object must also be considered. The most accurate diagnosis can be made immediately after injury, before swelling clouds the picture.
Healthy bone has an excellent blood supply with some exceptions in the metaphyseal area; but tendons, ligaments, discs, and cartilage are poorly vascularized. Yet, both bone and joints challenge the host's reparative and defensive mechanisms. The pressure of pus under hard bone blocks circulation, and consequent emboli, thrombosis, and vasospasm can cause additional devascularization. When circulation is deficient, local phagocytic function and nutrition are deficient. Healing is therefore inhibited.
When subjected to prolonged weight-bearing or occupational and traumatic overstress, bone demineralizes and undergoes degenerative changes, resulting in deformity of the articulating surfaces. Concurrently, the attending excoriation of the articular periosteal margins results in proliferative changes in the form of lipping and spur formations or eburnation. These facts must be balanced with the fact that diminished physical activity encourages osteoporosis and, conversely, exercise encourages the development of healthy bone structure.
Any stress applied to a joint that is greater than its structural resistance will fracture a bone or dislocate a joint. In this sense, stress is defined as the force exerted; eg, while it requires from 1,500—3,000 static pounds to fracture the neck of the femur, a weight of only 20 lbs dropped upon it from a distance of several feet will have the same result.
Many fracture and dislocation complications such as nerve and vessel injury occur not from the trauma itself but from poor first aid that does not provide adequate splinting before movement. Traumatic bone injury rarely occurs without significant soft-tissue damage. The physical examination must be gentle but thorough because deep soft-tissue trauma is poorly visible on roentgenograms for several days after injury.
Infection is infrequently found except in open wounds or aspirated hematomas. If bacteremia exists, a hematoma may become infected and produce suppuration. This is a greater possibility if the hematoma is sited in a relatively poorly vasculated area.
Myositis is an inflammation of muscle tissue, usually involving only the skeletal muscles. Contusion and trauma may cause an inflammation of muscles in which the involved muscles become red, swollen, tender, painful, and almost of wooden hardness. This type of myositis usually subsides without suppuration.
Disease of muscle tissue is often mistaken for disease of an adjacent joint, tendon sheath, or some type of neuralgia. Muscle pain is not localized subjectively with the same accuracy as is pain in the more superficial structures, thus such vague localization requires a most careful examination. The reason for this is that the sensory fibers of muscles course with motor fibers rather than with cutaneous afferents. Functional use of a muscle is painless if the inflammatory process lies entirely within the muscle sheath, but perimyositis may cause pain during function.
Myositis causes pain only when the muscle is deeply palpated or stretched. Whenever stretching a muscle causes pain, that muscle should be carefully palpated for sensitive areas and palpable swelling or induration. Sites of sharply defined tenderness (trigger points) can usually be found, and pressure upon such foci will usually initiate referred pain. In seeking signs of superficial muscle tenderness, portions of the muscle should be squeezed between the thumb and index finger (as opposed to pressing the muscle upon underlying bone) to avoid mistaking a periostitis for a myositis.
Traumatic Myositis Ossificans
Myositis ossificans is characterized by the formation of heterotopic bone in soft tissues. There are two types:
(1) A traumatic form (myositis ossificans circumscripta), which is the common concern following musculoskeletal injury. A similar type occurs in the lower extremity with severe brain injuries.
(2) A rare congenital form (myositis ossificans progressiva) that begins without trauma or shortly after birth.
Traumatic myositis ossificans is a condition of heterotopic bone formation that can occur in collagenous supportive tissues such as skeletal muscles, ligaments, tendons, and fascia following hematoma. It is most common in teenagers and young adult males and is frequently the effect of direct muscle bruising, especially repeated contusions as seen in contact sports. It occurs 80% of the time in the biceps brachialis after dislocations but frequently occurs in the deltoid, quadriceps, and hamstrings.
The connective tissue that surrounds an injured muscle rapidly invades the traumatized area, and connective tissue retains its embryonal ability to be transformed into more differentiated tissue. Following the primary interstitial myositis, there is a transformation of the connective tissue into bone. A fluffy calcification shows on roentgenography in 2—4 weeks after injury, it matures in 3 months, and in 5 months, ossification appears. The lesion is characterized by an indurated, tender, indistinct mass of a single muscle group that emits local heat.
Absorption is inhibited if bleeding is excessive or if a hematoma forms within lax tissues. When the clot retracts, a serum-filled cavity (presenting a fluctuant swelling) is left that is lined with organizing fibrin deposits.
Muscles enclosed and supported by strong fascial compartments may become involved in a muscle-fascia interface compartment syndrome. A condition may be produced in which pressure within an anatomical space is increased, resulting in circulatory embarrassment to the contents of the space. Any muscle crush or interference with circulation may result in muscle swelling restricted by the fascial sheath, leading to extreme pressure producing cellular death.
Compartment syndromes manifest in both the upper and lower extremities, but they most commonly occur in the forearm and leg. Typical locations in the upper extremity include the volar and dorsal compartments of the forearm and the intrinsic compartments of the hand. Lower extremity locations are found at the anterior, lateral, posterior superficial, and deep compartments of the leg.
Increased pressure within a compartment may effect vascular closure, a reflex vasospasm, and/or decreased perfusion pressure. The cause for the increased pressure may be traced to either an increase in compartment content or a decrease in compartment size by one or more factors. Hemorrhage, increased capillary permeability or pressure, infusion, and hypertrophy are common causes of an increased compartment content.
A decrease in compartment size is usually the effect of localized external pressure. Each syndrome has its individual clinical picture of pain, tenseness, weakened muscles, and sensory changes. Comparable signs of lower extremity compartment syndromes are shown in Table 1.10.
A diminished peripheral pulse may point to either a compartment syndrome or arterial occlusion. Hot red skin overlying an affected compartment suggests a complication of thrombophlebitis or cellulitis, both of which can lead to serious extension and systemic invasion. Kidney failure or myoglobinuria may add to and complicate the picture. A poorly responding case of shin splints with pain even on rest suggests some degree of compartment syndrome.
Table 1.10: Lower Extremity Compartment Syndromes|---------------------Compartment----------------------------------| Posterior Posterior Sign Anterior Lateral Superficial Deep Pain on passive Toe flexion Foot inversion Foot dorsiflexion Toe extension movement
Site of tissue Between Lateral fibula Bulk of calf Between tibia tenseness fibula and and Achilles tibia, anteriorly in posterior- medial lower leg.
Weakened Tibialis an- Peronei Gastrocnemiuus, Tibialis anter- muscles terior, toe soleus ior, toe extensors flexors
Sensory change First web Dorsum of No sign Plantar sur- distribution space (deep foot (deep face (pos- peroneal) and superficial terior tibial) peroneal)
Tendon sheaths are lined with specialized connective-tissue cells, similar to cells lining bursae and the synovial membrane of joints. Thus, reactions within tendon sheaths to external influences are akin to those seen in bursae and joint-cavity disorders. The term tenosynovitis generally includes all inflammatory affections of the tendons and their enveloping sheaths.
The inflammation is usually the result of:
(1) overuse or compression of a tendon possessing a synovial sheath or
(2) secondary to systemic infection. The disorder is usually acute, relieved by rest, but may become chronic and resemble rheumatoid arthritis. Chronic inflammation of the sheath always holds the danger of stenosis, especially at sites where tendons cross (eg, De Quervain's disease, snap finger).
Continual pain at a tendinous insertion can usually be traced to a sudden unexpected strain, to chronic stress, and rarely to contusion. Nerve entrapment, epicondylitis, soft-tissue nipping, and osteoarthritis may be confused or superimposed within the clinical picture. The two most common sites of tenosynovitis are at the origin of the extensor tendon at the lateral epicondyle (tennis elbow) and the origin of the adductor longus at the inferior surface of the pubis.
Symptomatology. Symptoms of tendinitis develop in 24—28 hours after injury. There is a gradual onset of pain radiating along the involved tendon upon active contraction or passive stretching. There is a soft, hot, frequently red, localized swelling at the musculotendinous junction that usually renders an audible silky or leathery crepitus whenever the tendon is moved. In the hemorrhagic type, the pain is dull and aching, a feeling of fullness is perceived at the site of the affected tendon sheath, and crepitation is not usually prominent.
Types. Traumatic tenosynovitis (peritendinitis crepitans) is divided into two types:
The common form is due to repeated overuse of a musculotendinous unit to a point of fatigue where the tissues cannot functionally adapt. Vigorous exercise in a sedentary weekend athlete is an example of overactivity that may bring on the characteristic symptoms. Within a few hours after a hard session of unaccustomed effort, the involved tendon sheath becomes edematous. Pathologic changes are particularly evident at the musculotendinous junction and in the peritendinous areolar tissue. Thrombosis of the venules occurs, and fibrin is thrown out into the aveolar tissue and between muscle fibers. A sticky fibrinous exudate is thus produced which may be accompanied by a serous effusion within the tendon sheath. The adjacent muscle fibers show degenerative changes, lose glycogen content, and accumulate lactic acid, which spreads over the tendon. This acidity causes the edematous swelling.
The second form is an acute hemorrhagic type resulting from direct contusion or a puncture wound that does not introduce infection. A sterile outpouring of bloody and serous fluid occurs within the tendon sheath.
Tendon rupture is exceedingly rare in individuals under the age of 40 years. Both complete and partial ruptures are most commonly seen of the Achilles tendon of middle-aged athletes. The cause is usually traced to overuse, direct violence during stretch, or a poorly placed injection. Its site is commonly found just away from the point of insertion into bone. The rare event of spontaneous tendon rupture occurs only when the tendon is weakened by degenerative processes.
Rupture Near Insertion. Tendon rupture near its bony insertion is characterized by sharp pain, often accompanied by perception of an abrupt "thud" at the site. The sharp pain soon subsides, but joint weakness does not. Partial rupture is characterized by acute pain during activity that persists until stress can be avoided. When activity is resumed, severe pain returns. A tender swelling is inevitably noted on palpation.
Rupture at the Musculotendinous Junction. This injury features a sudden stabbing pain followed by swelling and sometimes hematoma. Pain is increased when the affected muscle is contracted. A gap may be noted when swelling subsides to indicate a degree of muscle tear. Surgical correction is not usually necessary unless the separation is severe.
The tendons of the rotator cuff and the origin of the elbow extensors are the common sites of deposits of calcium. Deposition is usually abrupt and associated with an acute inflammation of the joint capsule and its lining, characterized by pain and spasm that limit movement. Relief may occur suddenly as a deposit is spontaneously ruptured into a bursa or joint cavity. Occasionally, deposition is a slow asymptomatic manifestation of tendinous degeneration.
Due to stress at points of tendinous insertion, cracks may appear in the cortex that cause the area to become invaded by osseous tissue. In late stages, compact bone may be found on roentgenography to extend well over an inch into the tendon. Such extensions are subject to fracture. Unless exposed to direct trauma or undue intrinsic stress, they are usually asymptomatic.
A localized cystic swelling is often the result of a mucinous degeneration of connective tissue occurring near a tendon sheath or joint capsule. The cause is unclear, but trauma is thought to be a factor. One large cyst may be felt, or several small cysts may coalesce to form a multilocular cyst. The walls are composed of dense fibrous tissue. Bundles of nerve fibers often occur in the areas of mucinous degeneration.
Such ganglia are usually seen on the dorsum of the wrist or foot. They give rise to localized swelling, of a gradual or sudden onset, which may vary in size from time to time. Weakness and mild neuralgia may be associated. If connected to a tendon sheath, the ganglion becomes prominent when the tendon is stretched.
Peripheral Nerve Trauma
Damage to an individual peripheral nerve is characterized by:
(1) flaccid, atrophic paralysis of the muscles supplied by the involved nerve and
(2) loss of all sensation, including proprioception, in the skin areas distal to the lesion.
When partial destruction to various peripheral nerves occurs, the effects are usually more prominent in the distal extremities. The condition is characterized by muscular weakness and atrophy and poorly demarcated areas of sensory changes. Associated trophic lesions of the joints, muscles (atrophy), skin, and nails are common. They blend and are somewhat explained as the results of vasomotor changes.
Classification of Nerve Trauma. Nerve trauma occurs from contusion, stretching, or laceration:
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 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. Nerve "pinch" or "stretch" syndromes are common in sports, but they are also seen after falls and industrial accidents. The syndromes appear throughout the cranium, 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 pinch 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 stretched, partially torn, or ruptured most anywhere in the nervous system from the cord to peripheral nerve terminals.
Nerve Entrapment Syndromes. A peripheral nerve entrapment syndrome represents 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 by normally surrounding tissues. Local impairment of blood supply may further damage the entrapped nerve if associated vessels become stretched, kinked, or compressed. So that a patient may avoid unnecessary pain and disability, it is important to identify a peripheral entrapment syndrome rapidly through careful 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. The major features of upper and lower-extremity nerve entrapment syndromes are shown in Table 1.11.
Table 1.11. Common Nerve Entrapment Syndromes
Upper-extremity syndromes Syndrome Site Nerve Major Findings* Anterior interosseous Proximal forearm (median) Anterior interosseous Abnormal pinch sign; normal sensations; weakness of flexor pollicis longus, pronator quadratus, and flexor digitorum profundi of index and middle fingers; poorly defined ache in forearm. Pain intensifies during the night. Carpal tunnel Wrist Median Pain, paresthesias, numbness, and poor two-point discrimination in thumb and radial 2| fingers; hypesthesia especially on palmar aspect of second digit; thenar weakness and wasting; positive Tinel's and Phalen’s signs; positive EMG signs. Cubital tunnel Elbow Ulnar Sensory loss in ulnar 1–1/2 fingers and ulnar aspect of the hand; weakness and wasting of ulnar intrinsic and flexor digitorum profundus; ache in medial elbow and forearm; little-finger numbness; positive Tinel's sign. Guyon's canal Wrist Ulnar Sensory loss in ulnar 1–1/2 fingers; weakness and wasting of ulnar intrinsic muscles. Postcondylar groove Elbow Ulnar Sensory loss in ulnar 1–1/2 fingers and ulnar aspect of the hand; weakness and wasting of ulnar intrinsic and flexor carpi ulnaris muscles; elbow joint deformity. Posterior interosseous Proximal forearm Posterior interosseous (radial) Normal sensation; wrist drop; dull ache in dorsal forearm; difficult finger extension. Pronator Proximal forearm Median Proximal forearm pain and tenderness; flexor pollicis longus and abductor pollicis brevis weakness; paresthesias in thumb and radial 3–1/2 fingers; forearm and hand pain; positive Tinel's sign. Radial Midarm, spiral groove Radial Sensory loss in radial side of dorsal hand; wrist drop; weak wrist and finger extensors; possible sensory impairment in web of thumb. Crutch or sleep palsy Axilla, humeral groove Radial Sensory loss of radial forearm; loss of elbow extension; wrist drop. Lower-extremity syndromes Syndrome Site Nerve Major Findings* Femoral Inguinal area of pelvis Femoral Sensory loss of anteromedial thigh; weakness and wasting of quadriceps femoris; local tenderness in groin; impaired knee jerk. Meralgia paresthetica Inguinal area Lateral cutaneous of thigh Sensory loss, paresthesias, burning pain, and numbness in anterolateral thigh; no motor weakness. Obturator Pelvis Obturator Sensory loss of superomedial thigh; thigh adductor weakness. Peroneal Neck of fibula Common peroneal Sensory loss of dorsal foot and lateral leg; foot drop; steppage gait; local tenderness; anterior and lateral compartment atrophy. Tarsal tunnel Ankle Posterior tibial Burning pain and paresthesias of sole and toes; weakness of intrinsic foot muscles. * Adapted from Reddy, with slight modifications. It should be noted that one or more of the major features presented in this table may be absent and that the symptoms and signs may vary in severity from one patient to another.
Differentiating Joint Dysfunction From Joint Disease: Guidelines
In a history of joint pain, there may be many clues pointing to the diagnosis of joint disease and many strongly suggesting joint dysfunction. This may represent separate problems overlapping on one another or one complex problem. For instance, joint pain may be the chief complaint in such systemic diseases as polyarteritis nodosa, systemic lupus erythematosus, dermatomyositis, erythema nodosum, and scleroderma.
It is also sometimes associated with kidney or pulmonary diseases, ulcerative colitis, acromegaly, or Henoch purpura and other hemorrhagic dyscrasias. In Henoch purpura, the abdominal symptoms usually predominate. It should be kept in mind that gout may occur in any limb joint and is occasionally found in the spine. It is not always associated with tophi or limited to the feet and hands.
Primary joint dysfunction is usually the effect of intrinsic joint stress occurring at an unguarded moment when the joint is active within its normal range of motion. Another cause is that of extrinsic joint stress following a definite but minor trauma and often classified as sprain and/or strain. Joint dysfunction implies the loss of one or more movements within the normal range of motion and associated pain, but it is only one possible problem that must be differentiated from other causes of joint pain.
Secondary joint dysfunction is often overlooked in traditional medicine. Yet joint dysfunction is, according to Mennell, "the most common cause of residual symptoms after severe bone and joint injury and after almost every joint disease when the primary pathological condition has been eradicated, has healed, or is quiescent."
Immobilization after surgery, immobilization from a fracture cast even if the fracture is far from a joint, and immobilization from a taped sprain all cause residual symptoms of joint dysfunction. Such symptoms also follow joint inflammation or resolution of systemic joint disease with or without internal adhesions.
When joint dysfunction causes residual symptoms after so called joint disease recovery, the symptoms change from that of joint disease to joint dysfunction. That is, during the active process, rest increases joint pain and stiffness. During the residual dysfunction, rest relieves and action aggravates the pain. These points should be brought out during the case history.
Specific features elicited in the history can point directly to certain diseases. For instance, migrating joint pain following systemic illness suggests rheumatic fever. A tubercular joint is often a single joint offering mild complaints yet associated with marked muscle atrophy. An acute gonococcal joint presents a single acutely painful joint that is protected by the patient as if it were a boil.
Hemarthrosis has a history of trauma and is characterized by slight but rapid swelling from the blood pool; the joint is hot and acutely painful. Synovitis may also have a history of trauma, but the swelling due to excess synovial fluid may not occur for many hours. The joint may feel warm rather than hot, aching rather than acutely painful.
In the hand(s), the location of joint involvement offers a general rule that helps the diagnosis:
(1) gout affects the metacarpophalangeal joints,
(2) rheumatoid arthritis involves the proximal interphalangeal joints, and
(3) osteoarthritis affects the distal interphalangeal joints. Mennell feels that osteoarthritis by itself does not cause joint pain; that is, the pain is from the associated joint dysfunction rather than the disease process itself.
The key history points of primary joint dysfunction are:
(1) the pain has a sudden onset and is sharp,
(2) it usually follows stress at some unguarded joint motion,
(3) the pain is limited to one or adjacent joints,
(4) the pain is aggravated by movement and usually is at some particular area of motion,
(5) rest relieves the pain and does not produce stiffness, and
(6) marked swelling or warmth is not associated.
Keep in mind that while the major problem may be of joint dysfunction, persistent pain following adequate treatment may indicate the presence of a secondary low-grade asymptomatic infection or irritation in spite of blood reports to the contrary. In such cases, suspicion should be directed toward a distant focus of infection such as the gastrointestinal or genitourinary tracts, the teeth, sinuses, or tonsils. In food preparation, adequate cooking heat will kill pathogenic bacteria but it has little affect upon toxins and spores.
Trigger Point Development
Myofascial pain may present as a primary complaint or as a crippling adjunct to any number of other problems (eg, unequal leg lengths, disuse, immobilization, chronic strains, poor posture, gait disturbances, connective-tissue diseases, arthritides). Trigger point syndromes often appear related to a lack of appropriate exercise; thus, they are less common (but not absent) in the large muscles of athletes and laborers than they are in sedentary workers.
Trigger points are foci of stress inflammation that result in binding cobweb adhesions that entrap sensory nerve endings to produce sharp demarcation of pain especially upon pressure. Thus, a trigger point is essentially a small hypersensitive area in a myofascial structure from which impulses bombard the CNS and give rise to referred pain. These areas are frequently unknown to the patient until revealed by palpation. Besides deep pressure, an application of heat, cold, electrical stimulation, needling, or some other stimulus may evoke a painful trigger-point reaction.
The power of such a reaction appears to be moderated by a number of general factors (eg, conditioning, genetic predisposition, hormonal balance, scar tissue from previous injury, and prolonged emotional stress).
Myofascial trigger mechanisms may be initiated by direct trauma to muscle or joint, chronic muscular strain, chilling of fatigued muscles, acute myositis, arthritis, nerve root injury, visceral ischemia or dyskinesia, and hysteria. The pain is initiated whenever the trigger site is stimulated by pressure, needling, extreme heat or cold, or motion that stretches the structure containing the trigger area.
The resistance to stretching leads to apparent shortening of the affected muscle with limitation of motion and weakness. High-intensity discharges from a trigger area may be accompanied by vasoconstriction and other autonomic effects limited to the reference zone of pain.
Although one or more trigger points may occur in any muscle, they usually form in clusters. Certain muscles and muscle groups (eg, the antigravity muscles) appear to be more liable than others. See Table 1.12.
Table 1.12. Common Trigger Point Syndromes
Location: Upper Body Primary Reference Zone or Symptoms ** Infraspinatus Posterior and lateral aspects of the shoulder. Intercostal muscles Thoracodynia, especially during inspiration. Levator scapulae Posterior neck, scalp, around the ear. Pectoralis major Anteromedial shoulder, arm. Pectoralis minor Muscle origin or insertion. Quadratus lumborum Anterior abdominal wall, 12th rib, iliac crest. Rectus abdominus Anterior abdominal wall. Semispinalis capitis Headache, facial pain, dizziness. Splenius cervicis Headache, facial pain, dizziness. Sternocleidomastoideus Headache, dizziness, neck pain, ipsilateral ptosis, lacrimation, conjunctival reddening, earache, facial and forehead pain. Trapezius Lower neck and upper thoracic pain, headache. Location: Lower Body Primary Reference Zone or Symptoms** Anterior tibialis Anterior leg and posterior ankle. Gastrocnemius/soleus Posterior leg, from popliteal space to heel. These trigger points may be involved in intermittent claudication. Gluteus medius Quadratus lumborum, tensor fascia lata, gluteus maximus and minimus, sacroiliac joints, hip, groin, posterior thigh and calf, cervical extensors, upper thoracic muscles. Tensor fascia lata Lateral aspect of the thigh, from ilium to the knee. *Adapted from Travell, Sola, and Smythe, with slight modifications. **Reference patterns vary considerably according to the severity and chronicity of the trigger point phenomenon involved.
Trigger point pain may be localized in one muscle or group, or it may also involve remote muscles or groups. Primary trigger points in the gluteus medius, for example, are commonly related to secondary trigger points in the neck and shoulder girdle. In addition, trigger areas in myofascial structures can maintain pain cycles indefinitely; ie, the pain cycle may continue long after the precipitating cause has vanished because the mechanism that set the pain cycle in motion initially is not necessarily the same as that which keeps it going.
Cycles of physiologic responses arising from trigger points typically involve:
(1) well-defined pathways (eg, motor reflexes, sensory changes),
(2) anticipated autonomic feedback reflexes, and
(3) microscopic tissue changes. Motor and sensory reactions are usually exhibited in local and general muscle fatigue, hypertonia, weakness, possibly a fine tremor, hyperirritability, pain, and hypesthesia.
The autonomic concomitants are similar to those seen with meridian acupoints. Travell believes that these are frequently expressed as decreased skin resistance, increased pilomotor reaction in the reference area, vasodilation (possibly with dermatographia), and skin temperature changes (coolness). In the typical myofascial syndrome, laboratory analyses and roentgenography fail to show significant bone, joint, or soft-tissue changes.