Joint Trauma: Perspectives of a Chiropractic Family Physician
Perspectives of a Chiropractic Family Physician
Clinical Monograph 8
By R. C. Schafer, DC, PhD, FICC
The general stability of synovial joints is established by action of surrounding muscles. Excessive joint stress results in strained muscles and tendons and sprained or ruptured ligaments and capsules. When stress is chronic, degenerative changes occur.
The lining of synovial joints is slightly phagocytic, is regenerative if damaged, and secretes synovial fluid that is a nutritive lubricant having bacteriostatic and anticoagulant characteristics. This anticoagulant effect may result in poor callus formation in intra-articular fractures where the fracture line is exposed to synovial fluid. Synovial versus mechanical causes of joint pain are shown in Table 1.
Table 1. Synovial vs Mechanical Causes of Joint Pain
|Onset||Symptoms fairly consistent, during use and at rest.||Symptoms arise chiefly during use|
|Location||Any joint may be involved.||Primarily involves weight-bearing joints.|
|Course||Usually fluctuates. Episodic flares are common.||Persistently worsening progression. No acute exacerbations.|
|Stiffness||Prolonged in the morning.||Little morning stiffness.|
|Anti-inflammatory effect||Aided by cold and other anti-inflammatory therapies.||Anti-inflammatory therapy of only minimum value.|
|Major pathologic features||Negative radiographic signs or diffuse cartilage loss, marginal bony erosions, but no osteophytes.||Radiographic signs of cartilage loss and osteophyte developments|
Tendinitis, tenosynovitis, peritendinitis, and bursitis near a joint are usually shown by signs of noninfectious inflammatory processes involving a tendon, a tendon sheath, or a bursa. They may be related to singular severe trauma or a series of microtrauma as is often seen in physical laborers, weight lifters, tennis players, and even piano players or typists. Some authorities believe that such inflammations may be the result of reduced microcirculation caused by reflex mechanisms weakening the site to normal stress. A basic guide to peripheral arthritis and related disorders is shown in Table 2.
Table 2. Basic Guide to Peripheral Arthritis and Related Disorders
|Bursitis||Inflammation around calcium deposits between tendon and bursa sac causing severe pain (usually in the shoulder). Subsides after a week or so but may become chronic.||Adults of both sexes.||Unknown, although new injury to tendons sometimes starts an attack.|
|Osteoarthritis||Bony spurs appear around joints, causing swelling, pain, and eventually erosion of cartilage. Develops slowly and is rarely disabling.||Approximately 6 million Americans are affected. Almost everyone past middle age develops conditions typical of this disease.||Heredity, overuse of a joint, repeated minor trauma, or a sudden severe injury; there may be a metabolic imbalance in body chemistry.|
|Rheumatoid arthritis||An inflammatory condition affecting not only joints but connective tissue, nerves, muscles, blood vessels, and other organs. Causes crippling stiffness of joints if not controlled.||About 4.5 million suffer from this raving form of arthritis: 75% are over 45 years of age, with women stricken three times more often than men.||An unknown virus, inborn hypersensitivity, or other factors that weaken the body’s resistance; family predisposition.|
|Gouty arthritis||Painful swelling of soft tissues, mainly the great toe. Enormous increase in uric acids.||Over 90% of cases occur in males over 50 years of age. Over 35,000 citizens are affected by this disorder.||A defect of metabolism causing an excess of blood uric acid collecting on or near cartilages. Heredity and obesity cofactors are common.|
|Rheumatic fever||Many joints may be inflamed in the acute phase of this disease, but they usually heal completely. Chief danger is injury to the heart.||Children below teens. Nearly all cases follow streptococcal infections with over 50% following tonsillitis or pharyngitis. Peak incidence is age 6-9.||Unknown.|
The major symptom is a gradual onset of pain radiating along the involved tendon during active contraction or passive stretching. The swelling is localized and soft, and the area may exhibit heat and redness. Typical abnormalities that may be discovered include:
- color changes such as ecchymoses and redness;
- local heat;
- soft-tissue swelling from synovial thickening, periarticular swelling, or nodules;
- swelling from bony enlargement;
- deformity from abnormal bone angulation, subluxation, scoliosis, kyphosis, lordosis;
- wasting from atrophy or dystrophy;
- tenderness on palpation;
- pain on motion;
- limitation of motion;
- joint instability; and
- carriage and gait abnormalities.
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, active and passive ranges of joint motions should not be conducted until after radiographs have demonstrated the mechanical integrity of the joint.
Analyzing the character, origin, timing, onset, and absence of pain can offer important clues to differentiate the pain of trauma from the pain of a precipitated disease. Categories of peripheral joint disorders are shown in Table 3, and Traumatic and nontraumatic causes for most cases of joint pain are listed in Table 4.
Table 3. Categories of Peripheral Joint Disorders
|Acute monarthritis||Chronic monarthritis|
|Acute gout||Chronic osteoarthritis|
|Acute infectious arthritis||Chronic infectious arthritis|
|Acute intermittent hydrarthrosis||Chronic traumatic arthritis|
|Acute pseudogout||Neuropathic arthropathy|
|Acute rheumatoid arthritis||Overuse stress with complications|
|Acute traumatic joint disease||Pseudogout|
|Acute polyarthritis||Chronic polyarthritis|
|Acute rheumatic fever||Chronic gouty polyarthritis|
|Acute rheumatoid polyarthritis and other acute connective-tissue diseases||Chronic polyrheumatoid arthritis and other chronic connective-tissue diseases|
|Acute sarcoidosis||Chronic polyosteoarthritis|
|Infectious polyarthritis||Chronic rheumatoid arthritis variants|
|Acute rheumatoid variants||Enteropathic arthropathy|
|Enteropathic arthropathy||Psoriatic arthritis|
|Psoriatic arthritis||Reiter’s syndrome|
|Reiter’s syndrome||Sojgren’s syndrome|
|Sojgren’s syndrome||Chronic sarcoidosis|
Table 4. Arthritic Conditions Accounting for Joint Pain
|Acute pyogenic arthritis||Marie-Strumpell’s disease||Rheumatoid arthritis|
|Gout and pseudogout||Osteoarthritis||Spondylosis|
|Disuse atrophy||Osteochondritis dissecans||Subluxation|
|Epiphyseal displacement||Periostitis||Traumatic arthritis|
|Fibrositis||Pneumococcal arthritis||Tubercular arthritis|
|Fracture||Psychogenic rheumatism||Von Bechterew’s arthr.|
|Diss. lupus erythematosus||Rheumatic fever|
Relatively uncommon incidental arthritides exhibiting joint pain:
|Bone tumor||Osteogenesis inperfec.||Serum sickness|
|Brucellosis||Osteomyelitis||Sub. bac. endocarditis|
|Chronic pulmonary disease||Paget’s disease||Sudeck’s atrophy|
|Congenital heart disease||Penicillin reaction||Syphilis|
|Diabetic pseudogout||Psoriasis||Ulcerative colitis|
Origin. Although bone proper is insensitive to pain, orthopedic pain originates from the periosteum, joint capsules, surrounding connective tissues, or irritated or inflamed bursa. Receptors are summarized in Table 5. A fractured bone produces pain from the periosteal rupture and pressure of soft-tissue hemorrhage. Arthritis is painful because of capsule inflammation. A history of a recent injection of antitoxin or the administration of a new drug may suggest joint symptoms having an allergic basis.
Table 5. Joints
|Location||Outer layers of joint capsule, grape-like clusters||Sparsely found in deep layers of joint capsule and in fat pads, grape-like clusters (2-4)||Joint ligaments, grape-like clusters (2-3)||Joint capsule (except synovial, joint ligaments, fat pads, periosteum; absent in articular fibrocartilage|
|Endings||Encapsulated||Thickly encapsulated||Thinly encapsulated||Free nerve endings, plexus|
|Fiber type and size||Myelinated, small||Myelinated, medium||Myelinated, large||Myelinated and unmyelinated; variable size|
|Action||Mechanoreceptor||Dynamic mechanoreceptor||Dynamic mechanoreceptor||Nociceptor|
|Function||Signals static position of joint, speed and direction of joint movement. Constant firing aids in regulating posture and muscle tone during joint motion.||Signals only rapid changes in movement: acceleration, deceleration; helps to initiate momentum||Signals direction of movement; guards against excessive joint movement by regulating muscle tone (braking mechanism).||Signal noxious changes: mechanical or chemical|
*Adapted from data of Kessler/Hertling and Wyke.
Sharp pain occurring only when the joint is moved a certain way and that’s usually relieved by rest or immobilization points to joint dysfunction, not joint disease. In degenerative joint disease of the weekend athlete, the pain that occurs on motion and is relieved by rest is the result of joint dysfunction rather than the arthrosis itself.
Onset. The onset of pain in several joints simultaneously points to joint disease unless several joints have been immobilized such as in multiple fractures or involved in severe trauma with multiple bruises. Gradually developing pain is often associated with chronic nonspecific arthritis. A rapid onset is seen in acute rheumatic conditions and gout. Both primary joint dysfunction and joint disease may present sudden pain following trauma or an episode of stress; however, joint swelling is uncharacteristic of joint dysfunction but is of joint disease.
Joint disease may have an insidious onset that is unusual in joint dysfunction. An exception to this would be intrinsic trauma causing joint dysfunction occurring during sleep or unconsciousness. Typical causes of pain near a single joint are listed in Table 6.
Roentgenography is helpful in differentiating the various arthritides. Table 7 lists the major roentgenographic features that differentiate rheumatoid arthritis from osteoarthritis. Roentgenographic features of gout versus atypical osteoarthritis are shown in Table 8.
Table 6. Typical Causes of Pain Near a Single Joint
|Acute pain||Subacute or chronic pain|
|Acute monarthritis||Avascular necrosis|
|Septic arthritis||Low-grade infection|
|Other inflammatory synovitis||Monarticular osteoarthritis|
|Osgood-Schlatter disease||Reflex sympathetic dystrophy|
Table 7. Roentgen Features: Rheumatoid Arthritis vs Osteoarthritis
|Involvement of many peripheral joints, especially metacarpophalangeal and proximal interphalangeal joint of hands, and first interphalangeal foot joints.TD WIDTH=”48%” VALIGN=”TOP”>Knees and hips especially. First carpometacarpal and acromioclavicular joints are often involved although nonweightbearing.|
|Early synovitis, characterized by fusiform soft-tissue swelling.||No signs of soft-tissue changes.|
|Diffuse loss of joint space.||Asymmetric loss of joint space.|
|Involved bones are osteoporotic.||Osteoporosis lacking.|
|Marginal erosions.||Development of subchondral cysts.|
|Little reactive new bone formation.||Reactive bony sclerosis; formation of osteophytes.|
|Eventual fibrous ankylosis.||Possible late bony ankylosis.|
Table 8. Roentgen Features of Gout vs Atypical Osteoarthritis
|Gouty Arthritis||Atypical Osteoarthritis|
|May involve any joint but most commonly attacks first metatarsophalangeal joint of the foot. Joint space is preserved in spite of eroded bones of the foot, other foot joints, and carpometatarsals.||Commonly involves hips, knees, metacarpophalangeal, midcarpal, and patellofemoral joints. Asymmetric joint-space narrowing, sclerosis, bone enlargement, osteophytes.|
|Erosions caused by tophi in cartilage, often with a spicule of surrounding bone; asymmetric soft-tissue swelling caused by urate deposits.||Formation of subchondral cysts; collapse of bony surface.|
Timing. Pain from a herniated disc gets progressively worse as the day goes on. A dull ache during rest that’s aggravated by motion suggests inflammatory arthritis. Pain lasting for several weeks or longer is common in chronic arthritis. In acute rheumatic fever and often in gonococcal arthritis, joint pain lasts for several hours, disappears, then reappears in other joints. Pain worse in the morning after rest that is relieved after mild exercise but worsens in the evening points to joint disease. Deep, aching, throbbing, dull or sharp pain that may be either constant or spasmodic is typical of joint disease.
Unusual Absence. Neuropathy is suspect when there is no pain but obvious joint disease. In such cases, diabetes mellitus is the usual fault. When pain fibers are destroyed or deadened in joint disease, injury is not safeguarded against and traumatic osteoarthritis advances rapidly. In history of a nonmedicated painless limp, muscle disease is the first suspicion, but a metabolic bone disease or an endocrine dysfunction may be involved in children.
The major points of significance during joint inspection and palpation are ummarized in Table 9. Two important factors to determine are the ranges of joint motion and joint flexibility. Middleton defines joint range of motion (ROM) as the available amount of movement in a joint (in each normal plane) and joint flexibility as the ability of joint soft tissues (muscles, tendons, and other connective tissues) to elongate through the available range of oint motion.
Table 9. Review of Major Points During Joint Inspection and Palpation
|1.||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 they are not. Fluid or semifluid exudates in joints may fill and smooth the natural depressions around the joint, or, if the exudate is large, may bulge the joint pockets. In the knee joint, four eminences may replace natural depressions: two above and two below the patella.|
|3.||Irregularities of contour: osteophytes or lipping (attached to bone); gouty tophi (not attached to bone); constriction line opposite the articulation; or protrusion of joint pockets in large effusions, filling natural depressions. Irregularities of contour are easily recognized, providing the normal contour is familiar.|
|4.||Limitation of motion. This is due to pain and effusion, muscular spasm, thickening or adhesions the capsule and periarticular structures, obstruction by bony overgrowths or gouty tophi or ankylosis.|
|5.||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 seem normal or are not grossly injured, the excessive motility of the joint is called a subluxation, but excessive motility may also be due to destruction of bone and other essential of the joint (eg, as in Charcot joints).|
|6.||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.|
|7.||Free bodies in the joint. These are not palpable externally and are recognized only by their symptoms, roentgenography, or invasive surgery.|
|8.||Trophic lesions over or near a joint (cold, sweaty, mottled, cyanosed, white or glossy skin, muscular atrophy).|
|9.||Sinus formation; the sinus leading to necrosed bone, gouty tophi, or an abscess in or near the joint.|
|10.||Distortion or malposition due to contractures in muscles near the joint, to necrosis, to exudation, or to subluxation.|
|11.||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 to the hip joint. One method is to mark the tip of each ASIS with a skin pencil and likewise the tip of each inner malleolus. Then, with the patient lying prone on a flat table, the distance from the ASIS to the inner malleolus is measured bilaterally on each side with a tape.|
A tough “springy” block exhibiting some rebound at the end of an arc usually indicates contracture or a deranged cartilage; motion may be normal in one direction and completely absent in another. In most cases of chronic extremity subluxations, resistance will be felt before passive motion induces pain.
If the extent of joint limitation depends on the position of another joint, it can generally be assured that the cause is extra-articular; ie, the cause is within a structure spanning the two joints. Hip flexion, for example, may be limited with the knee extended but not with the knee flexed, indicating shortened hamstrings. Another example can be seen in Volkmann’s ischemic contractures in which the fingers cannot be extended unless the wrist is first flexed. When a sudden protective spasm occurs at some point during motion (felt as a firm resistance), an active localized lesion should be suspected.
Neuritis associated with joint stiffness causes pain on active motion but a full passive range of movement exists. Pain induced by passive motion in one direction and active motion in the opposite direction signifies a lesion of a muscle or its tendon; ie, the muscle becomes painful when passively stretched by manipulation or contraction of its antagonists.
To distinguish muscle spasm from bony outgrowth as a cause of limited joint motion, remember that bony outgrowths allow free motion to a certain point and then motion is arrested suddenly and without pain. Muscle spasm, on the contrary, checks motion somewhat from the onset. Resistance and pain gradually increase until the examiner’s efforts are arrested at some point that feels like a “thick rubber” block. When passive motion causes sharp pain far before the end of motion has occurred and little internal resistance is felt on further motion, an acute inflammatory process, a mass, or a psychosomatic disorder should be suspected.
Contractures typically exhibit limited motion in one direction and painless motion in all other possible directions. A “snapping” sound results when a tendon abruptly slips over a bony prominence or fibrotic soft tissue. This is often seen in tendon displacements, osteoma, lax joints, and trigger fingers.
Tenosynovitis exhibits pain during both stretch and relaxation as the roughened tendon slides within its inflamed sheath. A mushy “boggy” sensation at the end point is the typical feature of chronic joint effusion in which synovitis is minimal. A firm “leathery” arrest occurring before the end of normal motion in some directions but not others suggests restraining fibrotic ligaments, adhesions, or capsule thickening as often seen in subacute arthritis.
Motion limited by capsular thickening and adhesions are not, as a rule, as painful after the first limbering-up process is over. There is no sudden arrest after a space of free mobility, but motion is limited very early and usually in all directions even if the muscles around the joint are not rigid. The possibility of limbering-out after active exercise (or passive motion) distinguishes this type of limitation. Restricted mobility from capsule restriction usually follows inadequately treated acute traumatic arthritis, degenerative joint disease, or prolonged immobilization.
Joint trauma is often profiled by a cool periarticular swelling that is extremely tender. Direct trauma or secondary inflammation can result in hemorrhage or effusion. Painless bony lumps and asymptomatic joint swelling can often be traced back to forgotten trauma, especially when associated with sport injuries. In degenerative joint diseases, the trauma may be only normal activity sufficient to elicit effusion.
Joint swelling can originate from edema arising in the joint proper, edema originating in the extra-articular tissues around the joint, and/or edema derived from the bones forming the joint. The key features of joint swelling are its variable character, shape, effect on motion restriction, and effect on joint positioning, and its visibility.
Character. Swelling around a joint that is warm and painful is characteristic of gout and rheumatic arthritis. Synovial inflammation is characteristic of the nonspecific arthritides, rheumatic fever, septic arthritis, gout, and various collagen-vascular diseases. A gonococcal wrist or ankle joint will usually be associated with nearby tenosynovitis.
Swelling about a joint can be caused by edema from fluid overload or venous insufficiency. When this occurs, pain and tenderness will be absent. Infiltration, effusion, or inflammation can cause direct joint swelling. Localized infiltration is seen in leukemia, myeloma, and amyloid disorders. The major differentiating signs of hemarthrosis and synovitis are shown in Table 10.
Table 10. Differentiation of Posttraumatic Joint Swelling
|Rapid onset||Slow onset, may not occur for 24 hours|
|Small periarticular swelling||Large periarticular swelling|
|Hot, painful joint||Warm, aching joint|
Shape. The shape of a swollen joint corresponds to that of the synovial membrane distended in toto. When a subcrural pouch becomes dilated, for instance, swelling of the knee joint may extend as much as 7 inches above the joint line. Another example is that distention of the tabular process of endothelium about the long head of the biceps in the shoulder may exhibit enlargement over the surgical neck of the humerus.
Location. A swollen joint is often the result of thickening synovial membrane or excessive fluid in the joint cavity. This swelling is often obscured by bones, muscles, and tendons overlying the joint cavity or its pouches; however, it is noticeable over thinly covered areas of the joint. For instance, swelling in the hip joint is almost impossible to detect.
Swelling in the elbow is observed only at the posterior aspect on the sides of the olecranon process because the anterior surface of the elbow joint is thickly covered with muscles and the lateral aspects by strong collateral ligaments that prevent protrusion. For the same reasons, a wrist swelling is least noticeable when viewed from the front and radial side and a knee swelling is least noticeable when viewed from the medial or posterior aspect.
Positioning. Because of the relative position of various bones and associated relaxation of the muscles around joints, every joint has one position in which the synovial cavity attains the greatest dimensions. When tension increases in the synovial cavity because of effusion, the patient will adopt a specific position that gives the greatest relief.
Motion Restriction. In general, joint motion becomes restricted from either pain or mechanical disability. Intra-articular swelling impairs both active and passive movements, while extra-articular swellings impair only one type of movement or none. Foreign bodies or fragments within a joint resulting in effusion are associated with intermittent motion restriction.
Traumatic arthritis presents with signs of pain, possible ecchymosis, and soft-tissue swelling of periarticular tissue that may be limited to effusion within the capsule or obliterate bony prominences. This depends on the severity of the trauma. As the process develops, spurs and lipping at fibrous tissue attachments, fibrocystic degeneration of articular surfaces, and possibly posttraumatic deformity in bone tissue are typical. In soft tissues, fibrous and fatty degeneration may be noted. Motion is usually limited because of pain, and there will be joint instability if the injury is sufficient to tear a tendon or joint capsule. Intra-articular fractures and fragments may be associated.
Second only to polyosteoarthritis, the most common cause of bone/joint degenerative disease is the result of posttraumatic degenerative arthritis from severe injury or chronic stress. The phases of chronic peripheral joint degeneration are shown in Table 11. Any joint may be involved, but the most common sites are the hip, knee, first metacarpophalangeal joint, first metatarsophalangeal joint, and apophyseal joints of the spine.
Table 11. Phases of Chronic Peripheral Joint Degeneration
|History||Strain/sprain.||Strain/sprain with likely history of previous injury.||Chronic episodes of pain|
|Signs and symptoms||Periarticular muscle spasm, pain aggravated by certain movements (eg, “catches”), tenderness, motion restriction, slight swelling at times.||Like features of dysfunction, except tendency toward collapse and feelings of weakness are usually reported, a periodic segmental shift may be seen during active motion.||Pain, area stiffness, incapacitating attacks after minor trauma, muscle weakness.|
|Biomechanics||Tension or compressive overstress leading to subluxation.||Hypermobile joint motion with frequent subluxation, cartilages likely malpositioned.||Hypomobile joint motion|
|Pathology||Small cartilage fissures, possible disc displacement, synovitis leading to fixation by intra-articular adhesions and/or articular cartilage degeneration, likely subluxation.||Lax capsule, coalesced probable subluxation. disc tears, possible nipping of synovia.||Fibrosis, cartilage bodies, severe joint space thinning, marginal osteophytes leading to ankylosis.|
Whenever joint trauma is the chief factor, an acute arthritis is likely to be induced. As with all trauma, the extent of the local reaction is relative to the severity of the injury and the resistance of the tissues. Arthritis resulting from a single severe injury, especially if improperly treated, may be indefinitely prolonged and result in chronic symptoms and permanent disability. Repeated injuries from excessive joint stress can cause pathologic reactions or derangement within the joint.
It was once thought that this common disorder was the result of joint trauma and overwork, but evidence collected during recent years shows that degenerative bone disease is just as common in the sedentary individual as it is in the manual laborer or professional athlete. Thus, the explanation of prolonged overstress can no longer be held valid as a general assumption.
While the cause of osteoarthritis is still unknown, it is possible that it will be found within investigations of the nutrition of articular cartilage. We do know that fibrocartilage and hyaline cartilage is nourished essentially by a pump-like action in which nutrients are pulled or sucked inward and metabolic products are exuded or expelled outward during reciprocatively opposite joint motions. If an articular fixation (motion restriction) exists, it is likely that this pump-like mechanism will not be effective.
If any tissue is not properly nourished, its power and reserves to withstand normal stress are diminished and lead to inflammation initially and degeneration when prolonged and tissue defenses are depleted. When degeneration is advanced, the structural design of the segment will not allow normal function and normal proprioceptive input to the CNS is severely altered.
Violent muscle strain damages the periosteum, and if severe enough to detach periosteum, a degree of hematoma develops. The bruised area is swollen, extremely tender, and movements are restricted. Physical examination makes one suspicious of fracture, but early roentgenographic findings are negative. Later, ossification of the hematoma is exhibited by induration of the swelling and new bone formation. New bone formation occurs from many causes whenever the outer periosteal membrane of bone is irritated (osteoblastic reaction). The formation of new bone may appear on film as either a solid or an interrupted mass, which can be an aid in differentiation.
Bursa are fluid-filled pads designed to aid motion between contiguous tissues. Bursitis is an inflammatory reaction of thickened synovium in which there is excessive secretion of fibrin-rich synovial fluid that may lead to an abscess if secondary infection occurs from local or systemic sources.
The microscopic picture of bursitis and tenosynovitis is almost identical, but prolonged friction is the most common cause of bursitis. The size of an inflamed bursa may increase many fold if not protected from further injury. The bursa located near the patella, olecranon, and hip are commonly involved.
Synovitic vs Mechanical Lesions
Articular and periarticular disorders present with one or more of three basic clinical patterns:
- joint inflammation or synovitis,
- mechanical or cartilaginous lesions, and/or
- nonarticular rheumatism that mimics arthritis. Bursitis and tendinitis also express themselves on periarticular structures, but signs of internal joint involvement are absent. Weakness of proximal muscles is a major finding in myositis, not swelling or tenderness about involved joints. Refer to Table 1.
Synovitic Lesions. Synovitic lesions may involve any synovial joint. In contrast, mechanical lesions primarily attack only the weight-bearing synovial joints. Thus, deformities of non-weight-bearing joints such as the elbows, wrists, and fingers generally indicate the effects of synovitis. Synovitic disorders are characterized by persistent symptoms during use and at rest that are helped by anti-inflammation therapy. There is prolonged morning stiffness, and the course fluctuates with exacerbations lasting from weeks to months.
Mechanical Lesions. Mechanical disorders are characterized by symptoms arising chiefly with use that respond poorly to anti-inflammatory therapy. Morning stiffness is minimal and short-lived after loosening movements. Damaged cartilage has little ability to repair itself. Thus, once mechanical lesions are produced, they tend to progress in severity with time and use. Asymptomatic intervals do not occur as they do with synovitic lesions.
Possibly Associated Nonarticular Rheumatism Involving Joints. Some types of periarticular inflammation or rheumatism may mimic rheumatoid or degenerative joint lesions or be superimposed on them. Fibrositis, polymyalgia rheumatica, palmar fascitis, reflex sympathetic dystrophy syndrome, and psychogenic rheumatism follow an intermittently or gradually worsening course and are thus likely to be mistaken for rheumatoid or degenerative joint disease. Hypertrophic osteoarthropathy should also be differentiated.
A capsule tear is usually the results of an unexpected joint force, often occurring in an abnormal plane of motion. The torn tissues produce hemorrhage and local tenderness. Damage to the synovial membrane is commonly associated, resulting in effusion and possible hemarthrosis. Unless joint instability is severe, capsule injuries improve well with conservative care. Early treatment is not remarkable. It should consider cold, pressure, rest, and a graduated muscle education and exercise regimen. After acute symptoms subside, contrast baths, deep heat, and more active movement can begin.
A sudden joint stress, often rotational, may cause some soft tissue to be pinched within articular structures. This is most frequently seen in the knee where infrapatellar fat is nipped, resulting in effusion and possibly hemorrhage. Management is the same as that for strain/sprain, but movement is delayed for several days because injured fat is slow to heal.
As with adhesions, pain arises from most cartilaginous tissues only when they are displaced or swollen and stretch or pressure is applied on adjacent pain-sensitive receptors. The periphery of most fibrocartilages (eg, IVDs, menisci of the knee and jaw) contains some nociceptors, but the degree that they are involved in a patient’s report of pain is difficult to determine. A cartilaginous loose body will certainly produce pain if it is caught between two apposing pain-sensitive articular surfaces.
Cartilaginous thickening and even chondrophytes at articular sites have been shown to be impregnated with sensory fibers; thus, pain can arise when they are compressed. If adjacent tissues are inflamed, then both compression and tensile forces will give rise to pain.
Injury to fibrocartilage is usually associated with the spine and knee but is occasionally related to the temporomandibular, sternoclavicular, and distal radioulnar joints. Moderate cases can usually be managed by adjustments, rest, physical therapy, and muscle reeducation, but crippling cases may require surgery.
When injured, cartilaginous and disc substances progressively undergo degenerative change with possible dehydration and fragmentation. IVD damage results from repeated vertebral subluxation and the strain of mechanical and postural incompetence that tend to weaken the annulus, and, in the cervical and lumbar spine areas especially, at the posterolateral aspects with possible bulging into the intervertebral foramen. Some DCs believe that there may also be a visceral reflex causing a slight vasospasm leading to degeneration.
An osseous dislocation (luxation) is defined as the displacement of the normal relationship of the articular surfaces of the bones that comprise a movable joint. It places considerable stress on the ligaments that normally maintain the involved joint’s position. There may be injury to these ligaments, the capsule they form around some joints, articular cartilage, synovial membrane, and other related soft tissues, as well as hemorrhage into or around the joint. Gross dislocations require x-ray analysis before reduction by a specialist.
A dislocation may result in a complete luxation or a subluxation. If articular surfaces lose contact during the disruption of trauma and lock in this position, a dislocation is formed. If articular surfaces lose contact but return to a position where the articular surfaces are in contact, an orthopedic subluxation is formed. Regardless, the finding of a dislocation or an orthopedic subluxation implies a sprain has occurred.
Following reduction of acute dislocation or mobilization of a fixated subluxation, the injury is treated as any severe sprain (acute or chronic). The fact that articular surfaces present in a dislocated or subluxated position or remain so for 30 seconds or 30 days gives no indication of the extent of ligament damage (grade of sprain). Thus, although static x-ray films may eliminate suspicions of fracture, they are no help in determining whether a mild sprain exists or a severe rupture has occurred requiring surgical repair.
In the extremities, a subluxation may be the effect of a spontaneously reduced dislocation and associated with considerable capsule and ligament damage. Pain, swelling, and deformity are centered about the joint. There usually is loss of motion. Related ligaments are frequently torn and may require surgical repair.
Emergency Care and Related Considerations. A dislocation is immobilized in the same way as a fracture: close to the joint. Cold compresses may be applied to the joint to relieve pain and reduce swelling, but the patient’s temperature must not be lowered to a point inviting shock.
Postreduction immobilization usually requires 6 weeks in the lower extremity and 3 weeks in the upper extremity. These durations should be reduced whenever possible to reduce the ill effects of immobilization. Inadequate care, especially in ankle, shoulder, and spinal dislocations/subluxations leads to chronic weakness, movement restrictions, instability, and recurrent dislocation in which subsequent surgery or conservative care has a poor prognosis in restoring preinjury status.
Growth plates in the young are highly susceptible to severe stress because of their vascularity.
Epiphyseal Displacements. Malpositions are often seen in the young and are almost always associated with trauma. They may occur spontaneously, especially in the hip where they are often associated with unexplained or misdiagnosed knee pain. The growth plate is weakest at the site of cell degeneration and provisional calcification, especially in children undergoing a rapid spurt in growth or who are overweight in proportion to their skeletal maturity. A common pitfall in orthopedics is to confuse an epiphyseal slip for a ligament injury; eg, at the knee joint. Epiphyseal slips should be treated as fractures, for fractures are what they are rather than a disease process.
Osteochondritis. Traumatic intrajoint changes as the result of overstress are featured by displacement, bony fragments, distortion or collapse, and irregular ossification during the late stages. Osteochondritis may occur at almost any epiphyseal plate, and it is often named after a descriptive author. For example:
Vertebral plates – Scheuermann’s disease
Femoral head – Perthe’s disease
Tibial tubercle – Osgood-Schlatter’s disease
Tarsal navicular – Kohler’s disease
Heel – Sever’s apophysitis
Metatarsal heads – Freiberg’s disease
Such terminology is confusing as the condition is not a disease, and this should be explained to the afflicted.
Osteochondritis Dissecans. This disorder features inflammation of subchondral bone and articular cartilage that results in split pieces of cartilage within an affected joint. The cause is not completely understood, but the damage is inevitably at a point where compression occurs in a jarring injury. The clinical picture reflects avascular necrosis where flakes or loose bodies of bone and/or cartilage are extruded into the joint. The knee, ankle, and elbow are most often affected.
PERIPHERAL NERVE TRAUMA
Direct trauma to a nerve is rare for most nerves are overlaid with protective muscle and fat. O’Donoghue lists exceptions to this as the axillary nerve at the shoulder the ulnar nerve at the elbow, the radial nerve in the forearm, and the peroneal nerve behind the head of the fibula.
Peripheral nerve disorders may be the cause of, a contribution to, or superimposed on articular disorders. Radiculogenic pain is distributed over the course of the nerve and may be altered by certain spinal movements but not usually by isolated use of the joint. In contrast, pain associated with vascular insufficiency is located distally and related to use of the joint. Nocturnal pain suggests neuropathy, a nerve root lesion, a bone lesion, or tendinitis, but it is not characteristic of advanced cases of degenerative arthritis.
Damage to an individual peripheral nerve is characterized by flaccid, atrophic paralysis of the muscles supplied by the involved nerve and loss of sensation, including proprioception, in the skin distal to the lesion. When partial destruction to various peripheral nerves occurs, the effects are usually more prominent in the distal extremities. The condition features muscle weakness and atrophy and poorly demarcated areas of sensory changes. Associated trophic lesions of joints, muscles, skin, and nails are common. They blend and are somewhat explained as the results of vasospasm.
In simple contusion, there is an immediate shocking sensation that is followed by numbness and pain that passes in a few minutes. In more severe contusion, there is persistent aching pain along the distribution of the nerve and weakness of the muscles supplied that are the effect of edema and congestion of the nerve and its sheath. In severe injuries, paralysis (eg, wrist drop, foot drop) may result. The major features of routine myotome tests, dermatome tests, and reflexes are shown in Table 12.
Table 12. Common Myotome Tests, Dermatome Tests, and Reflexes
|Key Sensory Areas|
|Reflexes to Test|
|Shoulder shrug, diaphragm action|
|Shoulder abduction, external rotation|
|Wrist extension, elbow flexion||Thumb, index finger, radial edge of hand||Biceps, radial, triceps|
|Wrist flexion, elbow extension||Middle fingers||Radial, triceps|
|Ulnar deviation of wrist. thumb abduction||Ring and small finger, ulnar edge of hand||Radial|
|Hip flexion||Medial thigh||Patella|
|Knee extension, hip flexion||Anteromedial and distal thigh||Patella|
|Knee extension, ankle dorsiflexion||Medial surface of large toe||Patella|
|Ankle eversion, large toe dorsiflexion.||Web space between large toe and 2nd toe|
|Plantar flexion, ankle eversion, knee flexion||Beneath lateral maleolus||Plantar, Achilles|
|Plantar flexion, knee flexion||Back of knee||Plantar, Achilles, bulbocavernous|
|Saddle region||Anal, bulbocavernous|
Posttraumatic paralysis may be immediate as the result of a severed nerve or a nerve block (eg, fracture) or slowly progressive because of the growth of a mass (eg, hematoma, scar tissue). Unless caused by a penetrating wound, few cases require surgical joining. Most cases recover completely and relatively rapidly, unless axons degenerate, with conservative therapy to the involved nerve and the musculature it supplies. However, any nerve injury requires careful monitoring. If necessary, surgical exploration should only be delayed for a reasonable time (30–60 days).
Three Classes of Peripheral Nerve Trauma
Contusion (Neurapraxia). Contusion may be the result of either a single blow or through persistent compression. Fractures and blunt trauma are often associated with nerve contusion and crush. Peripheral nerve contusions exhibit early symptoms when produced by falls or blows. Late symptoms arise from pressure by callus, scars, or supports. Mild cases produce pain, tingling, and numbness, with some degree of paresthesia. Moderate cases manifest these same symptoms with some degree of motor-sensory paralysis and atrophy. Recovery is usually achieved within 6 weeks.
Crush (Axonotmesis). Recovery rate is about an inch per month between the site of trauma and the next innervated muscle. If innervation is delayed from this schedule or if the distance is more than a few inches, early referral for surgical correction should be considered.
Laceration (Neurotmesis). Laceration follows sharp or penetrating wounds and is less frequently seen associated with tears from a fractured bone’s fragments. Surgery is usually required. A traction injury typically features several sites of laceration along the nerve. Stretching injury is usually but not always limited to the brachial plexus.
Nerve Pinch or Stretch Injuries
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 pulled, partially torn, or ruptured most anywhere in the nervous system -from the cord to peripheral nerve terminals.
Nerve “pinch” or “stretch” syndromes are common in sports, but they are also seen after falls and industrial accidents. The syndromes can appear in the face, spine, pelvis, and extremities. Hardly any peripheral nerve is exempt. A nerve pinch syndrome may be due to direct trauma (contusion and swelling), subluxation, dislocation, an expanding mass (eg, hematoma), or fracture (callus formation and associated posttraumatic adhesions). Any telescoping, hyperflexion, hyperextension, or hyperrotational blow or force to a limb may result in a nerve pinch syndrome where pain may be local or extending distally.
Nerve Entrapment Syndromes
A peripheral nerve entrapment syndrome is a distinct type of neuropathy in which a single nerve is compressed at a specific site (eg, within fibrous tissue, a fibrous-osseous tunnel, or a muscle), either by external forces or surrounding tissues in an abnormal state. Peripheral entrapment syndromes are often related to congenital defects, overuse, and scar-tissue development following trauma or surgery. A locally impaired blood supply may further damage the entrapped nerve if associated vessels become stretched, kinked, or compressed, or if blood flow is obstructed in some way.
So the patient may avoid unnecessary pain and disability, it is important to identify a peripheral entrapment syndrome rapidly through examination and appropriate diagnostic studies such as electromyography, nerve conduction evaluations, and roentgenography. Severe impairment of nerve function is usually only reversible in its early stages.
Vulnerability to Trauma
If the nerves of the body were placed end to end, they would span an average distance of 45 miles. Fortunately, most large nerves of the body lie deep where they are protected by muscle and bone. In only a few areas are major peripheral nerves particularly exposed to direct contusion from a blow:
The axillary nerve in the shoulder
The radial nerve in the midarm
The ulna nerve at the elbow
The peroneal nerve behind the head of the fibula.
General Neuromuscular Mechanisms
Healthy muscle is characterized by active contraction in response to the reaction of the nervous system to the environment. This readiness to act results in firing of motor units as stimuli from the environment impose upon the nervous system; it is expressed as muscle tone. Muscles losing their tone through lack of activity, primary muscle disease, or nerve damage become flaccid.
The tone of musculature is due to the constant steady contraction and relaxation of different fibers in individual muscles that help to maintain the “chemical engine” of the muscle cells. Even minor exercise helps to maintain tone by renewing blood supply to muscle cells.
Acute trauma can be superimposed on a subclinical peripheral nerve isease, which will often offer a confusing clinical picture. The primary causes of peripheral neuropathy are shown in Table 13.
Table 13. Causes of Peripheral Nerve Disease
|Collagen vascular disease||Paraneoplastic lesions|
|Hereditary factors||Chemical solvents|
|Peroneal muscular atrophy||Trauma|
|Refsum’s disease||Direct or indirect|
|Infection||Tumors involving nerves|
|Acute intermittent porphyria||Vitamin deficiency|
|Diabetes mellitus||B-12 (malabsorption)|
|Liver disease||Thyroid disease|
Pathologic peripheral nerve disorders are characterized by paresthesias (eg, numbness, pins and needles), dysesthesias (eg, hypesthesia, hyperesthesia, anesthesia), weakness, cramping with rapid fatigue, and muscle atrophy. The causative lesion, which may or may not have trauma in its history, can be in a root (radiculopathy), plexus (plexopathy), individual nerve (mononeuropathy), or several nerves (polyneuropathy). As the peripheral nervous system is a direct extension of and two-way communicator with the central nervous system, the concept of a pure peripheral disorder is theoretical.
Besides trauma, peripheral neuropathy may be associated with a large number of diseases. Diabetes, cancer, liver or kidney failure, immunologic impairments, and endocrine or metabolic disturbances are the most frequent agents. Folic acid, niacin, pyridoxine, thiamin, and vitamin B12 deficiencies have also been linked to peripheral neuropathy.
Various medications, industrial solvents, commercial poisons and pesticides, and exposure to heavy metals are also common causes of diffuse peripheral neuropathy. Any of these conditions may be underlying or superimposed on what first appears to be a simple joint disorder. Differential diagnosis can be a complex process.
When peripheral neuropathy is suspected, the physical work-up should include evaluation of reflexes, muscle strength, pain, temperature (hot and cold), joint position, and vibration. Appropriate blood tests include sedimentation rate, hematocrit, CBC and differential, glucose tolerance, blood culture, serum electrolytes, serum calcium, serum acid and alkaline phosphatase, and drug screens. Urine should be examined for heavy metals. In many chiropractic offices, electrodiagnostic evaluations are considered a standard part of the neurologic examination rather than a laboratory procedure. Electromyographic recordings should be taken if the equipment is available.
Joint infection may obviously be the result of extension, be blood borne, or be the result of a penetrating wound. Hematoma or hemarthrosis is an invitation to a subclinical blood-borne condition to manifest. 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.
In some cases, the clinical picture may not be from a true infection. It could be a sterile inflammatory irritation from malfunction in an organ that reflexly produces vasospasm in the joint and, hence, associated pain and lowered resistance. Irritation produced by malfunction of a viscus can produce many remote symptoms difficult to diagnose. Several factors determine the characteristics of bone or joint infection in any particular case:
The duration and virulence of the disease
The degree of destructive activity
The degree and extent of soft-tissue atrophy
The amount of reactive swelling
The degree of repair accompanying destruction
The type of decalcification involved.
Once bone marrow is invaded, infection usually spreads throughout the marrow to a degree depending upon host resistance and the virulence of the microorganism. When an infection becomes localized, the abscess will produce a small focus of cancellous or cortical bone destruction. This site becomes limited by adjacent sclerotic bone: a natural defensive reaction.
During the early stage, the area contains purulent exudate, granulation tissue invades neighboring bone, and the area destroyed may be completely replaced by fibrous tissue. Surviving bone at the site of active infection becomes osteoporotic from disuse atrophy and the amount of inflammation. When the infection begins to diminish and function begins to return, radiographic density increases.
Special Considerations of Childhood. Edeiken explains that infection in bones and joints is different in infants, children, and adults. In the infant, many vessels penetrate the epiphyseal plate into the epiphysis and vice versa. Thus, in the metaphyseal area, infections are easily spread to the epiphysis and into the soft tissues of the joint since the epiphysis is intra-articular.
Fewer vessels penetrate the epiphyseal plate as the child matures, thus there is less chance of epiphyseal infection and joint involvement from metaphyseal infection. Because infants have a loose periosteum, infections readily strip the periosteum and extend to the articular end of the bone. The metaphyseal vessels in the child loop backward into sinusoids allowing a fertile area for the implantation of infection. Infections easily extend to the joint once the epiphyseal plate closes as there is a direct connection with the epiphyseal vessels.
Osteomyelitis is a general term referring to any acute or chronic infectious bone inflammation, especially that involving marrow. The acute form is common in children; the chronic form, in adults. It can rarely be treated conservatively for clinical features arise only in the advanced stage.
Acute Forms. With the exception of operative surgery, compound fractures, repeated injuries, piercing wounds, and surgical procedures, acute osteomyelitis infrequently occurs. Symptomatology includes bone pain in the affected part that is increased by pressure, inflammation of overlying skin that presents warmth and erythemia, general fever and hyperhidrosis, chills, leukocytosis, splinting of overlying muscles, and possible suppuration. If suppuration occurs, it is usually associated with a draining skin sinus. This can be a life-threatening stage in children. Consider the possibility that an underlying pulmonary or gastrointestinal infection may be the primary focus.
Diagnosis is made by blood culture, culture of aspirations, routine blood profiles for septicemia, and roentgenography. Common differentiating roentgenographic patterns of bone destruction occur. Mercier points out that no matter what type of osseous resorption takes place, as much as half the bone must be destroyed before evidence appears radiographically.
Chronic Forms. The most common site of chronic osteomyelitis is below a weight-bearing joint (eg, vertebra, knee, ankle). The nidus of infection may become surrounded by dense bone and fibrotic tissue and be asymptomatic but unable to be cleared by the body’s immunologic defenses or antibiotic therapy. Subsequent superimposed trauma may reactivate the inflammation, cellulitis, and sinus drainage.
Adhesions are a product of infection (extrinsic or intrinsic) or sterile inflammation, usually traumatic. Strong fibrous bands usually bridge from one fascial surface to another but may span between any two structures. At times, they may resemble a ligament and serve a beneficial function. In other circumstances, they may restrict normal articular motion, compress vessels or nerves, glue normally mobile adjacent tissues, or in some other way interfere with normal function where they become a therapeutic challenge.
Adhesions are not elastic. They are strong bands of fiber. For example, adhesions forming after pericarditis have been known to restrict normal movement of the heart. Unpropitious adhesions are commonly found in the abdomen following surgery or near any extremity part that has been traumatized and received inadequate care.
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 the fact that there is a pronounced structural hypomobility when adhesions are present.
A common encounter is the painful adhesions that develop after surgery or major trauma. However, joint adhesions may develop as the result of adhesive capsulitis, rheumatoid arthritis, septic arthritis, etc. Pain originating in capsules tightened by adhesions occurs immediately when the capsule is stretched. If the adhesions are stretched further, a sharper pain may ensue. Its intensity 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. The surrounding muscles are flaccid.
In profiling a traumatized patient’s status, an underlying nutritional deficiency may fail to be considered because overt signs of deficiency are not apparent. While it is true that gross signs of malnutrition are infrequently seen in the United States, this does not exclude the role that subclinical vitamin, mineral, and trace nutrient deficiencies have in contributing to neuromusculoskeletal disorders and hindering or impairing healing.
Basic Factors Leading to Malnutrition
Digestion and assimilation are not mechanical acts that produce the same results in all human beings. Anything that interferes with the absorption and utilization of nutrients contributes to malnutrition. Typical examples are gastrointestinal disorders and emotional stress producing abnormal gastric and intestinal activity. Food allergies readily interfere with digestion. Excessive perspiration, diarrhea, and polyuria commonly cause an increased loss of nutrients. In addition, excessively low or high temperatures during physical activity or high humidity increase nutritive requirements.
Physical Conditioning Factors Contributing to Malnutrition
Continuous participation in athletics or strenuous work increases an individual’s caloric and nutrient requirements, just as do the effects of a fever. Thus, a diet adequate under normal sedentary conditions may be far inadequate to meet the needs of demanding activity, growth, or illness. Nutritional inadequacies do not happen suddenly, they exhibit after a long insidious course. In its early stages, the only symptoms noticed may be tiredness, irritability, low morale, lowered efficiency, and reduced resistance to disease.
Stages of Malnutrition
Dolan/Holladay describe the development of malnutrition in athletics in four stages. The same can be assumed for physical laborers.
First Stage. The stage of tissue depletion and weight loss in which the tissues become depleted of their stored nutrients. This depletion progresses at a rate relative to the severity and chronicity of the deficiency state.
Second Stage. The stage of biochemical “lesions” in which alterations in the normal constituents of the blood occurs, exhibited in a distinct shortness of breath on exertion.
Third Stage. The stage of functional changes and overt symptom development. The patient may require longer warm-up periods to loosen muscle tissues of the extremities. Postexercise soreness lasts longer, and injuries take longer to heal. Peripheral neuritis may result from a thiamin deficiency.
Fourth Stage. Progressing symptoms are so severe that strenuous activities become impossible before this stage is reached. Overt clinical signs appear in bones, muscles, and nerves, and with vision and behavior.
Vitamins and minerals are fundamentally involved in the nutrition of most if not all body cells. An inadequate supply over a long period results in disease and possibly death. Fortunately, as enzymes and catalysts, vitamins are needed in extremely small amounts. Evidence does not indicate that moderate exercise or labor significantly increases the body’s requirements for vitamins, nor have massive amounts of specific vitamins or combinations been shown to safeguard against infection, prevent injury, improve endurance, or benefit performance. However, logic dictates that optimal nutrition will enhance the healing process and sustain defensive reserves.
The term “overnutrition” is a misnomer if taken in a general sense. A better synonym would be “hyperphagia,” especially diets rich in fats and sugars. But this would not take into consideration the effect of inactivity on metabolism or appetite regulation, of endocrine imbalance, or of hypothalamic lesions affecting the theoretical “set point.” Pollock/Wilmore quote Jean Mayer, world-famous nutritionist, as saying, “I am convinced that inactivity is the most important factor in explaining the frequency of ‘creeping’ overweight in modern Western societies.” Several studies are reported to support this conclusion.
Malnutrition in the Physically Active
Continuous participation in athletics increases an individual’s caloric and nutrient requirements, just as seen in the effects of a high fever. The conclusion of a government study determined that human motion can be viewed from its workload (caloric) requirements: light (2.5-5.0 kcal/minute), moderate (5.1-7.5), heavy (10.1- 12.5), exhausting (12.6+).
A diet sufficient under sedentary conditions may be far inadequate to meet the needs of prolonged physical activity, growth, or illness. When exercise needs are combined with growth needs in the young, there is a definite nutritional challenge. Malnutrition in the physically active does not occur suddenly, it exhibits during a long insidious period. In its early stages, the only symptoms noticed may be of easy fatigue, chronic tiredness, irritability, low morale, lowered efficiency, and reduced resistance to disease.
Anything interfering with the absorption, assimilation, metabolism, or utilization of nutrients contributes to malnutrition. Typical examples are gastrointestinal disorders and emotional stress causing excessive gastric and intestinal activity. Food allergies readily interfere with digestion. Excessive perspiration, diarrhea, and polyuria are common factors causing an increased loss of nutrients. In addition, excessively low or high temperatures during strenuous physical activity or in an atmosphere of high humidity increase nutritive requirements.
The indications, applications, and contraindications for common modalities and other applied physiologic therapeutics are described in Jaskoviak PA, Schafer RC: Applied Physiotherapy.
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