THE RATIONALE OF REHABILITATIVE THERAPY
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Survey the situation for a medical emergency, and take whatever first-aid measures are necessary, record patient status and vital signs, and record as much of a detailed history as possible under the circumstances. Record findings of inspection and tolerated palpation and moverment of the part involved. Auscultate the area for crepitus, observe abnormal limb position suggesting fracture or dislocation, and seek signs of CNS injury or hemorrhage. Record integrity of normal superficial and deep reflexes and occurrence of pathologic reflexes, and order roentgenography if fracture or dislocation is suspected. Record findings of involved joint range of motion studies and muscle strength to the degree possible at the stage existing at the time of examination, order electromyographic and/or thermographic studies as indicated, and order pertinent laboratory studies. Coordinate findings, patient’s objectives, and prognosis, and set clinical goals, treat and monitor, periodically reassess patient progress with the working diagnosis and clinical goals, and retest when confirmation is necessary.
Recording oral temperature, comparing extremity pulses and limb blood pressure, and auscultating the heart and lungs should be routine in any examination. Traumatic injury is no exception.
For many centuries, therapeutic rehabilitation was a product of personal experience passed on from clinician to clinician. In the last 20 years, however, it has become an applied science. In its application, of course, much empiricism remains that can be called an intuitive art --and this is true for all forms of professional health care.
The word trauma means more than the injuries so common with falls, accidents, and collision sports. Taber* defines it as "A physical injury or wound often caused by an external force or violence" or "an emotional or psychologic shock that may produce disordered feelings or behavior." This is an extremely narrow definition for trauma can also be caused by intrinsic forces as seen in common strain. In addition to its cause being extrinsic or intrinsic, with a physical and emotional aspect, it also can be the result of either a strong overt force or repetitive microforces. This latter factor, so important in treating a unique patient's specific pathophysiology, is too often neglected outside the chiropractic profession.
Taber defines rehabilitation as "The process of treatment and education that lead the disabled individual to attainment of maximum function, a sense of well being and a personally satisfying level of independence. The person requiring rehabilitation may be disabled from a birth defect or from an illness. The combined effects of the individual, family, friends, medical, nursing, allied health personnel, and community resources make rehabilitation possible." It is surprising that Taber excludes trauma as a prerequisite for rehabilitation for it is the most common factor involved.
Other authors define rehabilitation strictly in terms of exercise and restorative therapeutic modalities and regimens. Some limit the term to preventing or reversing the noxious effects of the inactivity or lessened activity associated with the healing process. While it is true that these definitions hold significant components of clinical reconditioning and restoration, the scope of rehabilitation means much more to the chiropractic physician.
It has been the custom of the majority health-care profession not to consider rehabilitative procedures until late in case management. Like Welch**, allopaths generally place it 6th in the cycle of managing the body's response to injury: (1) injury → (2) pain, bleeding and traumatized tissue → (3) inflammation → (4) repair and regeneration → (5) atrophy → rehabilitation. Chiropractic clinicians ask, "Why wait for signs of atrophy to begin rehabilitation? Nonparalytic atrophy beacons a neglected patient."
Throughout the manuscript, emphasis is placed on minimizing the noxious effects of fibrosis. Fibrosis parallels atrophy and leads to:
(1) impaired cellular nutrition and drainage,
(2) stiff, shortened soft tissues,
(3) trigger-point development,
(4) adhesion development, and
(5) articular fixations restricting normal ranges of motion. Restricted joint mobility, in turn, encourages further atrophy, stasis, and a lack of mechanoreceptor input. Thus, a vicious cycle is established leading to a greater risk of residual impairment, reinjury, and progressive degeneration. After bleeding and pain are controlled, a primary objective is the normalization of soft-tissue flexibility, elasticity, and pliability as soon as possible.
Posttraumatic rehabilitative procedures ideally begin at the time the doctor first sees the patient. Hopefully, this will be an early stage --one occurring soon after injury. Alert care will usually control the ill effects of inflammation, enhance repair and regeneration mechanisms, and halt, if not nullify, the progress of atrophy and the formation of fibrosis. In many cases, customary surgery may be avoided. With individualized care, the result is a greater likelihood of obtaining an optimal goal of full function, strength, power, resistance, agility, and endurance.
All experienced clinicians recognize the need to treat the entire kinematic chain and related functions involved in an injury and not a particular joint or part manifesting acute symptoms. Protocols, templates, and regimens are used throughout this manuscript simply as guidelines. They should not be considered "the standard" or "the only way to do it." Every person is unique in many ways. The way each responds to trauma and pain and its treatment is no exception. Thus, a "cookbook" approach to rehabilitative therapy is irrational if suggestions are taken as a directive rather than a framework for thought
--a framework, not a cage.
Without a doubt, no other health-care approach equals the efficacy of chiropractic in the general field of conservative neuromusculoskeletal rehabilitation. This introductory chapter reviews the understructure and rationale of a clinical plan of action.
Most texts concerning rehabilitative therapy directed to allied health-care professions appear to be developed from the standpoint of a perfectly healthy individual who has suffered an injury. The young practitioner should keep in mind that this is rarely the case. The typical traumatized patient presents with an array of underlying overt and subclinical pathologic, dyfunctional, and emotional disorders that must be considered in arriving at a practical treatment plan.
An examiner should keep in mind that trauma is not always the cause of all an injured patient’s complaints. A painful injury may only be the precipitating factor bringing the patient to the doctor’s office. Trauma produces overstress, and overstress frequently brings out subclinical disorders because of the tax on the immunologic system and other body reserves. The differentiation of the immediate from predisposing factors is just one component of the clinical art.
If a doctor were to concern himself solely with injury prevention, care, and rehabilitation, his role would be much easier. But many other factors are involved. For instance, consider patient motivation and cooperation —without which case management is an uphill battle. The average patient bears many pressures. These pressures may blind the patient to the fact that continuing usual activities at this time may make a minor condition worse or that the continuation of treatment after pain has subsided is necessary to reach optimal goals.
Physical activity beyond the point of exhaustion or tissue strength or continuing stressful activity with an injury where further insult may lead to permanent injury is illogical from a clinical viewpoint, but common behavior. And for various reasons, some people may avoid reporting injury or even try to hide its effects.
The attending physician should mentally target that he is only responsible to the patient and his professional code of conduct. He is not responsible to any other person except the parent of a minor or a legal guardian. Thus the questions must be asked: Who has the authority to return an injured employee to work: the attending physician, the company doctor, or the patient’s employer? Who has the authority to return an injured athlete to play or practice: the attending physician, the trainer, or the coach?
BASIC DIAGNOSTIC AND SUPPORT PROCEDURES
This and the following two sections describe basic diagnostic procedures, offer a brief review of fundamental disorders, and explain the basic clinical template on which all subsequent chapters of the manual are framed. The chapter concludes with an explanation of physiologic performance, conditioning rationale, and exclusion criteria for potentially harmful activity.
CASE MANAGEMENT PLAN
Each doctor usually has a general case management plan that can be readily adapted to the situation at hand. An example is listed below.
THE HISTORY INTERVIEW
The personal data collected should be similar to that recorded routinely such as name, address, date of birth, age, sex, present complaints, present and past occupations, type of work and the number of hours, recreational activities, medical and surgical history, accidents and injuries history, drug and food sensitivities, allergies, congenital difficulties, diet, smoking and drinking habits, insurance data, etc. The history should also define the types of primary and secondary physical activities, the number of hours involved, the-level of achievement, the age at which active involvement began, etc.
A thorough history forms the basis for differentiating acute from chronic disorders. See Table 1.1.
Table 1.1. Differentiation of Acute and Chronic Disorders
Survey the situation for a medical emergency, and take whatever first-aid measures are necessary, record patient status and vital signs, and record as much of a detailed history as possible under the circumstances.
Record findings of inspection and tolerated palpation and moverment of the part involved. Auscultate the area for crepitus, observe abnormal limb position suggesting fracture or dislocation, and seek signs of CNS injury or hemorrhage.
Record integrity of normal superficial and deep reflexes and occurrence of pathologic reflexes, and order roentgenography if fracture or dislocation is suspected.
Record findings of involved joint range of motion studies and muscle strength to the degree possible at the stage existing at the time of examination, order electromyographic and/or thermographic studies as indicated, and order pertinent laboratory studies.
Coordinate findings, patient’s objectives, and prognosis, and set clinical goals, treat and monitor, periodically reassess patient progress with the working diagnosis and clinical goals, and retest when confirmation is necessary.
Recording oral temperature, comparing extremity pulses and limb blood pressure, and auscultating the heart and lungs should be routine in any examination. Traumatic injury is no exception.
|Clinical Finding||Acute Inflammation||Chronic Inflammation|
|Pain||Relatively constant; likely referred over a diffuse segmental area. In intrinsic disorders, pain is increased on movement in any direction. In periarticular disorders, pain is increased on movement only in certain planes.||Increased by specific movements, relieved by rest; likely to be relatively localized near, but not necessarily over, the site of the lesion.|
|Passive motion||Muscle spasm or empty end-feel at the end of motion.||No muscle spasm or empty end-feel at the end of motion, possible blocking.|
|Tenderness||Severe.||From slight to moderate.|
|Skin temperature||Measurable increase.||No measurable increase.|
|Sleeping pattern||Difficulty in falling asleep, staying asleep, or both.|
Color changes such as ecchymosis and redness
Swelling from synovial thickening, periarticular edema, nodules, or bony enlargement
Deformity from abnormal bone angulation or subluxation
Wasting from atrophy or dystrophy
Tenderness on palpation
Pain on motion
Limitation of motion
Carriage and gait abnormalities.
In examining a patient in pain, certain types of pain are clinically significant. For example, a sharp severe pain associated with muscle changes and sensory disturbances radiating along the distribution of a nerve is characteristic of acute nerve compression. The pain from fracture is severe, throbbing, and acutely aggravated by movement of the part.
SPINE-BOARD TRANSPORTATION OF THE INJURED
Moving an injured person frequently requires extreme care. In moving a severely injured person from one location to another, a spine board is more appropriate than the common stretcher because the board helps to prevent further aggravation of a possible vertebral or spinal cord lesion. Craig warns that transporting an injured athlete from the field must be well-planned, orderly, and conducted in an unhurried manner. Four general steps are involved in transporting any injured person:
The patient should be placed supine with care taken that the head, neck, and spine are in normal alignment. The spine board is placed close and parallel to the patient’s body. Note, however, that a conscious patient with a painful disorder is understandably reluctant to change a position that seems comfortable, thus tending to favor a position that usually involves minimum movement.
Usually, the patient’s arm next to the board is placed at the subject’s side and the patient’s other arm is extended over the head if it is not injured. The patient is then gently rolled onto the side opposite the patient’s extended arm. The patient should be rolled like a “log” to maintain body alignment. An exception to this would be suspicion of a spinal fracture, whereon the player should be kept on the side and not rolled supine. This may require seven people in a spinal or head injury, otherwise two people will usually suffice unless the player is extremely large.
The spine board is inserted under the back of the patient (not under the patient’s side). Then, gently roll the patient onto the spine board. In cases of unconsciousness, facial or mouth fractures, bleeding from the mouth or nose, the patient is kept laterally recumbent to allow drainage and an open airway.
Assure that the injured person is in a comfortable position, then snug straps around the board and patient to secure the injured person to the spine board during transportation. If possible, remove rings from injured hands before swelling occurs.
EMERGENCY IMMOBILIZATION BY SPLINTS
To prevent further damage during referral, a fractured bone must be immobilized by immediately splinting the joints above and below the fracture because movement of these joints would disturb the bone segments. The splint should be well padded to protect the skin from injury, loss of circulation, inflammation, and infection. A pneumatic inflatable splint is especially useful in limb fracture because it allows both immobilization and compression to minimize effusion and hemorrhage. It must be applied only snug enough to support any fracture 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. The bandages or straps 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 would suggest that one or more bandages are too taut. Security bandages should never be tied directly across the site of injury.
A dislocation is immobilized during referral in the same way as a fracture: close to the joint. Area ligaments are usually torn and may require surgical repair. Cold compresses can be applied to the area to relieve pain and reduce swelling. The patient’s temperature must not be lowered because this would invite shock.
Postreduction immobilization of a dislocation in the lower extremity usually requires 6 weeks and in the upper extremity requires 3 weeks. Inadequate care, especially for ankle and shoulder dislocations, leads to chronic weakness, movement restrictions, instability, and recurrent dislocation in which subsequent surgery has a poor prognosis in restoring preinjury status. Except for recurring dislocations, almost all overt dislocations require anesthesia before reduction.
Courson reminds us that any rehabilitation program should include returning the patient to optimal preinjury status and developing a preventive maintenance program to minimize the possibility of injury recurrence.
Assessing Physical Fitness
A reduced level of fitness predisposes injury and likely the extent of injury at both its macroscopic and microscopic aspects. For example, physical training increases the bulk of muscle fibers and increases muscle interstitial vascularity. Both factors have an influence on the effects of acute muscle strain in that (1) an untrained muscle is more apt to bleed and form a hematoma than a trained muscle, and (2) the physiologic mechanisms necessary to absorb extravasated fluid is more efficient in a trained muscle than an untrained muscle.
Many people in modern civilization spend much of their mature life at an energy level close to the resting state because of technologic advancements and modern conveniences. To what exact degree this affects human resistance to disease, longevity, adaptability, and general well-being has not been determined, although it is generally recognized to be extensive. In this context, the role of physical training has still to be accurately defined to the satisfaction of all. Williams/Sperryn look to physical fitness as an “artificial state in so far as it is specially cultivated rather than inherent in the individual”. Functional status can apparently be increased more in young subjects than in the elderly.
People participating in vigorous occupations and sports should have a complete examination at least annually, and re-evaluation is often necessary at seasonal intervals. Re-assessment is always necessary when the patient has suffered a severe injury, illness, or surgery.
Questioning. Because of drilled routine, doctors are well schooled in the taking of a proper case history. But with an athletic or work injury, both obvious and subtle questions often appear. How extensive was the individual’s conditioning? How much time for warm-up is allowed before vigorous activity? What precautions are taken for heat exhaustion, heat stroke, concussion, overuse strains and sprains, and so forth? Does the supervisor or coach make substitution for proper evaluation immediately on the first sign of disability? How adequate is protective gear? How many associates have suffered this injury? Who, what, when, where, how, and WHY? A detailed history of past illness and injury is vital. In organized sports, an outline of the regimen of training should be a part of the history, as well as a record of performance.
Determining Disability. The term “disability evaluation” in clinical practice roughly describes the physician’s function in claims proceedings. The doctor determines the degree of functional impairment, usually in a percentage to denote an impairment in comparison with a person’s entire range of activities typical with the patient’s age and sex. The doctor’s responsibility is to determine functional impairment only, not to determine occupational disability, as the later is the responsibility of a workers’ compensation board. In sports care, however, “disability” has a more profound meaning that includes not only the physical factor of functional impairment but other considerations such as a player’s talent, experience, position, present and future risk to a part or organ, etc. A defect may bar a candidate from a specific occupation, sport, or position but not another, or it may be only a deterrent until it is corrected or compensated. Many famous athletes have become great in spite of a severe handicap.
Depth of Examination
Any occupational or athletic health examination has dual functions:
(1) to assess health status (limits and capacities), and
(2) to recognize problems that may be precipitated during common activity.
These functions must be kept in mind during the examination of a laborer, professional athlete, or a weekend athlete. If there is undue risk of present injury or future permanent injury of any type under employment or sports conditioning, practice, or competition situations, the patient should be kept from participation regardless of the patient’s (or another person’s) objections.
The typical initial physical examination should evaluate height, weight, sitting blood pressure and pulse, temperature, eyes and vision, ears and hearing, nose, mouth and throat, chest and lungs, female breast, heart, abdomen, rectum, genitalia, feet, and spinal and overall postural mechanics. A pelvic gynecologic examination should be considered for any female athlete over the age of 20 that has not been examined within a year.
A basic orthopedic evaluation should be conducted in regard to limb circumference measurements, joint flexibility, and range of active motion for the cervical spine, shoulders, back, hips, knees, and ankles. Neurologic deep-tendon reflexes, superficial reflexes, and coordination tests should be assessed, with more sophisticated tests reserved to confirm any abnormalities found.
Laboratory work-ups should be conducted as indicated from the physical examination. However, many clinicians feel that all patients should have as minimum a blood work-up and urinalysis, and an ECG if possible. X-ray films are not considered routine procedures unless necessary to confirm suspicions. The examiner should avoid collecting information without a clear purpose.
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.
The Motion Barrier. When a joint is passively tested for ranges of motions, the examiner will find an increasing resistance to motion (a “bind”) or the physiologic motion barrier. When a joint is moved past this point, the attempt becomes at least uncomfortable to the patient. This point is the anatomical motion barrier. In evaluating degrees of passive motion, joints should be moved to but not forced through the anatomical motion barrier (which may be unstable). Thus, joint motion is evaluated by passively carrying the joint(s) through ranges of movement until the motion barrier in each plane is encountered. The degrees of movement allowed should be recorded.
Joint Play. There is a small but precise accessory movement within synovial joints (joint play) that cannot be perceived except by dynamic palpation. Although joint play is necessary for normal joint function, it is not influenced by a patient’s volition. Thus, joint play is that degree of end movement allowed passively that cannot be achieved through voluntary effort. Total joint motion is the sum of the voluntary range of movement plus or minus any joint play perceived by the examiner.
Joint play occurs because normal joint surfaces do not appose tightly. There are small spaces created by articular incongruencies necessary for hydrodynamic lubrication. In addition, because synovial joint surfaces are of varying radii, movement cannot occur about a rigid axis. The capsule must allow some “play” for full motion to occur. 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 protective 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.
Although joint play cannot be produced by voluntary muscle contraction, volitional action is greatly influenced by normal joint play. This occurs because restricted joint play produces a painful joint that becomes involuntarily protected by secondary muscle spasm (splinting). Joint play should exist in all ranges of motion normal for a particular joint. If a joint normally 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 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.
Impaired muscle function leads to impaired joint function, and impaired joint function leads to impaired muscle function. In this cycle, muscle and joint function or dysfunction cannot be separated.
Besides translatory joint play, some distraction capability normally exists. If the act of axial lengthening is impaired for some reason, articular surfaces become closely packed and motion will be restricted. This subject of closely packed joints will be explained in greater detail later in this chapter. See “Implications of Closed-Packed Joint Positions.”
Bony Restrictions. Bony outgrowths may be obvious (as in Heberden’s nodes), but if they are near the periphery of a joint, they may be recognized physically 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 many cases, roentgenography is necessary for diagnosis. Bony outgrowths within a joint are sometimes recognized only 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 and 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 obstructing myositis ossificans) has developed. If force is continued beyond the point of a bony block is painless, a neuropathic arthropathy is likely but a rare finding.
Bone vs Muscle Resistance. Striated muscle spasm is distinguished from bony outgrowth as a cause of limited joint motion by two features:
(1) Bony outgrowths allow free motion to a certain point, after which motion is arrested suddenly, completely, and without great pain.
(2) Muscle spasm, on the contrary, slightly checks motion from the onset. Resistance and pain gradually increase until the examiner’s efforts are stopped at some point in the arc.
Joint 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 worse after rest; eg, in the morning or arising after sitting for a long period. Stiffness lasting for more than half an hour points toward one of the inflammatory arthritides (in which the stiffness may last for several hours).
Stiffness from structural changes can usually be traced to cartilage degeneration or capsule tears. It is common for previous trauma or inflammation to result 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.
Loose Bodies. Suspended bodies in joint fluid 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 commonly occur in the temporomandibular joint, knee, and spine. They arise less frequently in the elbow, hip, and ankle joints. Keep in mind that loose-body formation is an outstanding effect of osteochondritis dissecans or osteochondromatosis. However, there are other conditions in which loose bodies arrive 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” and “melon-seed” bodies, and intra-articular fractures (especially compression fractures).
Calcareous Bodies. Calcareous bodies are abnormal calcifications within a joint of such an age 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. Remember that fragments of a fractured cartilage are rarely visible on films unless a degree of calcification has ensued.
An involved joint with a closed wound should also be palpated for masses and points of tenderness that may indicate displacement, osteoarthritis, synovitis, or a torn ligament or meniscus. Soft-tissue palpation should be conducted for tenderness, masses, muscle tone, fasciculations, and spasm. It has been estimated that from 50% to 60% of the pains and discomforts that the average ambulatory patient has is 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.
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.
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 the 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.
Pitting on Pressure. Pitting is a sign of liquid infiltration into the underlying tissues. Tenderness associated with pitting is indicative of inflammatory edema. While edema gives rise to a 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 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 by the tip of one forefinger placed 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 this event, Paget’s test can be used: pressing the mass with a fingertip. A solid swelling feels hard in the center, while a cyst feels soft in its center.
Muscle Mass. Palpation and mensuration are used to determine extremity muscle volume. On 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 show the same circumference approximately unless there is a large degree of unilateral occupational activity. A decrease in size (eg, arm, forearm, thigh, or calf) indicates atrophy and is usually associated with some degree of hypotonicity.
Muscle Tone. The typical feeling of a normal muscle on palpation is one of resilience. An increased perception of tone by the examiner denotes a hypertonic muscle; a decreased perception of tone, a hypotonic muscle.
Spasticity. 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 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 found near an area of muscle that has entered a state of fatty degeneration. When located through palpation, the lesion should be differentiated from a common lipoma.
Stretch Reflex Effects in Spasticity. A spastic resistance is essentially a stretch reflex activity whose receptors are muscle spindles scattered but parallel with muscle fibers. In common spastic disorders, the muscles relax when the part is comfortably rested with support but become spastic with volitional movements, tendon tapping, vibration, or even startling noises. Three hypotheses have been put forward by debaucher 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. Damage to or dysfunction of the corticospinal pathways weakens 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.
Joint Clicks. The importance of atmospheric pressure and surface tension of synovial fluid in joint stability is readily heard during knuckle cracking or by the audible click accompanying a chiropractic dynamic adjustment. A 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. This 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.
Crepitation. There are types of musculoskeletal crepitus 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. Crepitation from an epiphyseal separation resembles that of a broken bone but is softer in character than the crepitus from a fracture. 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 then be felt when the fingers are placed with mild pressure over the affected area. To amplify crepitation, it is often helpful to apply a stethoscope to the joint during passive motions.
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 crepitus is transmitted to the palm of the palpating hand, osteoarthritis, chronic rheumatoid arthritis, or tubercular tenosynovitis is usually involved. Intermittent crepitus of bone against bone suggests that the articular cartilage is extensively worn. Crepitus may also 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 rapidly open his hand several times. The presence of effusion produces a palpable and/or audible transmission.
PAIN: GENERAL CONSIDERATIONS
All joints contain nociceptors in their ligaments, tendon insertions, periosteum, fibrocartilages (sparsely), capsules, and vascular walls. Authorities differ in whether or not synovia contains nociceptors; most believe that it does not. 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.
Significance of Hyperalgesia
A painful tenderness produced by external pressure frequently results from traumatic lesions of sensitive subdermal tissue, trigger points, the development of a toxic accumulations, or a deep-seated inflammatory irritation. 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 often associated with acute and subacute visceral disease than with chronic disorders.
Characteristics of Extremity Pain
The cause of limb pain may be of mechanical, chemical, thermal, toxic, nutritional, metabolic, or circulatory origin, or a combination of several of these factors depending on the pathologic process involved. Peripheral nerve disease will sometimes reveal a history of an entrapment neuropathy. Nutritional disorders can result in a polyneuropathy because of unfavorable metabolic activities within the neural apparatus. When an inflammatory process involves sensory fibers, the pain is frequently perceived along the total course of the nerve. The 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 alleviates the symptoms (at least temporarily).
Characteristics of Neuralgia
Neuralgia is any sharp, severe, stabbing, paroxysmal, remittent pain with temporary abatement in severity that travels along the course of one or more nerves. It is usually associated with tenderness along the course of the nerve and violent episodic spasms in the muscles innervated. Pain accentuated by heat points to neuritis or congestion. In contrast, pain that is relieved by heat suggests something producing abnormal myotonia or possibly ischemia. Pain of intrinsic neurologic origin is generally accompanied by paresthesias and root signs. When throbbing pain occurs, vascular engorgement, crush syndrome, a vasomotor disturbance, or possibly Paget’s disease should be the first suspicions. It’s difficult for the patient to describe its character because it is unlike any other type of pain and usually is a combination of painful sensations.
Neuralgia is provoked by any peripheral stimulation in the involved zone, and stimulated trigger points cause spontaneous paroxysms. Morphologic changes cannot be detected early in a pure neuralgia or neurodynia syndrome. The term neurodynia describes a similar pain that is less severe; ie, a deep ache. The patient vigilantly guards the involved part and shows great apprehension. The pain manifests in the involved nerve’s distribution —superficially or deep. It usually radiates, and there is an exorbitant response to stimulation. 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 sometimes arise.
Skin and Tendon Reflexes
Evaluation of pertinent superficial and deep tendon reflexes should be checked as a standard procedure. Upper-limb tendon and periosteal reflexes are supplied essentially by C5—T1 segments of the cord; lower-limb reflexes, essentially by the L2—S3 segments. A summary of normal reflexes is shown in Table 1.2.
|Superfical Reflexes||Afferent Nerve||Center||Efferent Nerve|
|Lower abdominal||T10—T12||Cord level||T10—T12|
|Nasal (sneeze)||Trigeminal||Brainstem, upper cord||Cranial V, VII, IX, X, and spinal nerves of respiration|
|Upper abdominal||T7—T10||Cord level||T7—T10|
|Tendon and Periosteal Reflexes||Afferent Nerve||Center||Efferent Nerve|
|Visceral Reflexes||Afferent Nerve||Center||Efferent Nerve|
|Ciliospinal||Sensory nerve||T1—T2||Cervical sympathetics|
Roentgenography should be used to confirm or dispose of suspicions arising during the history and physical examination, and not used as the sole basis of the diagnosis. When a film is used solely to confirm a prior clinical opinion, other clues exhibited on a view may be missed that indicate a different approach. This occurs when an outstanding feature, visible at a distance, overwhelms a desire to seek other evidence. Nevertheless, whatever is presented on the film must be evaluated; eg, an asymptomatic chronic disease process may be underlying an acute injury.
X-ray films are often helpful in determining dislocations, overt fractures, stress fractures, joint-space alterations, ossification, calcification, and sometimes cartilage fractures, fat pad alterations, and masses and swelling. Common radiographic signs of various bone lesions are shown in Table 1.4. Once relevant features classify an abnormality, a search should be made for details enabling it to be distinguished from others in the same class. This takes careful evaluation of frequently subtle soft-tissue changes which confirm osseous alterations.
The examiner must be well acquainted with the nature of all substances visible on a film. This is a medicolegal responsibility. Healthy tissue features and common variances should be recognized at a glance. Joint abnormalities show 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. In addition to roentgenography of distressed joint(s), spinal and chest films are almost always included if the possibility of referred pain or systemic symptoms is involved.
|Grade 5 100%||Normal||Complete range of motion against gravity with full resistance.|
|Grade 4 75%||Good||Complete range of motion against gravity with some resistance.|
|Grade 3 50%||Fair||Complete range of motion against gravity.|
|Grade 2 25%||Poor||Complete 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|
Size. Body length (height), width, and depth of parts are linear measurements. These dimensions are usually obtained by using calipers, tapes, or gird photographs. Linear measurements offer direct evidence of bony framework length. Body part depth and width influence motor activity as they affect body mass and relative size. Broad hands and feet are an aid to the lifter and swimmer, for example. Broad hands are a control advantage to the basketball handler. Large feet offer a wide base of support.
Weight. Dead weight is the weight of the body not involved in locomotion (eg, fat, inactive muscles, viscera). Greater mass (dead weight) is a distinct disadvantage in acceleration (eg, runners), and an advantage in being difficult to move (eg, furniture movers, truck loaders, football linemen, wrestlers) or stop once in motion (eg, football backs). Endurance and acceleration are the primary concerns that resistance exercises are used to develop strength without greatly increasing muscle bulk. Dead weight from inactive muscle mass is as useless as fat. When weight is gained strictly through an increase in muscular weight, the undesirable effects of increasing body mass are offset by the increase in strength available for movement. On the other hand, a football lineman employs his dead weight in gaining momentum (velocity X mass) and uses his fat component to absorb the shock of impact.
Mass. Because of gravity, body weight in human movement is a significant structural-mechanical variable. Body mass is defined as body weight divided by the gravitational constant (32 ft/sec²). In many vigorous physical activities, body weight is important because of the impact force: the greater the mass, the greater the amount of force required for movement. This may be an advantage or a disadvantage, depending on objectives.
Build. Evaluation of body proportions is helpful in determining an individual’s center of gravity and body build (type). A person’s common center of gravity affects motor equilibrium (kinetic and static). The center of gravity is the point of application of the gravitational (vectorial) force acting on the body; in addition to the whole body, each part or segment has its individual center of gravity. Gravitational weight of the body as a whole or its segments differs from subject to subject depending on body type, height, size, density, age, and sex. The position of a person’s normal center of gravity may be slightly changed through the influence of training and conditioning, blood supply, and diet.
Physique. Physique is one’s physical structure, organization, and development; the characteristic appearance or physical power of an individual or a race. Body type greatly influences physical performance, and it is determined by weight, linear measurements, and girth dimensions. The intermediate (mesomorphic) type’s streamlined physique and lean muscle mass contribute to rapid motor talents (sprinting). The stability of the heavy endomorph is seen in wrestling and football linemen. The advantages of the long-limbed ectomorph are quickly recognized in the basketball center and football end.
Leverage. The rigid bones and mobile joints of the body along with the forces acting on them represent a system of levers and, as all levers, transmit force and motion at a distance. Contracting muscles in the body normally constitute the force, with resistance supplied by a body part’s center of gravity plus any extra weight that may be in contact with the part.
Height. During motor activity, greater height is usually related to longer limbs, which mean longer levers (eg, high jump), longer stride (eg, running), greater velocity (eg, discus, javelin), a wider arc of reach (eg, blocking), a larger target (eg, catching), and height dominance over a raised goal such as a basketball hoop or starting at a point further from the ground (eg, shot put). Height presents a disadvantage because of the increased leverage in weight lifting, in activities requiring quick changes in direction, in lack of stability due to the higher center of gravity (eg, judo, wrestling), and in lack of long-limb manipulative balance (eg, soccer). Thus, long limbs are a disadvantage in any job or sport where equilibrium and strength are the priority, and they are an advantage where range of motion and velocity are critical.
Body Type and Career Fit. Several studies have shown that body type and physical performance have a close correlation. There are exceptions, but they are rare at the professional level. This means that there are many people striving for high levels of physical achievement that they probably can never attain. Some authorities believe as high as 80% of the population should never aspire to great heights in terms of purely physical performance. This underscores the fact that the techniques and achievements of champions, commonly used in calculating standards, may not be suitable for different physiques within identical events. An important element that the voluminous literature on somatyping does not include is the great variable of personal motivation.
An injury or potential risk of injury must be evaluated relative to the person as a whole. Physical activity is a complicated phenomenon involving all joints, related tissues, and remote sections of the body when movement requires more than single joint or limb action. Regardless of the size or intensity of human motion, the articulations of the limbs and pelvis constitute the basic elements involved.
Goniometry. The objective measurement of joint motion is an important evaluative procedure in physical examination of the joints because it offers an accurate record of joint motion and the extent of disability as part of a patient’s permanent record.
Inclinometry. Because the use of a goniometer is awkward in measuring spinal motions, the use of an inclinometer is preferred. An inclinometer is a half-circle level, commonly used by carpenters. Its use is now a standard in spinal impairment evaluation.
When measurements are taken of a unilateral disabled joint, a comparison is made with the contralateral unaffected joint. Boone and associates show that, for greater continuity in procedure, the same individual should make goniometric measurements when the effects of treatment are evaluated. For reference to average percentages, refer to the ACA text, Basic Chiropractic Procedural Manual (ed 5) where goniometry and inclinometry are described for specific joints along with average measurements.
The quantity of one’s muscle fibers does not vary much after birth. Exercise primarily increases muscle quality, not quantity; it allows muscle fibers to become larger, stronger, and better developed.
Muscle and Ligament Function
Muscles can contract only in the direction of the muscle fibers. Movement may take place that reduces the joint angle (concentric contraction) or increases the joint angle (eccentric contraction). A slightly stretched muscle contracts with a great amount of force, but a shortened muscle contracts with very little force. Muscle contraction consumes nutrients and oxygen and produces acids and heat (major source). Acids accumulating as a result of continued activity contribute to fatigue.
Ligaments play a much greater part in supporting loads than generally thought. Electromyographic studies in situations involving fatigue from forces acting across a joint prove that muscles play only a secondary role. This fatigue is basically a form of pain originating in ligaments rather than muscles. Thus, some researchers believe that if the muscles involved in a problem are weak to begin with, there is an immediate strain on the ligaments producing the characteristic fatigue syndrome.
Mechanical Factors Affecting Normal Muscle Contraction
MacDonald/Stanish showed that the mechanical factors governing muscle contraction are the angle of pull, the length of the muscle, and 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. A suddenly prestretched muscle has an increased contractile capacity. Improved flexibility through static stretching exercises, which does not activate the stretch reflex, appears to reduce soft-tissue restrictions and enhance antagonist relaxation.
Temperature Values Affecting Normal Muscle Contraction
Hill 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 strenuous physical labor or athletic participation is underscored. Reducing muscle temperature appears to increase the threshold of irritability, which causes weakened and more sluggish contractions.
Manual muscle testing is a procedure that depends greatly on the skill, knowledge, objectivity, and experience of the examiner. In fact, the major fault with this method is that evaluation rests on the subjective skill of the examiner. Thus it is important that the same examiner records initial and follow-up evaluations of the degree of “resistance” perceived. Also, muscles often test differently in various positions such as from supine to weight-bearing.
The criteria shown in Table 1.3 are commonly used in recording muscle strength. One muscle or group should be tested at a time, thus the subject should be requested not to recruit allied muscles during resistance. Caution is used during resistance to avoid creating cramps, stretch injuries, or excessive fatigue.
Infection Singular Malignant Bone Lesion Formation of sequestration and involucrum Permeactive or moth-eaten destruction Irregular periosteal reaction frequent, (wide transition zone) no speculation Extraosseous extension with soft-tissue Diaphyseal site most common mass, occasional fluffy calcifications Variable bone destruction Irregular (sometimes spiculated) Destruction of adjacent cartilage crossing periosteal reaction joints (most malignancies lack this trait Metaphyseal area is the most common site Metastatic Lesions Benign Bone Lesions Moth-eaten destruction of cortex and Enlargement of an intact cortex medulla Homogeneous periosteal reaction Pathologic fractures Sclerotic margins (narrow transition zone) Diaphyseal site most common Periosteal reaction absent Multiple bone involvement
Manually Resisted Joint Motion. The goal of an examiner applying passive resistance to patient active motion is to reveal and isolate pain, weakness, hypermobility, hypomobility, and associated patient reactions. It is important during testing that the joint is held near mid-range, the resistance is strong enough to avoid joint motion, and, when possible, specific muscles are isolated. 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 produces pain from periosteal tears, fractures, bursitis, or when a tender structure (eg, an abscess, neuroma) is compressed by the action.
In testing muscle strength subjectively, the patient is asked to do various actions against the examiner’s resistance. For example, the patient could press the thumb and middle finger of the same hand tightly together, and the examiner could try to pry the fingers apart with the patient resisting. Normally, it would be difficult for the examiner to do this. Another example is to have the patient flex or extend an arm or leg against the examiner’s resistance. The strength of an involved joint is tested, compared bilaterally, and the results recorded.
The type of response a patient makes during resisted motion can add much toward an accurate diagnosis. See Table 1.5.
|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 resisted movements||Arterial flow deficit.|
|Strong and unchanged pain in all directions||Referred pain syndrome.|
|Strong, painful, and hypomobile||Guarded joint for some reason.|
|Strong, painless, and hypomobile||Contracture, adhesion.|
|Weak and sharply painful pathology||Fracture, dislocation, rupture, gross|
|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.|
Objective Muscle Testing. Until recently, the hand dynamometer and electromyograph were the only objective clinical instruments available to record the force of muscle contractions. However, recently more practical equipment has been developed. 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, and Kin-Com are examples. With modern equipment, the strength of almost every joint motion of the body can be assessed objectively.
ELECTRODIAGNOSIS AND ELECTROMYOGRAPHY
Electrodiagnosis is used to grossly test the integrity of muscles and nerves. As an adjunct to the examination of the motor system, it has become a valuable tool in evaluating whether or not partial degeneration of a nerve or muscle fibers is suspected. Such tests help to determine if disease of an upper or lower motor neuron is involved, if the nerve is interrupted, and if the muscles are undergoing degeneration.
Electromyography (EMG) allows the recording of oscillations in potential variations of skeletal muscles at rest and during activity. It basically provides a tracing of electrical activity transmitted from muscle to an electrode and then to an oscilloscope. Tracings aid in determining whether a patient’s illness is directly affecting the spinal cord, muscles, or peripheral nerves. EMG recordings aid the scientific basis for diagnostic conclusions and monitor the effectiveness of therapy.
ELECTROCARDIOGRAPHY, THERMOGRAPHY, AND SPIROMETRY
An electrocardiogram (ECG or EKG) offers a graphic representation of the electrical phenomena associated with the heart beat. It does not represent the mechanical events of the heart. The recorded P, QRS, and T waves reflect the rhythmic electrical depolarization or repolarization of the myocardium that precedes or follows cardiac contractions. The electrocardiogram should therefore be employed as a supplementary technique in the study of heart disease. Only infrequently is it a diagnostic sine qua non for a clinician.
Thermography is used to measure slight 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 used to record specific temperatures, either by color changes or a direct display of temperatures. Dudley reports that when a spinal subluxation exists, it causes unequal contraction of muscles. This unequal contraction, an effect of the subluxation, should be observable by heat-detecting equipment. Once detected, the subluxation can be traced, corrected by adjustment, and the imbalance of the nervous system arrested. He also mentions that frequent alteration of the upper dorsal heat pattern has led to other companion signs being noted. For instance, Adson’s sign is always positive on the same side as the elevation of temperature of the levator scapula and some parts of the trapezius. If the patient is adjusted to remove the causative subluxation and rescanned, the temperature becomes nearly normal, thus registering improvement of muscle function and vascular normalization.
Spirometry can be helpful when a patient presents a history of pulmonary difficulty, repeated episodes of fainting, cardiac symptoms, chest injury, or certain nervous system diseases and dysfunctions that affect lung function. Most tests are performed by having the patient breathe into a spirometer to record the amount of air put through it and the rate of air passage for a specified time. The more common tests for pulmonary function are vital capacity, forced expiratory volume, and maximal voluntary ventilation.
Blood, urine, and other analyses should be used whenever the clinical picture warrants it. The most commonly used profiles for acute joint complaints are:
|Blood sugar||Platelet count|
|Blood uric acid||R-A test|
|CBC and differential||Sedimentation rate|
|Febrile agglutins||VD serology|
Effects of Soft-Tissue Overstress. In chronic balance defects, strain, fatigue, and sprain cannot be discussed in unrelated terms. Strain commonly arises when the body is forced to be used in a position that is not favorable to muscle function or when joint facets are at their physiologic limit of articulation. Thus, pull and stabilization come from ligaments rather than muscles. The result is tissue insult leading to edema, pain, and physical deformity that is referred to the structures on which the strain is imposed or the cutaneous branches of the spinal nerve root supplying the strained tissues. Long-term muscle strain results in adaptive changes occurring in the involved joints and their ligaments to meet the needs of the malaligment. Thus, low-key chronic sprain is a part of the picture. Abnormal fatigue and reduced performance are the result of wasted energy.
Effects of Mechanical Disadvantage. The more pronounced an abnormal spinal curve or unilateral spasticity, the greater the mechanical disadvantage to which the supporting structures are subjected. Thus, again, the process becomes a vicious cycle. Along with chronic strain and fatigue, constant overstress produces small tears in ligament and tendon attachments and facial supports. This results in a series of subperiosteal hemorrhages that later may calcify into exostoses, becoming acutely painful on further overstress. This may occur in any joint subjected to prolonged stress, but it is especially common in the spine and other weight-bearing joints.
Neuralgic Syndromes. There appears to be some degree of intervertebral foramina insult present when spinal imbalance exists. Neuralgic pains in the thorax and legs are common. Less common, because it mimics visceral disease, is intercostal neuralgia. If originating in the cervical region and associated with hypertrophic changes, pain is often referred about the shoulders and down the arms, frequently being mistaken for angina pectoris or carpal tendon syndrome. Similar neuralgic pains in the chest walls can be mistaken for pleurisy, pleural adhesions, or pulmonary lesions. Chest auscultation, palpation, and percussion serve in the differentiation.
Vascular Syndromes. Circulatory disturbances are rarely absent in balanced defects. The low diaphragm results in venous congestion in its failure to assist blood returning to the heart. Sagging viscera stretch mesenteric vessels and narrow their lumina. Thus, circulatory symptoms may arise throughout the body. For instance, allopathic-oriented researchers have recorded the relief of eye strain and mild myopia in children by postural correction alone. They explain this as a relief of venous congestion in the head. In extreme cases, such impaired circulatory inefficiency may be sufficient to produce a marked fall in blood pressure and loss of consciousness. This is said to be the result of general muscle relaxation with blood pooling in venous reservoirs, especially in the abdomen, thus reducing the practical blood volume. More often it produces only dyspnea and weakness, sometimes accompanied by palpitation. Precordial pain resembling angina pectoris is not rare.
Visceral Syndromes. Faulty posture mechanics may cause the liver to rotate anteriorly and to the right. Traction is thereby exerted on the common duct and sometimes seriously interferes with biliary drainage. Ptosis of the kidneys, especially the left kidney, results in traction on the renal veins that may obstruct venous outflow causing passive congestion and albuminuria. Mild digestive symptoms may be present in the apparently healthy person. This can sometimes be traced to a degree of visceroptosis resulting in dysfunction of the displaced organs. Abdominal dilatation and motility disturbances are not infrequent occurrences. This is likely the outcome of stretching of the sympathetic nerves. Stretched nerves within muscle can produce transient paralysis. In addition, when the abdominal cavity becomes shortened longitudinally, the viscera become crowded as do the glands of internal secretion. Nerve ganglia may be involved as well. Thus, orthostatic albuminuria, dysmenorrhea, and constipation may sometimes be associated.
As a result of visceroptosis, a compensating lumbar lordosis, and the insult at intervertebral foramina, symptoms can be diffuse and subtle. Duodenal stasis may be attributed to increased tension on the superior mesenteric vessels. One study showed that postural correction relieved 65% of cases exhibiting a picture of duodenal obstruction and 75% of cases presenting gastric distress, nausea, and abdominal pain associated with visceroptosis. Narrowing of the intervertebral foramen may cause severe pain that has a segmental distribution and evidenced in the skin, muscle, or parietal peritoneum. This condition is usually misleading in origin as it suggests the presence of some intra-abdominal disorder.
A contusion, states O’Donoghue, is the effect of any type of trauma causing bruised skin and subcutaneous tissue that results in capillary rupture and an infiltrative type of bleeding followed by edema and an inflammatory reaction. Soft-tissue damage is usually more painful and can be more serious than bone injury. Bone heals with calcium. Soft tissue heals with fibrous scar tissue and is different from the original tissue by lacking its elasticity, pliability, plasticity, flexibility, and viability. Soft tissue also takes longer to heal than osseous tissue. Bone may actually be stronger after the healing process has taken effect, whereas soft tissue is usually weaker and less adaptable after repair.
Acute hemorrhage is defined as the sudden or rapid loss of blood from the circulatory system within a few minutes or hours as a result of an opening or openings in the system. Life is threatened if blood loss reaches 25%—50% of total volume. Concealed bleeding is difficult to estimate. Williams/Sperryn point out that over a quart of blood may be lost into the tissues in a closed fracture of the tibia, yet this is minor compared to be what may be lost within pleural or peritoneal cavities in chest or abdominal injuries. The seriousness of hemorrhage lies in both the rate and the quantity of blood volume reduction, which are related to the number, type, and location of the opened vessels.
Whenever an artery or vein is opened, the injured vessel reflexively constricts and, if severed, retracts into the tissue, thereby reducing the size of the opening and facilitating clot formation (scalp vessels are an exception). In addition, other blood vessels temporarily constrict as a part of the general reaction to injury. This generalized vasoconstriction helps maintain blood pressure by reducing the capacity of the circulatory system. The body in general and the cardiovascular system in particular react to stress of injury to the circulatory system by shock that is apparent after sudden loss of 15% or more of the circulating blood volume. At the site of injury, blood tends to clot and plug the opened vessel. If vasoconstriction and blood clotting are unsuccessful, the resulting blood volume reduction causes a fall in blood pressure which, among its other effects, facilitates clot formation. If hemorrhage persists, the person dies of lack of oxygen and other nutrients.
Thrombophlebitis and Embolism
Of the many complication dangers involved in handling an injury victim, throbophlebitis and the potentiality of embolism are common concerns. Venous stasis and pressure or other injury to vein walls predispose the development of thrombophlebitis. The overt signs and symptoms are cramping pain in the calf; possible redness, warmth, and swelling along the course of the involved vein; and pain which may appear only on dorsiflexion of the foot. The most common sites are in the veins of the pelvis and legs.
The affected limb should never be rubbed or massaged. It should be placed horizontal and at rest, supported by pillows. Cotton elastic bandages may be used if available on each extremity from foot to groin to assist venous circulation.
Be alert to any complaint or other evidence of respiratory difficulty or chest pain due to a possible embolism. Sudden dyspnea, violent coughing, hemoptysis, or severe stabbing chest pain may be the first sign of a dislodged thrombus. Sudden signs of shock and collapse should be anticipated.
The management of external hemorrhage is best accomplished if the wound is first exposed to view. Clothing or other material over the injury should be cut, torn, or lifted away carefully so that additional harm is not inflicted. Unnecessary movement or exposure of the patient to general cold should be avoided if to the extent that it may induce or hasten the lowering of body temperature.
External Venous Hemorrhage. Venous bleeding can be profuse during physical competition or vigorous work because of the increased blood flow to active limbs. However, the bleeding is often quickly stopped by a pad, firm bandage, and cold pack applied to the elevated part. Nothing more is usually necessary for the next 24 hours unless referral for surgical cleansing or suturing is required.
External Arterial Hemorrhage. Arterial injuries may be classed as either (1) complete, where the entire vessel wall is disrupted, or (2) incomplete, where only the outer coats or, at most, a portion of the circumference is damaged. These injuries originate from contusions, incised and lacerated wounds, and puncture wounds. The early manifestations are hemorrhage and possibly the appearance of a hematoma. In the later stages, thrombosis, traumatic aneurysms, and secondary hemorrhage are to be feared.
Internal Hemorrhage. Internal bleeding is a medical emergency. Treatment should only be first-aid measures to benefit the patient until transportation can be made to an appropriate trauma center or emergency ward. In some cases, such facilities may be many miles away. Initial actions can be life saving. If on-the-scene attention is made, the examiner should seek evidence of “pattern bleeding” in which the pattern of clothing texture is imprinted on the skin. This indicates severe compression and suggests possible visceral rupture. Note the presence of blood in vomitus, sputum, or excretions. Hemorrhage within the cranium or lungs may be indicated by bleeding from the nose, mouth, or ears. Evidence of internal bleeding may also be represented in such signs as restlessness, apprehension, thirst, falling blood pressure, and increasing pulse rate. Swelling and discoloration may be seen. Treat for shock, and prepare the patient for referral for hospitalization and blood transfusion.
A pressure point is any site where a main artery supplying the wounded area lies near the skin surface and over a bone or firm tissue. Pressure at these points is applied with the fingers, thumb, or hand. The object of the pressure is to compress the artery against a firm substance to occlude the flow of blood from the heart to the wound. Since it is often difficult to maintain occluding pressure manually on a pressure point, the pressure point method is used only until a pressure dressing can be applied.
A sterile dressing applied with pressure to a hemorrhaging wound enhances clot formation, compresses open blood vessels, and protects the injury from further invasion by infectious organisms. Sometimes more harm is done to the patient by secondary infection than the trauma itself.
Direct pressure on a wound is usually ineffective in controlling hemorrhage. Pressure is applied for the purpose of minimizing the size of the vessel opening by compression, temporarily or for an extended period, thereby lessening the amount and the velocity of the escaping blood and aiding clot formation. Firm pressure may be applied to a wound if there is no broken bone in or near the wound. Hemorrhage does not always stop immediately. At times, firm pressure on the dressing over the wound may be required for many minutes until a clot has formed with sufficient strength to hold with only the help of dressing ties. If a clot does not form quickly, a tourniquet must be considered (if feasible).
The dressing should be of absorbent material that spreads and slows the blood it absorbs. This spreading and slowing action exposes a relatively large and thin surface of the outflowing blood to the air and thereby aids clot formation. Accordingly, one dressing partially filled with the victim’s blood is more effective in controlling hemorrhage than is a series of others because clot formation is in progress within the bloody dressing. Clot formation tends to spread back toward and into the wound until diminished air exposure, coupled with an adequate circulating speed, brings the bleeding to a halt. It is the clot that stops the hemorrhage. If the blood had no ability to clot, the absorbent dressing applied would merely draw blood out through the wound and do more harm than good. When blood is about to clot, it begins to turn darker and becomes progressively darker as the clot takes form. A hard clot is almost black as its iron content oxidizes. Unnecessary prolonged pressure must be avoided. The dressing should be anchored snugly to prevent slipping, but not tightly. The wounded part, especially if it is an arm or leg, will swell after a time, tightening the bandage still more and impairing or stopping circulation within the part to the detriment of the patient.
An external wound easily becomes contaminated with microorganisms at the moment of occurrence, thus the prompt application of a sterile dressing serves to limit the entrance of infectious organisms. Once a dressing is applied, it should remain in place if at all possible. Removal permits entrance of additional microorganisms and may disturb the clot so that hemorrhage recurs. Also, leaving the original dressing in place helps the surgeon viewing it later to estimate the amount of blood the patient has lost. When a wound is dressed, care must be taken to avoid touching the wound or the surface of the dressing that is to be placed directly on the wound, breathing onto the dressing or wound, stirring up dust about the patient area, or allowing other actions which would permit infectious organisms to enter the wound.
Elevation of a Wounded Limb
Hemorrhage, especially of the venous type, can frequently be lessened appreciably by raising the injured limb to a height slightly above that of the heart. Because elevation tends to drain the elevated limb by gravity, an initial gush of blood downward from open veins should be expected when the limb is first elevated. Elevation helps to lower the blood pressure at the wound site. It may be used before, during, or after application of a pressure dressing, depending mainly on the type and severity of the wound. The patient may be instructed to elevate an less serious wound while waiting for a dressing and to maintain the height after the dressing is applied. Serious hemorrhage, especially of the arterial type, may require simultaneous and continuous application of elevation, dressing, pressure, and cold. If there is a broken bone in the wounded limb, elevation must be postponed until after the limb is splinted.
Use of a Tourniquet
A tourniquet is any constricting band placed around the circumference of one of the extremities to stop hemorrhage. In an emergency, careful judgment is required in making the decision to apply or withhold a true tourniquet. Both arterial and venous blood flow stops at the tourniquet. Without circulating blood, the part distal to the tourniquet begins to die. Rarely will a tourniquet be required unless a limb is severely mangled. When a tourniquet is used unskillfully, more harm can be done than from not using one.
Professional Judgment. While later surgical amputation of the limb distal to the point of application of the tourniquet does not necessarily always follow, the person who decides to apply a tourniquet must do so with the realization that this distal portion will probably be sacrificed. Thus, a tourniquet applied to a patient must represent a choice between saving a life or saving a limb. It must not represent a choice between the quick results a tourniquet produces and the sometimes tiring application of a pressure dressing.
Commitment. The decision to apply a tourniquet is irreversible. Once a tourniquet is applied, it must be left in place until removed by a surgeon as soon as possible. It must not be loosened and retightened in the mistaken belief that the portion of the limb distal to the tourniquet is being kept alive. The patient whose system is stabilized after the tourniquet has reduced the capacity of his circulatory system may not be able to withstand the shock of its sudden enlargement if the tourniquet is loosened.
General Guidelines. The need of a tourniquet is minimized when good techniques are used in pressure points, pressure dressings, elevation, local cold, and rest. Nonetheless, bleeding from a major artery of the thigh, lower leg, or upper arm, or hemorrhage from multiple arteries that is seen in traumatic amputation may prove beyond control by these methods. There is no set rule as to how long one should continue to try to control hemorrhage by pressure dressing, elevation, etc. However, in the emergency treatment situation, the absorbent capacity of the injured person’s first-aid dressing may be used as a guideline.
The Danger of Reactionary Hemorrhage
The possibility of delayed hemorrhage occurring either externally or internally as a postinjury complication is not remote. Reactionary bleeding may occur within a few hours after injury when blood pressure and circulation return to normal after shock. This increased pressure may also cause bleeding by displaced blood clots previously formed. If signs of renewed hemorrhage from a wound appear after a dressing is snugly in place, reapplication of manual pressure may be all that is necessary to assist clot formation. Sufficient pressure must be used to occlude the opened vessel(s). Signs of renewed or continued hemorrhage are (1) the appearance or enlargement of a bloodstain on the outer surface of the dressing and (2) the appearance or continuance of blood trickling between the dressing and the skin.
A clot protruding beyond the surface of the skin is presumptive evidence of arterial damage. The circulation of the part distal to the injury may be jeopardized because of marked damage to vital vessels or be merely a result of pressure resulting from a hematoma. If subcutaneous fat is exposed, the rule of thumb is that the wound should be sutured. An emergency attendant is rarely involved in the handling of wound closure materials such as suture needles or thread. However, it may be necessary to apply specially prepared adhesive strips for a sutureless wound closure before transporting the victim.
A hematoma arises from a rapid extravasation of blood and tissue fluid that pools into a singular large fluctuant mass. After injury, it may localize within a tissue space, a compartment, or an organ at any depth at most any site in the body. More specifically, O’Donoghue defines hematoma as a collection of pooled blood, within a relatively restricted area, that has collected in a localized area (self-made space) and has maintained its identity as blood. Bleeding within an anatomically closed space such as a joint, bursa, or viscus is not commonly called a hematoma.
Etiology. Interstitial hematomas are usually the result of contusion, while intramuscular hematomas are the product 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 in deep and subcutaneous connective tissues to compound the problem. When intramuscular tension returns after injury, bleeding points tend to become compressed. Firm clotting occurs within a few hours, but slight trauma (eg, massage, bump) may cause further hemorrhage even after 2—3 days. Resolution follows with a degree of absorption and fibrosis.
Inspection and Palpation. After a hematoma develops, the body’s reaction is to make an inflammatory response enabling it to cope with the blood pool. This reaction increases local tenderness and heat (similar to that seen in cellulitis) for 2—3 days until the stage of reactionary inflammation subsides. A large hematoma is never absorbed, it undergoes organization, fibrosis, and scar. The extent of a palpable hematoma should be noted, along with tissue tension and the presence of a bruit. If the hematoma pulsates, it may be due to transmitted arterial impulses or the development of an aneurysm. With aneurysm, a bruit can usually be auscultated. A hematoma itself is not tender, but adjacent soft tissues are frequently so. As the hematoma begins to age, the initial pool firms. If palpable, it will feel from doughy to fluctuant depending on its stage.
Management. First air for typical hemorrhage is compression, cold pack, elevation, and rest. Although a distinctly large extremity hematoma may become obliterated in 1—2 days with this treatment, local compression and padding should be continued for 1 or 2 weeks to assure complete resolution. Certain enzymes tend to help disbursement of a hematoma, but they are less effective than evacuation.
Referral. In severe cases or when fluctuation is obviously evident, referral for aspiration may be necessary. If so, it must be done early as a firm clot cannot be aspirated; open drainage must be used for evacuation. Aspiration should be followed by continued compression. If a semifirm clot resists aspiration, continued compression and padding are applied to encourage clot liquefaction. This should occur in 2—5 days. Open surgery is rarely necessary; when it is, the probability of secondary infection is always a problem. A dozen or more sterile needle aspirations are safer than one incision.
Uniqueness of Athletic Injury. The well-conditioned athlete (or hard laborer) not only has increased work capacity but also has altered typical metabolism at the microscopic level. Injury interrupts training and work causing a diminished level of physical fitness. It also produces a different type of lesion than that seen in general practice. This is due to the effects of training that increase muscle-fiber bulk and interstitial tissue vascularity. Because of the increased muscle bulk, vascularity, and conditioning to demands in the physically active individual, bleeding is more marked than in the unconditioned individual. Well-trained muscle offers more efficient physiologic mechanisms to remove extravasated blood from muscle, and absorption is much more rapid. Thus, in the management of hematoma or any similar injury, treatment must be modified when dealing with the rigorously trained or with the sedentary person.
Shock is a reaction to injury or disease, a manifestation of the rebellion of the body against a major insult or injury —an alarm reaction. It may appear suddenly after trauma or develop insidiously. There is inadequate circulating blood to fill the vascular system. There is interference with the basic physiologic process of the blood stream delivering oxygen and other essential elements to body tissues and removing waste products. Besides the predominant characteristic of a reduction in volume of circulating blood and initial vasoconstriction, vasodilatation, hypotension, tachycardia, and prostration follow. The initial circulatory deficiency is rapidly complicated by widespread oxygen deprivation and by a lessening of function of all tissues, especially the brain, liver, heart, and kidneys.
Typical Causes in Sports and Manual Labor
Reduction of blood volume in circulation can result from:
(1) loss of blood through internal or external hemorrhage;
(2) loss of plasma by seepage into tissues at the site of injury (eg, burns, contusions, crash injuries);
(3) excessive loss of fluids and electrolytes from the intestinal tract through severe vomiting or diarrhea; or
(4) an abnormally sudden increase in the volume capacity of the vascular system because of extensive vasodilatation. In the latter instance, many blood vessels dilate at the same time and, although there is no actual loss in the amount of blood, blood fails to move forward in the dilated vessels, thus mimicking cardiac output failure.
The signs and symptoms of shock are related to ineffective circulation and depression of vital body processes. The classical signs of shock exhibit the body’s attempt to compensate. They are:
Progressive loss of blood from active circulation, which may lead to failing heart output and insufficient oxygen to cells vital for survival. Cold perspiration, pallor, and possibly slight cyanosis, reflect the body’s attempt to produce peripheral vasoconstriction.
Sustained, progressively failing hypotension, which may lead to kidney and liver failure reflected by oliguria, indicative of physiologic-compensation failure.
Rapid-shallow breathing (air hunger), tachycardia, and a rapid weak thready pulse in compensation for cerebral anoxia. Anxiety, excitement leading to confusion, listlessness, irrelevant phrase repetition, apathy, and coma are also effects of cerebral anoxia.
Early syncope, which is mainly neurogenic and may be fatal. During this process, the patient will usually present a staring or vacant expression in the eyes. The pupils are dilated unless morphine has been given or taken.
Shock should be anticipated in any person subjected to known causes of shock such as unusual physical and emotional stress, any severe injury, loss of blood, or loss of other body fluids. It may develop slowly. In fact, characteristic signs might not appear for several hours. In incipient or impending shock that has not yet developed, no sign may manifest but preventive measures should be taken if shock is considered possible.
Prevention goals are met through the control or relief of factors tending to reduce aeration and circulation of an adequate blood volume. Aside from hemorrhage or even in its absence, circulatory collapse can be hastened or aggravated by such factors as fear, fatigue, or pain; dehydration resulting from excessive sweating, vomiting, or diarrhea; movement of injured parts; or use of morphine.
The patient should be kept horizontal so available circulating blood does not have to move against gravity. If the patient must be moved, move the victim gently. Cover the person lightly to preserve heat in a cold environment, but not so many blankets that would increase core temperature. Do whatever is possible to relieve pain. Establish a quiet atmosphere and a calm attitude to reassure and secure the patient. Check vital signs frequently to seek signs of irregularities and sudden changes.
Williams/Sperryn warn that the worst treatment given is overheating as this increases peripheral vascularity depriving deeper essential circulation. Elevated body temperature places stress on the cardiovascular system. As the superficial vessels dilate in an attempt to cool the blood within them, the system may become too large for the amount of blood it contains. In addition, there is an increased loss of electrolytes, particularly sodium and chloride. In a warm or hot atmosphere, padding used beneath the patient should not be made of wool. The patient should be shaded from the sun.
Temperature, pulse, and blood pressure should be checked every 15 minutes. A critical point for effective kidney function is reached when systolic blood pressure drops below 80 mm Hg. This can be a fatal complication. The only effective treatment of severe shock is transfusion of whole blood. Until this can be arranged, assure that the patient’s airway is open. Other measures are explained below.
Position the patient supine if conscious or in the three-quarter coma position if unconscious. The victim’s limbs should be raised to a level about 6-inches above the head to let gravity assist venous drainage. Pillows can be placed beneath the patient’s feet (with flexion at the knees) and buttocks. The good method is to raise the foot end of a spineboard, cot, or litter. This creates pooling of blood in the abdominal area without pressure on the diaphragm. Placing the head of a sitting victim down is not good procedure because respiration is hindered from the weight of the viscera producing an elevated diaphragm. The semiprone coma position may be used when the patient is unconscious; when there is a wound of the head, face, neck (except fracture or dislocation), or chest; or when vomiting is likely. When the patient is in this position, drainage from the respiratory tract is assisted.
Loosen tight clothing around the neck, chest, waist, and at any other areas in which clothing tends to bind. Loosen but do not remove shoes.
Keep the patient comfortable. The patient should not be allowed to become either cold or overheated. A drop in skin temperature gives rise to constriction of the superficial blood vessels, thereby reducing the volume of the vascular system. In a cool or cold atmosphere, the patient’s body and limbs should be covered with blankets. Wet clothing should be removed and blanket coverings tucked close to the patient’s skin. Clothing may be left on and exposed to the atmosphere, provided a breeze does not evaporate perspiration in the clothing so rapidly as to chill the patient. The victim should also be protected against atmospheric temperature changes such as those brought on with nightfall.
Relieve thirst in the conscious patient who is not vomiting and has no wound in the abdominal cavity or alimentary canal. Warm sweet drinks may be offered. Never offer an alcoholic beverage because it will dilate the vessels, and never force fluids by mouth.
Oxygen must be started immediately at 6 liters/minute if cyanosis of lips, nailbeds, or earlobes is noticed. Reassure the patient if conscious that his or her best interests are being served.
Treatment should be discontinued gradually when vital signs return to normal and stabilize. One valuable test of returned circulatory control is the ability of the patient to maintain stable vital signs as the patient changes position gradually upright. No sudden or abrupt movements should be allowed.
GENERAL SUBLUXATION-FIXATION IMPLICATIONS
The kinetic aspects of spinal biomechanics are an important consideration in traumatology since the totality of function is essentially the sum of its individual components. However, although reminders are frequently given, the multitude of causes and effects of an articular subluxation complex (spinal or extraspinal) will not be detailed in this text that is primarily directed to chiropractic clinicians and advanced students who are well acquainted with standard hypotheses. For a detailed description, the reader is referred to Schafer RC: Basic Principles of Chiropractic: The Neuroscience Foundation of Clinical Practice. Arlington, Virginia, American Chiropractic Association,1990.
The biomechanical efficiency of any one of the 25 vertebral motor units, from atlas to sacrum, can be described as that condition (individually and collectively) in which each gravitationally dependent segment above is free to seek its normal resting position in relation to its supporting structure below, is free to move efficiently through its normal ranges of motion, and is free to return to its normal resting position after movement. The degree of fixed derangement (subluxation-fixation) of a bony segment within its articular bed and normal range of motion may be an effect in the range of microtrauma to macroscopic damage. Regardless, it is always attended by some degree of mobility dysfunction; neurologic insult; and overstress of the muscles, tendons, and ligaments involved and their respective mechanoreceptors.
Once produced, the lesion becomes a focus of sustained pathologic irritation in which a barrage of impulses streams into the spinal cord where internuncial neurons receive and relay them to motor pathways. The contraction that provoked the subluxation initially is thereby reinforced, thus perpetuating both the subluxation and the pathologic process engendered. Sensory reflex phenomena can also be involved, and they frequently are. The nerve impulse creates a multitude of cellular reactions and responses besides those of even the most intricate, subtle, and variable sensations and motor activities. Once this is appreciated, we must add the complexities of trophic effects, neuroendocrine interrelations, biochemical affinities, proprioceptive buildup, summation increments, facilitation patterns, the input of the ascending and descending reticular activating mechanisms, genetic neurologic diatheses, synaptic overlaps, demoralization and disintegration of synaptic thresholds, the neurologic spread and buildup, reflex instability, predisposition to sensorial aberrations, undue cerebrovisceral or viscerocerebral interactions, psychosomatic overtones, and those many phenomena that science is only beginning to understand or are beyond our present understanding. This underscores that the quality and sometimes quantity of nerve function relates directly or indirectly to practically every bodily function and contributes significantly to the beginning of physiologic dysfunction and the development of pathologic processes.
Inequality in muscle balance leading to a subluxation complex may be initiated by trauma, postural distortion phenomena, biochemical reactions, psychomotor responses, paralytic effects, somatic and visceral reflexes.
Trauma. Frank trauma may cause inflammation, degeneration, etc, and particularly the muscular splinting reaction that muscles make when their surrounding tissues are injured or overstressed. This alters the position and motion of the structural tissues involved. Sustained microtrauma, though of a less acute nature, may produce a slow continual irritation and eventually create degenerative pathologic changes that similarly alter muscular reaction. The obvious trauma of a fall or blow that surprises a joint with the intrinsic muscles unprepared will cause a sprain with all its normal effects. A sudden slip during a lift is equally damaging to an unprepared or weak joint.
Indirect Stress. Depending on the degree of stress produced, any internal or external overstress factor involves the nervous system directly or indirectly, resulting in decreased mobility of the vertebra of the involved neuromere. This decreased mobility may be the result of (1) muscle splinting, especially on the side of greatest stimulation according to Fluger’s Law or (2) from abnormal weight distribution to the superior facets and other structures of the vertebrae involved. Fluger’s Law states that if a stimulus received by a sensory nerve extends to a motor nerve of the opposite side, contraction occurs only from corresponding muscles; and, if contraction is unequal bilaterally, the stronger contraction always occurs on the side stimulated. When involving one or more vertebrae, this state of decreased mobility of the motor unit encourages neurodysfunction leading to pathologic processes in the areas supplied by the affected nerve root or neuromere, depending on the degree and chronicity of involvement.
Psychomotor Responses. These responses refer to the reaction of musculature to emotional effects on the nervous system as the body depicts a state of psychologic stress. They may be environmentally, socially, or intrinsically initiated. Psychosomatic, psychovisceral, somatopsychic, or visceropsychic reflexes may be involved singularly or in combination.
The phrase “ligament sprain” is redundant. A sprain is joint injury in which the ligaments or capsule are partially torn or severely stretched without dislocation being fixed; ie, there may have been a partial dislocation that spontaneously reduced itself. O’Donoghue defines a sprain as any overstress ligament injury that produces some degree of damage to ligament fibers or their attachment. If an attachment is involved, the status may be called a sprain-fracture for some degree of periosteal avulsion has occurred.
The extent of damage depends on the amount, direction, and duration of the force and the strength of the tissues involved. Keep in mind that joint ligaments are designed as reinforcing straps that permit normal ranges of motion but restrict abnormal motion. Thus, a sprain cannot exist without some degree of instability, pain, swelling, or limitation of movement. The patient may recall hearing a pop or snap during a severe sprain.
Sprains are classed by severity as acute, subacute, or chronic, or by the area of involvement such as cervical, thoracic, thoracocervical, brachiocervical, thoracocostal, thoracolumbar, lumbar, lumbosacral, sacroiliac, iliofemoral, knee, ankle, shoulder, elbow, wrist, etc. Although the terms subacute and chronic may refer to diagnostic entities, they are confusing. An explanation of the specific subacute or chronic joint instability is more descriptive and desirable. Grading according to the extent to which the integrity of the involved ligaments have been compromised is favored by Garrick/Webb and many other authorities.
In differentiating sprain and strain, the examiner must keep in mind that sprain involves the ligaments and capsule of a joint and strain involves muscles and tendons. However, any tissue may be strained in injury if the word “strain” is being used as a verb. When used as a noun or state of being, sprain refers solely to ligament and/or capsule injury and strain solely to muscle or tendon injury. Sprain usually elicits pain on movement of the affected joint even without muscular effort. In contrast, strain produces pain on muscle effort even without joint movement (eg, in resisted contraction).
Periarticular and intra-articular ligaments can normally be stretched by passive movements of the related joint to the limit of their range of motion without inducing pain. Irritated or hardened ligaments become painful by stretching and deep pressure. When palpable, an irritated ligament will be tender; and if it can be squeezed, pain will be evoked.
Ligaments are generally much stronger than necessary to resist normal forces. If overstress is chronic or occurs at an unguarded moment, the ligaments are so overstretched to allow the articulating bones to slide (subluxate) out of their normal positions for a given motion.
Ligaments play a much greater part in supporting loads than are generally thought. Electromyographic studies involving fatigue from forces acting across a joint prove that muscles play only a secondary role. Such fatigue is basically a form of pain originating in the ligaments rather than muscle. Thus, some researchers feel that if the muscles involved in a problem are weak to begin with, there is a more immediate ligament action that produces the characteristic fatigue syndrome.
Chronic ligament pain usually develops when a joint is under strong 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) is held at a limit of motion. The ache arises from the stimulation of ligament, capsule, and periosteal mechanoreceptors.
In chronic conditions, the stretching of fibrous bands under continuous overtension is due partly to fiber elongation. However, most of the stretch 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 of some tissues and laxity of other 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 aligned and supported until ligament laxity is corrected.
When ligaments are subjected to continuous stress, they becomes chronically inflamed and invaded by collagen substance and mineral salts. This results in sclerosis and varying degrees of calcification. In addition, when ligaments and capsules are subjected to acute traumatic overstress, they may be rupture of some of the comprising fasciculi with attended minute hemorrhages. If the involved ligaments possessed elastic fibers, there will be a definite shortening as an after-effect.
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 leading to stretching of supporting ligaments and a flattening of the arch.
Acute Sprain Added to Chronic Sprain
An examiner must keep in mind that when connective tissue is subjected to continuous pull, it becomes chronically inflamed and invaded by collagen substance and mineral salts. This results in sclerosis and varying degrees of calcification. In addition, when these altered tissues are subjected to acute traumatic stress, some of the constituent fasciculi rupture. This is attended by an array of minute hemorrhages. Further attempts at repair result in collagen tissue deposition and mineral invasion that also produce sclerosis and calcification. If the involved ligament possessed elastic fibers, there will be a definite shortening. This knowledge is at the core of all rational rehabilitation programs involving sprain.
Classes of Acute Sprain
Sprains can be classed by severity, stage, or the area of involvement. In differentiating sprain and strain, textbooks frequently remind the examiner to 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). However, this author has rarely found the need to differentiate joint strain from sprain in posttraumatic joint injury because they inevitably coincide in variable degrees and their management, with exceptions to be explained, is generally the same. Thus, the term sprain/strain will be frequently used in this manual.
First-Degree Sprain. In a mild sprain, there is a small amount of internal bleeding in a localized area of the affected ligaments with only a few fibers separated. No actual loss of function or reduced strength is found. The involved ligaments generally require no protection and are not weakened. Mild sprain is characterized by tenderness on palpation that is not marked at the bony insertion by swelling or other features of overt inflammation. Joint instability is negligible.
Second-Degree Sprain. This is a moderate sprain with a partial tear, characterized by increased severity of first-degree symptoms. A tendency to recurrence is a complication, as is the potentiality of traumatic arthritis and permanent instability if improperly treated. A moderate sprain results from severe tearing of many fibers with at least half remaining undamaged. This type of sprain shows some loss of function in the injured area even if the torn ligaments are not widely separated. These fibers rejoin during the natural healing process unless the damage is great or treatment is inadequate. If damage is great, considerable scar tissue may form, and a permanent weakness of this section of the ligament may result is appropriate actions are not taken. Moderate sprain is characterized by a greater degree of symptoms than exhibited 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 complete ligament tears, characterized by severe swelling, hemorrhage, tenderness, complete loss of function, abnormal motion, and possible deformity. When a sprain is classed 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 series of bilateral stress radiographs or cineroentgenography. 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, but this should not be the basis for dismissal. Postsurgical chiropractic rehabilitative procedures are far more beneficial long-term than those provided by most orthopedic surgeons.
Garrick/Webb believe that rigid immobilization for a sprain much beyond 48 hours is counterproductive because of the invitation for disuse atrophy, taut capsule, and adhesion formation. A torn ligament is no stronger after immobilization than before and assisting joint muscle stabilizers have weakened proportionately. Sprains producing complete rupture requiring surgical repair may be an exception to this 48-hour rule, but the nefarious effects of immobilization remain.
Ligaments are stabilizers, not motor elements. Muscle-tendon units are motor units. While the term sprain is limited to ligament and capsule injury, strain is confined to injuries of the muscle-tendon unit. The phrase “muscle strain” is redundant.
Injuries to muscles and tendons are difficult to differentiate and need not be from a clinical standpoint. Rarely will surgery reveal a tendon injury with completely uninvolved muscle fibers, or vice versa. Another misconception is that strains are always the result of overstretching a muscle. More common, report Garrick/Webb, the injury occurs because tension within the musculotendinous unit is actively increased abruptly. This intensified tension may be the result of a sharp antagonistic contraction where the agonist tears before it can lengthen. A third misunderstanding is that a weak muscle is taut not flaccid. A very weak muscle fatigues easily, and a muscle forced beyond its capacity in strength or endurance will tighten defensively. Taut braiding spinal erectors are classic examples of this. They will not be found in the well-conditioned athlete.
Tendon attachments are contiguous with periosteum, with some fibers entering the bony cortex. Tendons have great intrinsic strength capable of withstanding the action of strong muscle contraction yet are often incapable of withstanding a sudden unexpected stretching force (eg, misstep). For protection, the Golgi tendon-stretch receptors (when healthy) signal a safety collapse reflex on excessive muscle contraction. This tends to counterbalance the stretch receptors in muscle that excite contraction on stretching.
Lymph vessels are not found in voluntary muscle. The degree of vascularity in the capillary network between skeletal muscle fibers and associated tissues depends greatly on physical conditioning. The quantity of interstitial fat, most marked in atrophied muscle, is also determined by the muscle’s degree of conditioning (eg, physical training).
A muscle in traumatic or reflex spasm becomes somewhat inflamed. Some transudation precipitation of fibrin, collagen, and mineral salt deposition may result and, if extended, produce chronic myositis and myofibrosis. Myofascial planes (especially of erectors) also may become inflamed at points of overstress. Myofascial transudation and fibrin formation commonly result in potentially disabling myofascial adhesions if not properly treated.
Pain from a damaged tendon usually arises when attached muscle fibers contract. Torn tendon fibers will usually not cause pain when the muscle is relaxed but will with the least muscle shortening. The pain of tendinitis is superficial, essentially resulting from associated tenosynovitis. It can be evoked by passively rolling the tendon back and forth within its sheath.
Tendon sheaths (synovium) are lined with specialized connective tissue cells similar to those lining bursae and the synovial membrane of joints. Thus, inflammatory reactions within tendon sheaths to traumatic influences (strains) are akin to those seen in bursae and joint-cavity disorders. The term tenosynovitis generally includes all inflammatory disorders involving tendons and their enveloping sheaths. The cause may be either trauma (direct blow, overuse) or infection (sterile or unsterile).
Etiology. Tenosynovitis is usually acute, relieved by rest, but may become chronic and resemble rheumatoid arthritis. The normally avascular synovium reacts with an increased blood volume, inflammatory cells invade, synovial fluid is oversecreted with an increased fibrin content. This results in the formation of “sticky” adhesions between tendons and adjacent tissue. These adhesions produce palpable “snowball crepitation” as the tendon moves within its sheath. Chronic inflammation of the sheath always holds the danger of stenosis, especially at sites where tendons cross (eg, De Quervain’s disease, snap finger).
Types. Traumatic tenosynovitis (peritendinitis crepitans) has 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 habitually sedentary weekend athlete is an example of overactivity that may bring on characteristic symptoms. Within a few hours after a hard session of unaccustomed effort, the involved tendon sheath becomes edematous.
Pathology. Adjacent muscle fibers show degenerative changes, lose glycogen content, and accumulate lactic acid, which spreads over the tendon. This acidity causes the edematous swelling. 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 that may be accompanied by a serous effusion within the tendon sheath. It is proper treatment especially at this stage of injury that is so important toward ideal rehabilitation
Clinical Features. Symptoms peak in 24—28 hours after injury. There is a gradual onset of pain radiating along the involved tendon on active contraction or passive stretching. There is a soft, warm, frequently red, localized swelling at the musculotendinous junction that usually renders an audible silky or leathery crepitus whenever the tendon is moved.
A less frequently seen form of tenosynovitis is an acute hemorrhagic type resulting from direct contusion or a puncture wound that does not introduce infection. A bloody and serous sterile fluid forms within the tendon sheath. 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.
The differentiation of joint swelling between hemarthrosis and synovitis is an important part of any joint examination following trauma. This is important because joint aspiration is usually contraindicated in simple synovitis but early aspiration is almost mandatory in hemarthrosis. 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).
Inflammation of areolar tissue around a tendon (peritendinitis) is a common result of sudden increases in physical work or training. It features swelling, pain which is relieved by activity, tenderness, and palpable crepitus.
Fascial hernias develop from contusions or small puncture wounds producing a weakness in the fascial sheath that envelops all muscles. They may also develop in weakened aponeuroses in patients with chronic compartment syndromes because of the increased pressure. Such hernias are sometimes found after injury where a muscle’s nerves emerge from its fascia. Palpation then reveals a tumor-like mass when the muscle is relaxed, which may disappear when the muscle is activated. This is the opposite finding of a hidden lipoma.
Etiology. Muscle action not balanced by reciprocal inhibition of the antagonistic muscle (eg, a blow, an unexpected force) may result in its rupture through its sheath by violent sudden contraction or a less common injury to its antagonist by overstretching. Muscles previously weakened by fatigue or disease are more apt to rupture. While complete muscle rupture is rare, a split in a muscle sheath due to weakness or a break may allow some muscle tissue to herniate during contraction. This may follow injury or be a postsurgical complication. The sheath opening may be large or small. 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. In the elderly, muscle rupture can occur under minimal loads as a result of degeneration within the muscle’s tendon.
Clinical Features. A soft mass is noted at the site of the opening during palpation. As with fascial hernia, it disappears when the muscle is contracted and reappears on relaxation. Weakness may be a complaint. In true cases, permanent correction can only be made by surgery. The syndrome 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 tendon’s attachment to the muscle belly. Normal continuity is broken and obvious on palpation unless 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 believed to be an effect of banding of overlying fascia. Rupture in youth features painful voluntary contraction, ecchymosis at an area of local tenderness, swelling, edema, and hemorrhage. Palpation often reveals the defect. After the acute stage, persistent weakness remains and there is an increase in muscle bulk proximal to the rupture site on contraction. In the elderly, muscle ruptures feature considerably less pain, swelling, tenderness, and ecchymosis; however, they do present with late persistent weakness and increased bulk on contraction.
Tendon rupture is rare in people under the age of 40 years. Both complete and partial ruptures are most often 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 usually found just proximal from the point of insertion into bone. The rare event of spontaneous tendon rupture occurs only when the tendon is weakened by advanced degenerative processes.
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 contracts. A gap may be noted when swelling subsides that gives a clue to the extent of muscle tear. Surgical correction is not usually necessary unless the separation is severe, but alert rehabilitation measures is always necessary to restore full function.
Rupture Near Insertion into Bone. Tendon rupture near its bony insertion features sharp pain often accompanied by perception of an abrupt dull snap 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.
Classification of Acute Strain
Strains, as sprains, are classed by either severity or area. When classified by area, names of specific muscles are used such as gluteal, intercostal, abdominal, and perivertebral strain. 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 according to the following descriptions.
First-Degree Strain. This is a mild muscle overstress causing trauma to a part of the musculoskeletal unit from forceful stretch resulting in a low-grade inflammation and some muscle- and/or tendon-fiber disruption. Hemorrhage and disability are mild. The injury 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 overstressed muscle caused by trauma to the musculoskeletal unit from excessive stretch or violent contraction resulting in torn fibers without complete disruption. It is characterized by increased first-degree-strain symptoms. There are moderate hemorrhage and swelling. Muscle spasm and function loss, especially, are greater. 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 usually felt at the site. The injury 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 tendon’s attachment to periosteum. Surgical joining is usually necessary, and postoperative chiropractic rehabilitation measures are recommended.
The tendons of the rotator cuff and the origin of the elbow extensors are common sites of calcium deposits. Deposition is usually abrupt and associated with a subdued inflammation of the joint capsule and its lining. Major characteristics are pain and muscle spasm limiting 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 tendon degeneration.
Due to chronic overstress at points of tendon insertion, fatigue fractures may appear in the cortex of the bone, causing the area to be invaded by bone cells. In late stages, compact bone may be found on roentgenography to extend well over an inch into the tendon and very frequently mistaken for a bone spur. Such extensions are subject to fracture; but unless exposed to direct trauma or undue intrinsic overstress, they are usually asymptomatic.
Traumatic Myositis Ossificans
Myositis ossificans is heterotopic bone formation occurring after contusion and hematoma near bone in collagenous supportive tissues such as skeletal muscles, ligaments, tendons, and fascia. It is commonly the effect of direct muscle bruising, especially repeated contusions (as seen in contact sports and certain occupations), on the anterior aspects of thighs and arms. True myositis need not be part of its cause. Ossification of infiltrated blood along the muscle origin on bone is all that is necessary.
Background. Connective tissue surrounding muscle rapidly invades a traumatized area, and this tissue retains its embryonal ability to be transformed into more differentiated tissue. Following 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. The calcification 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 exhibits local heat. It is common in teenagers and young adult males, and occurs 80% of the time in the biceps brachialis after dislocations. It is also frequently seen in the thigh (quadriceps). Periosteal tears undoubtedly encourage ossification.
Management. Early cold, rest, and compression to the injured muscle help to reduce potential ossification. Immobilization is usually required for about 2 weeks after injury, followed by progressive active range-of-motion exercises. Exercise should not begin early as it provokes extension of the calcareous deposits. Heat is helpful in the later stages. Extremely large and painful lesions may require surgery after ossification is mature and when the site is near a joint and disturbing function. Protection of the part is the best preventive measure.
Absorption is inhibited after injury if bleeding is excessive or if a hematoma forms within lax tissues. When the clot retracts, a serum-filled cavity (presenting a fluctuant swelling) remains that is lined with organizing fibrin deposits. Referral for aspiration is seldom successful; surgical drainage is indicated. Progressive exercises may begin gently even when the pressure bandage is still applied because an inserted drain is rarely necessary.
Localized cystic swelling is sometimes applied is the result of mucinous degeneration of connective tissue occurring near a tendon sheath or joint capsule. The cause is unclear, but trauma or degeneration is thought to be a factor. A defect in the fibrous sheath of a joint or tendon permitting a segment of underlying synovium to herniate should always be a suspicion. The initial irritation accompanying the herniation stimulates further fluid accumulation so that the sac or encapsulation enlarges, sometimes to a large degree. In the late stages, the synovial hernia firms and sometimes hardens. Early transillumination and palpation will reveal a translucent fluctuant mass.
Findings. One large cyst may be felt, or several small cysts may coalesce to form a multilocular lesion. Its walls are composed of dense fibrous tissue. Bundles of nerve fibers are often seen microscopically in the areas of mucinous degeneration. Ganglions are usually obvious when on the dorsum of the wrist or foot. They give rise to a localized swelling, gradual or sudden in onset, that may vary in size from time to time. Associated weakness and mild neuralgia may be reported, but most complaints will be of a cosmetic nature. When connected to a tendon sheath, the ganglion becomes prominent when the tendon is stretched.
Management. Small ganglia can be therapeutically ruptured by pressure or a sudden blow, but they frequently recur. After disruption of the gelatinous material into the tissues, the area should be firmly compressed for a few days. The classic practice of smashing a ganglion with Gray’s Anatomy, however, is not successful if the ganglion is attached to a joint capsule. Aspiration followed by corticotherapy is often recommended by allopaths. Surgical incision may be necessary and is a far more appropriate solution.
The osteocytes forming bone have the ability to select calcium and other minerals from blood and tissue fluid and to deposit the salts in the connective tissue fibers between cells. Bones become harder and brittle as age advances because there are higher proportions of minerals and fewer active osteocytes. The osteocytes in periosteum (which is rich in nerves and blood vessels) are active during growth and repair of injuries. The combination of hard and dense compact bone and porous cancellous bone produces maximum strength with minimal weight.
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. Physical examination must be gentle but thorough because deep soft-tissue trauma is poorly visible on radiographs until many days after injury.
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 emboli, thrombosis, and vasospasm can cause additional devascularization. When circulation is deficient, local phagocytic function and nutrition go begging. Healing is therefore inhibited.
When subjected to prolonged weight-bearing or traumatic overstress, bone demineralizes and undergoes degenerative changes, resulting in deformity of the articulating surfaces. Concurrently, the attending excoriation of the periosteal articular margins results in proliferative changes such as lipping, 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. Common radiologic patterns of bone destruction are shown in Table 1.6.
|Type of Bone Destruction||Major Features||Examples|
|Moth-eaten||Multiple, coalescing holes, moderate size, similar to an aggressive process.||Osteomyelitis|
|Permeative||Multiple, small holes that tend to become smaller and fewer near the periphery of the lesion, producing a wide transition zone from normal to abnormal bone.||Unlocalized infection|
|Geographic||Single or multiple, sharply marginated, relatively large, punched-out holes.||Multiple myeloma|
|Reaction Type Interrupted||Examples|
Lamellated (onion skin)
Perpendicular (spiculated or sunburst
Infection, Ewing's sarcoma, osteosarcoma
Infection, Ewing's sarcoma, osteosarcoma
Infection, hemorrhage, malignancy
|Solid Reaction Type||Examples|
Dense and elliptical with destruction
Thin and undulating
|Chronic infection or advanced malignancy|
Osteoid osteoma, eosinophilic granuloma
Hypertrophic pulmonary osteoarthropathy
Periostitis. Periostitis is usually associated with joint injury, especially that of the knee and elbow. It results from violent muscle strain that damages periosteum. If severe enough to detach the periosteum, a degree of hematoma develops. The bruised joint is swollen, extremely tender, and movements are restricted. Physical examination may spur suspicions of fracture, but early roentgenographic findings are negative. Later, ossification of the hematoma is shown by induration of the swelling and new bone formation. If severe hematoma is associated, aspiration may be necessary. In milder cases, firm support and physical therapy are appropriate. Periostitis is slow to heal and usually requires at least several months restriction from forceful activity or contact sports.
Osteomyelitis. With the exception of infested compound fractures, repeated injuries, surgery, and piercing wounds, the incidence of osteomyelitis is low. When diagnosed, antibiotics are invariably required for control. Staphylococcus aureus is the common agent in all ages, and over 50% of the strains are penicillin resistant. Blacks are prone to develop a subacute form of osteomyelitis, especially if there is an indication of sickle cell anemia. The time between initial infection and circulatory troubles is often rather short. If effective treatment is delayed and partial circulatory embarrassment is allowed for more than just 72 hours after the infection begins, surgery may be the only alternative and loss of joint function may be the result.
Intra-articular fractures are not uncommon. They involve articular surfaces and associated cartilage. Osteoarthrosis results if reduction is not accurate. However, a displaced fragment need not be removed if it does not interfere with function. Dislocations with complicating fractures often involve joint impaction and fragmentation. They usually present great instability and require operative repair.
Clinical Features. A working diagnosis of fracture may be based on any combination of signs and symptoms. Additional assistance in diagnosis may be obtained from the history and confirmed by roentgenography. For instance, a history of falling, receiving a blow, or having felt or heard a bone snap may help in the discovery of more evidence such as:
Swelling and discoloration at the site of injury that increase with time may indicate fracture. With fracture, 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. Protrusion of a bone segment, unnatural depression, or abnormal flexion may also indicate fracture.
Tenderness or pain on slight pressure on the injured part may indicate a fracture. Deep, sharp pain on an attempt to move the involved bone is presumptive evidence of fracture. Grating of bone ends against each other during movement 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.
Some diagnostic pitfalls in orthopedics are pointed out by Iversen/Clawson. They include (1) considering accessory ossicles as fractures; (2) overlooking an osteochondral, a tibial-spine, or a stress fracture; (3) forgetting that an upper-tibial fracture might progress into valgus; (4) failing to realize the instability of an apparently undisplaced lateral condyle fracture of the humerus; and (5) not appreciating the frequency of distal forearm fractures that slip.
The Repair Process. Although bone is noted for its hardness and supportive characteristics, bone is similar to soft tissue in that it is resilient, highly vascular, and constantly changing. It adapts to disease and heals itself when fractured. Bone growth and repair are most efficient during youth and adolescence in which fractures heal rapidly. Abnormally slow healing can almost always be contributed to a deficiency in minerals and vitamins, rarely to endocrine or metabolic etiologies. However, if control is poor for site motion, joint distraction, and infection, complications can cause delayed union or nonunion.
Fractures repair, as do all living tissues, by cellular growth, yet there are some unique characteristics due to bone’s high mineral content. Nevertheless, many similarities exist in the healing of connective tissue that can be generalized to direct proper treatment. That is, if the healing of a fracture is understood, the healing of any connective tissue can be understood and enhanced.
After fracture, a hematoma develops between the split ends. This space becomes invaded within a few days by granulation tissue, which in time becomes converted into fibrocartilage. This fibrocartilage is an osteoid tissue where new bone is laid down for union. After this stage, resorption and remodeling occur to reduce the initial callus formation in an attempt to restore the bone to its original size and shape. While healthy bone is highly vascular, readily repairs itself, and resists infection, avascular bone is defenseless in participating in the reparative process. Thus, after injury, treatment must be directed to prevent further devascularization and to encourage improved vascularity. Intra-articular and metaphyseal fractures enjoy an abundant blood supply, thus early and active movement of the joint should be encouraged. However, proper stabilization of distal and proximal joints must be maintained in diaphyseal fractures because of the relatively poor blood supply. Thus, special concern must be given to increasing circulation and preventing stiffness.
Emergency Care. The first step is to make a brief but thorough examination to determine the extent of injuries. Treatment of any life-endangering condition such as respiratory failure, cardiac arrest, or hemorrhage takes precedence over that for fracture. The care applied directly to the fracture is a part of the prevention or lessening of shock because pain is lessened and the likelihood of further trauma is reduced. In the initial treatment for fractures, the rule, “Splint them where they lie”, applies. Open fractures are dressed before splints are applied. Special care must be taken to avoid moving the fractured part because the razor-sharp ends of fractured bone can easily cut through vessels, nerves, muscles, and skin. Such additional damage would, of course, increase the possibility of hemorrhage, shock, and loss of limb or life. If movement of the patient is unavoidable or is essential in treatment, the fractured part must be supported if further damage is to be avoided. Slight traction distal to the part may be necessary to restore circulation, the lack of which is shown by absence of the pulse distal to the fracture. Circulatory impairment is especially common after elbow fracture. With the individual suffering multiple injuries, the most commonly overlooked injuries are fractures of the basilar skull, C7 vertebra, femoral neck, orbit, pelvis, radial head, talus, tibial plateau, T12 and L1 vertebrae, and zygomatic arch. Associated dislocations of the lunate, perilunate, posterior femoral head, posterior shoulder, and scaphoid are common.
Stress (Fatigue) Fracture. Bone-fatigue fractures may be the effect of an improper relation between overstress and adaptability of bone. They indicate a reaction to stress in an unconditioned person. The most common example of this is the so-called “march foot” of infantrymen, mailmen, and new track recruits. It’s commonly the result of 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 almost every bone of the body after trauma. These will not usually be evident in films taken immediately after injury. Often, 7—10 days must elapse before they can be visualized on film. On occasion, they are seen only by overlying periosteal elevation and 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 ordered to rule out fracture. Because of the associated weakness, swelling, and tenderness, differentiation from strain/sprain is difficult by physical examination. Protection and rest until the callus matures to bone is all the treatment usually necessary. However, stress fractures of the neck of the femur, anterior midthird of the tibia, tarsal navicular, and base of the fifth metatarsal deserve orthopedic consultation.
Chondral Fracture. Until recent years, chondral and osteochondral fractures have been overlooked. O’Donoghue reports that they are especially common in the knee and ankle. Early diagnosis is difficult because symptoms in the acute stage are obscure and disability is slight. A misdiagnosis of chronic sprain, idiopathic synovitis with effusion, or chondromalacia (especially patellar) is often made. At the knee, a joint mouse and/or osteochondritis dissecans may be an effect.
MYALGIA, MYOSITIS, AND RELATED CONDITIONS
Muscle pain is not localized subjectively with the same accuracy as is pain in more superficial structures, thus such vague localization requires a most careful examination. Muscle inflammation is often mistaken for disease of the adjacent joint, tendon sheath, or some type of neuralgia. The examiner should keep in mind that any type of excessive motor fiber stimulation results in pathologic, involuntary, and painful muscle spasm. Severe spasm places considerable tension on highly sensitive periosteum via its tendon attachment. It is one thing to find muscle spasm and another to determine if it is protective, compensatory, hysterical, or a causative factor.
Motion limitations due to spasm are seen frequently 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 direct irritation or trauma; stretching or pressure on a nerve trunk, plexus, or peripheral nerve branches; secondary to trauma of an adjacent structure; toxic irritation of the anterior horn cells; or psychogenic origins.
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.
Pain arising from an injury to muscle tissue may be provoked by making the muscle contract against resistance without allowing it to shorten; ie, preventing movement of adjacent joints. This test, although possibly helpful 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. Another factor is that pain arising from a chronic contraction of an involved muscle is not increased by contracting the muscle further.
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. This process allows a continuous exchange of tissue fluids and maintains a constant pressure of interstitial fluid.
The flow of lymph increases during activity as does capillary circulation, but the flow can be impeded by excessive pressure exerted by a constantly hypertonic or phasically contracted muscle. De Sterno shows that inhibited lymph drainage contributes to muscle pain during prolonged activity by (1) causing a build-up 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.
It is the author's belief that much of the success of chiropractic treatment of traumatized tissues is from the special concern given to normalizing lymphatic and venous homeostasis as soon as possible. The effect is minimization of fibrosis when coupled with early articular mobility.
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 woody hardness. This type of myositis usually subsides without suppuration.
Muscle function remains painless if an inflammatory process lies entirely within the muscle sheath, but perimyositis may cause pain during function. Myositis produces pain only when the muscle is palpated or stretched. Whenever stretching a muscle causes pain, that muscle should be carefully palpated for sensitive areas, swelling, or induration. Points of sharply defined tenderness can usually be found. In seeking muscle tenderness, portions of the muscle should be pressed between two fingers rather than pressing the muscle on underlying bone to avoid mistaking periostitis for myositis.
This disorder is characterized by chronic joint inflammation producing stiffness and deep aching. It’s of unknown etiology but often precipitates in the underconditioned or those past middle age following overstress. Attacks usually involve the shoulder and hip areas. Aching is perceived in the joints, and paresthesias are felt in the fingers. The proximal muscles, which are painfully stiff but not weak or atrophic, are chiefly involved, and their tendon insertions and associated joint capsules may become thick and tender. However, persistent synovitis or bony erosions are not characteristic of polymalgia rheumatica (PMR).
A mild form of giant cell arteritis is related in 16% of PMR patients. Unlike patients with fibrositis, patients with polymyalgia express such systemic symptoms and signs as a constantly elevated erythrocyte sedimentation rate, weight loss, malaise, headache, anorexia, fever, and mild anemia. Diagnosis is difficult to arrive at except by exclusion.
Striated muscles, especially the erectors, become painfully splinted (intrinsically immobilized) by involuntary spasm when fatigued. In time, trophic changes occur and tone is lost. In ordinary spasm, relaxation of affected muscles occurs at rest. This is not so for splinted muscles. 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 long after the initial cause has been erased.
Splinting is explained by understanding the stretch reflex. This reflex is not normally initiated by voluntary contraction. 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 than by a slow stretch. It is also well to remember that 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.
Prolonged pain from bone, muscle, tendon, and joint lesions with resultant long-term splinting or pseudoparalysis leads 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.
When muscles become acutely spastic or chronically indurated, normal movement is impaired and the foci for referred pain are established. Both spastic and indurated muscles are characterized by circulatory stasis that is essentially the effect of compressed vessels. This leads to cellular nutrition impairment and the accumulation of metabolic debris. Palpation often reveals tender areas that feel taut, gristly, ropy, or nodular. The degree of impairment is essentially determined by the severity of spasm, the amount of induration, and the extent of functional disability. Even with proper conditioning and warm-up procedures, myalgic syndromes are commonly seen when treating athletes or stoic individuals because they habitually ignore the warning signals of pain.
Treatment is commonly aimed at normalizing the continuous motor firing, dislodging collections of metabolic debris, and improving circulation and drainage. Despite the modality or manual procedure used, its intensity should be maintained below the threshold of pain to prevent a protective contraction of the involved muscles. Stretching, heat, sine-wave muscle stimulation, negative galvanism, vibromassage, and goading have all been effective, separately and in combination. When deep mechanical vibration is used, several clinicians report that pressure across muscle fibers tends to release accumulated metabolic by-products, while pressure parallel to muscle fibers (directed to the heart) enhances drainage. Lowe recommends that when spastic areas do not release adequately or conventional methods only offer temporary relief, a nutritional evaluation should be made. A calcium, Vitamin D, and/or magnesium deficiency may be a contributing cause.
On examination, spasticity and stiffness have similar physical findings, but the causes are different. As described above, spasticity is the result of contracted muscles. Stiffness is caused by taut connective tissues that have lost their normal elasticity, plasticity, and/or pliability —indicating the initiation of fibrosis. In chronic states, low-grade spasticity and progressing stiffness are often superimposed.
The relief of stiffness is one of the first goals of rehabilitation after the control of pain. Common techniques include continuous passive manual stretch, spray and stretch, continuous traction, and prolonged stretch with weights. Middleton also includes the use of walk-away casts and dynasplints. However, proprioceptive neuromuscular facilitation (PNF) techniques increase joint flexibility more efficiently than static or dynamic stretching procedures. PNF techniques are described later in this chapter.
A large number of localized tender sites, widely dispersed and symmetrical, suggests fibrositis. In contrast to fibrositis, a small number of points clustered in a single region and unassociated with diffuse aching stiffness and fatigue suggests a referred pain syndrome. Smythe defines primary fibrositis (fibromyalgia) as a syndrome of pain and stiffness lasting at least 3 months that is confined chiefly to tendon insertions, areas of bony prominences, and periarticular areas. His studies found that it is common in women of the 25—35 age group and frequently seen in broad muscles of both genders following prolonged overstress. Signs of joint involvement and muscle wasting are minimal or absent. Roentgenographic signs and laboratory data are indefinite. Common sites of fibrositis are shown in Table 1.8.
|1. Low cervical||Anterior surface of intertransverse spaces C5—C7.|
|2. Trapezius||Center of upper fold.|
|3. Costochondral||Just lateral and cephalad to 2nd costochondral junction.|
|4. Supraspinatus||Near the scapula’s medial border, above the scapular spine.|
|5. Lateral elbow||About 1½ inches distal to the lateral epicondyle, in the lateral inter-muscular space (“tennis elbow” point).|
|6. Low lumbar||L4—S1 interspinous ligaments.|
|7. Gluteus medius||Superior-lateral aspect of buttocks (deep).|
|8. Medial fat pad||Over superomedial knee ligaments, cephalad to joint line.|
|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 abdominis||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.|
The power of a reaction appears to be moderated by several general factors. Examples include conditioning, genetic predisposition, hormonal balance, scar tissue from previous injury, malnutrition, or prolonged emotional stress. The 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, or hysteria. Pain also occurs 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 shortening of the affected muscle with limitation of motion and weakness.
Certain muscles and muscle groups such as the antigravity muscles appear to be affected more than others. The 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. 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 usually manifest in local and general muscle fatigue, hypertonia, weakness, possibly a fine tremor, hyperirritability, pain, and hypesthesia.
The 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. These autonomic concomitants are similar to those seen with acupoint meridians. Travell believes that these are frequently expressed as decreased skin resistance, increased pilomotor reaction in the reference area, vasodilatation (possibly with dermatographia), and skin temperature changes (coolness).
Muscles enclosed and supported by strong fascial compartments may become involved in a muscle-fascia interface syndrome. It may be caused by intrinsic or extrinsic overstress or some type of circulatory obstruction in which pressure within a restricted anatomical space increases enough to produce circulatory embarrassment to the contents of the space. Compartment syndromes manifest in both the upper and lower extremities, but they 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.
The Pathophysiologic Process. Any muscle crush or interference with circulation (eg, arteriosclerosis) may result in muscle swelling restricted by the fascial sheath, leading to extreme pressure producing cellular death. Arteriosclerosis should not be thought of as strictly a disease of the elderly. Autopsies of young soldiers in the Vietnam War showed findings of extensive arteriosclerosis. 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 several 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.
Clinical Features. A diminished peripheral pulse may point to either a compartment syndrome or arterial occlusion. Hot red skin over 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. Because people appear to have a predisposition toward compartment syndromes, they should be identified as early as possible and examined frequently because the syndrome is usually progressive. In severe cases, referral for early decompression may be indicated, based on especially detailed records.
In athletes and physical laborers, secondary local phlebitis often accompanies contusions, sprains, strains, and varicose veins. Its effects can be minimized by rest and enhancing posttraumatic circulation; eg, early mild muscle activity after injury. It is important to differentiate simple inflammation from clot formation that may lead to a dangerous embolism. If a febrile reaction occurs, hospitalization should be considered.
An area of chronically indurated or weakened muscle is often next to an area of muscle that has entered a state of fatty degeneration. When found through palpation, this area should not be confused with a lipoma (adipoma). Lipomata are soft benign fatty tumors, frequently multiple but not metastatic, that vary in size from a pea to a large egg. While most lipomata are located subcutaneously, those embedded deep within skeletal muscle tend to rise to the surface when the involved muscle is exercised and to recede during rest.
Common posttraumatic stasis has been described earlier in this chapter. Posttraumatic lymphadenitis and lymphangitis, exhibited by warm red tender streaks extending toward neighboring tender swollen lymph nodes accompany infection. These potentially serious inflammatory infections are usually complications to hand and foot abrasions and fungal infections. Rarely does suppuration arise. If signs are not quickly abated by elevation and indirect warmth, referral should be made without delay for culture and appropriate antibiotic therapy.
Psychogenic rheumatism is a common example of psychic conversion. It is characterized by variable symptoms that include fleeting joint pains that shift from site to site and typically worsen under times of emotional stress rather than physical activity or changes in weather. The patient reports “good days” interposed between “bad days” that are unrelated to a common factor. There is an overreaction to gentle palpation such as facial grimaces and rapid “touch me not” withdrawal. It is sometimes seen in unmotivated youngsters that are coerced into athletic or certain work activity by parents or peers.
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 1.10.
|Feature||Synovitic Lesions||Mechanical Lesions|
|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 antiinflammatory 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.|
Name Description Incidence Cause Bursitis Inflammation around Adults of both sexes Unknown, although calcium deposits between new injury to tendons tendon and bursa sac causing sometimes starts an severe pain (usually in the attack. shoulder). Subsides after a week or so but may become chronic.
Osteo- Bony spurs appear around Approximately 6 million Heredity, overuse arthritis joints, causing swelling, Americans are affected. of a joint, repeated pain, and eventually erosion Almost everyone past minor trauma, or a of cartilage. Develops middle age develops sudden severe injury; slowly and is rarely conditions typical of may be a metabolic disabling. this disease. imbalance in the body chemistry.
Rheumatoid An inflammatory condition About 4.5 million suffer An unknown virus, arthritis affecting not only joints from this raving form of inborn hypersensi- but connective tissue, arthritis: 75% are over ivity, or other nerves muscles, blood 45 years of age, with factors that weaken vessels, and other organs. women stricken three the body's resistance; Causes crippling stiffness times more often family predisposition. of joints if not controlled. than men.
Gouty Painful swelling of soft Over 90% of cases A defect of metabolism arthritis tissues, mainly the great occur in males. that causes an excess toe, body chemistry, Over 35,000 citizens of uric acid in the blood, enormous increase in are affected by this which collects on or uric acids. disorder. near cartilages. Heredity and obesity cofactors are common.
Rheumatic Many joints may be inflamed Children below teens. Unknown. fever in the acute phase of this Nearly all cases follow disease, but they usually streptococcal infections heal completely. Chief danger with, over 50% following is injury to the heart. tonsillitis or pharyngitis. Peak incidence is age 6–9.
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:
(1) color changes such as ecchymoses 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, subluxation, scoliosis, kyphosis, lordosis;
(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.
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 1.12, and Traumatic and nontraumatic causes for most cases of joint pain are listed in Table 1.13.
Acute infectious arthritis
Acute intermittent hydrarthrosis
Acute rheumatoid arthritis
Acute traumatic joint disease
Acute rheumatic fever
Acute rheumatoid polyarthritis
and other acute connective-tissue
Acute rheumatoid variants
Chronic infectious arthritis
Chronic traumatic arthritis
Overuse stress with complications
Chronic gouty polyarthritis
Chronic polyrheumatoid arthritis
and other chronic connective-tissue
Chronic rheumatoid variants
|Conditions accounting for most cases of joint pain:|
|Acute pyogenic arthritis|
Gout and pseudogout
Disseminated lupus erythematosus
Von Bechterew's arthritis
|Relatively uncommon incidental arthritides exhibiting joint pain:|
Chronic pulmonary disease
Congenital heart disease
|Meningococcal arthritis |
Subacute bacterial endocarditis
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 1.14. 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.
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 1.15.
|Acute pain||Subacute or chronic pain|
|Acute monarthritis |
Other inflammatory synovitis
Reflex sympathetic dystrophy
|Involvement of many peripheral joints, especially metacarpophalangeal and proximal interphalangeal joint of hands, and first interphalangeal foot joints.||Involvement of weight-bearing joints, especially knees and hips. First carpometacarpal and acromioclavicular joints are often involved though non-weight-bearing.|
|Early synovitis, characterized by fusiform softtissue 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.|
|Gouty Arthritis||Atypical Osteoarthritis|
|May involve any joint but most commonly attacks first metatarsophalangeal joint of the of foot, other foot joints, and carpometacarpal joints.||Common involves hips, knees, metacarpophalangeal, midcarpal, and patellofemoral joints.|
|Joint space is preserved in spite of eroded bone.||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 summarized in Table 1.18. 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 joint motion.
|1.||Pain, tenderness, and heat in, near, or at a distance from the joint.|
|2.||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 netween 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 norma 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, wwhite, 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 with a tape on each side.|
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 1.19.
|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 1.20. 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. 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 derangements within the joint.
Table 1.20 too complex for this format
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: (1) joint inflammation or synovitis, (2) mechanical or cartilaginous lesions, and/or (3) nonarticular rheumatism that mimics arthritis. Bursitis and tendinitis also express themselves on periarticular structures, but signs of internal joint involvement are absent. Weakness of proximal muscles is a major finding in myositis, not swelling or tenderness about involved joints. Refer to Table 1.10. (See Above)
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 he 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|
|Metatarsal heads||Freiberg’s disease|
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 1.21.
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).
The 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 disease, which will often offer a confusing clinical picture. The primary causes of peripheral neuropathy are shown in Table 1.22.
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:
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.
The indications, applications, and contraindications for common modalities and other applied physiologic therapeutics are described in Jaskoviak PA, Schafer RC: Applied Physiotherapy. Arlington, Virginia, American Chiropractic Association, 1986. A second edition is currently in development.
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 study of human biomechanics includes the mechanical principles involved, the physiologic considerations of muscle length-tension relations, and an understanding of the controlling neuromotor mechanisms and the sensory feedback apparatus, reflecting both locomotor activity and cerebral function. Applied biomechanics is the application of the practical principles of mechanics (the study of forces and their effects) to the body in movement and at rest.
The more biomechanics are understood, the better musculoskeletal disorders in sports and the workplace can be appreciated. The same can be said physical work and recreational activities. The athlete is constantly attempting to improve performance by applying biomechanical principles to specific movements. The same is true for ergonomics in the workplace. From the viewpoint of the doctor, knowledge of the mechanisms involved in an injury is necessary to evaluate an injury accurately.
From a pure musculoskeletal standpoint, the human body is a mechanical device. All mechanical devices are subject to wear during use that reflects their history of destructive forces. Unique to living tissue is its ability to heal, adapt, and strengthen, which provides a dialogue between catabolic and anabolic forces. While machines convert thermal or chemical energy into mechanical energy, muscle tissue transforms nutrients directly into mechanical energy without a thermal intermediary. Body energy enables it to overcome resistance to motion, to produce a physical effect, and to accomplish work.
The body’s kinetic energy is reflected in its velocity, and its potential energy is reflected in its position. Work is the result of a force acting through a distance. Power relates to the time element and the work accomplished. There is a close association in the same unit of time between the work accomplished by a weight lifter and that of a sprinter.
Muscle contraction (work) reflects the consumption of mechanical energy. Some of this energy is unproductively used to overcome internal friction and loading, and some is stored for later use within elastic (contractile) tissues. The effect of muscle contraction essentially depends on: (1) the unique fiber arrangement determining the relationship of force that the muscle can produce and the distance over which it can contract, (2) the angle of pull, and (3) the muscle’s location relative to the joint axis.
The resistance offered to musculoskeletal forces may arise from gravity, friction, stationary structures, elasticity of structures, or manual resistance. The effectiveness of resistance or load is determined by the angle of the line of resistance applied and the distance of the load from the axis of the lever system involved. Gravity is the most common load on the body and provides a line of force in a constant direction.
Although forces of all types may cause subluxations, dislocations, fractures, strains and sprains, and so forth, the biomechanics involved determine the type and extent of the injury produced depending on the applications of force and its resistance. Thus, different types of force may cause bending fractures, stress fractures, or compression fractures. When the examiner understands how an injury was caused, the tissues involved are more readily located and the injury extent is more quickly evaluated.
Biomechanical Forces on Joints
Joint structure is the product of the quality and quantity of the chemical constituents of bone and associated tissues to cope with the action of external and internal forces. Joint stress is defined as the force exerted. Pressure always results in compression stress, and a pull produces tensile stress that is an action directly opposed to compression. Common tensile and compression stresses (axial forces) operate along the axis of a body part without altering it. A force directed against a structure at an angle to its axis permitting one part to slide over the other produces a shearing stress. Both parts may be movable with the parts sliding in opposite directions or one part fixed. A spinal curvature in any direction involves a constant state of abnormal tension and compression of bones, cartilage, and muscles. Spinal bending involves the dual actions of tension, compression, and torsion.
Stress is greatest on the short arm of first-class levers (eg, elbow, knee). Understanding the biomechanical principles involved helps us to prevent injury and restore functional integrity. While our lever-like extremities transmit forces and motion at a distance, they also favor musculoskeletal injuries by amplifying forces (usually external, occasionally internal) acting on the body’s biomechanical system.
Another clinical consideration is that an applied force greater than structural resistance will fracture a bone or dislocate a joint. For example, while it requires from about 1,500—3,000 lbs of static weight to fracture the neck of the femur, a weight of only 20 lbs dropped on it from a few feet will have the same result. In weight lifting during a dead lift of 200 lbs by a 170-lb person, a 2000-lb force is exerted on the lumbosacral disc. If a deep-squat lift is done exactly as defined in competitive weight lifting, severe stress on inappropriate tissues is inevitable. Thus, the athlete whose goal is solely to strengthen his leg extensors by lifting weights should seek one of the many alternatives to the deep-squat position (eg, partial squat, leg-press machine, Klein bench).
Newton’s basic laws of mechanical physics are the foundation of logical raining. Despite what degree of force is induced on a part, there is always a counteracting stress because for every action there must be a reaction. A downward pressure will be equal an opposing upward thrust. A force pulling right will be equal to a pull toward the left, expressed in terms of centripetal and centrifugal force. A twisting force in one direction must be followed by an equal twisting force in the opposite direction. A force allowing a part to slide downward must be resisted by an adequate upward force. And a force tending to bend a structure along its axis must be resisted by a force equal to prevent such bending.
The various body motions are not the sole result of muscular action alone; they are also the effect of the structure, balance, and position of the various bones forming the joints acted upon. This cooperative action of muscles and bones is the result of leverage, and levers operate according to mechanical laws.
What is the limit of human physical potential? Each year we see athletic performance draw closer to the structural limits of human capacity. Toward the goal of ideal fitness, Pollock/Wilmore emphasize that attention must be given to maintaining optimal function of the musculoskeletal system. “Prevention of poor posture, lower back complaints, fat-free tissue loss, and osteoporosis depends on the incorporation of a comprehensive strength and flexibility training program into the daily workout.” The reader will see the obvious parallelism between the conclusions of these scientists and the chiropractic approach.
Implications of Closed-Packed Joint Positions
Alternating compression and distraction within a joint has a distinct influence on articular surface nutrition and lubrication. These alternating motions also comprise the basis of proprioceptive neuromuscular facilitation techniques.
Some joint movements are accompanied by compression, others by distraction, and others by compression and distraction depending on 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 approximation (compression) such as when moving toward the closed-packed position or separation (distraction) when moving away from the closed-packed position.
The closed-packed positions for many joints are shown in Table 1.23. The clinician’s knowledge of the closed-packed position of each joint should include what movements involve compression and which involve distraction. This should be determined because most subluxations, dislocations, and fractures occur when a joint is in the closed-packed position. Most sprains, however, 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 intra-articular structures.
Most long-bone joints are in the ovoid class in which the cross-sectional surface curves to make a smoothly changing radius. As an opposing articular surface moves along an ovoid surface, the apposing surfaces do not closely fit (impure swing) except at one particular point, which every joint has, where congruency is relatively close. This is the closed-packed position. It is at this point that movement normally halts.
An impure swing during joint motion requires conjugate rotation. This type of rotation produces a twisting action on 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 on 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 enough, either a joint must dislocate or a bone must fracture.
Pain Produced by Faulty Biomechanics>
Owing to the constancy involved, postural and mechanical faults may exhibit severe pain from what appears to be mild postural defects and exhibit little or no pain in obvious cases of severe postural deficit. Minor postural deficits are often associated with considerable joint stiffness, and a very faulty posture may be seen in a very flexible subject whose body positions change readily. It is also observed that cumulative effects of constant or repeated small stresses over a long duration can give rise to the same difficulties as severe sudden stress.
No clear picture can be drawn of pain associated with postural faults. In some cases only acute symptoms may appear; some cases have an acute onset that progresses into chronic symptoms. Some cases exhibit chronic symptoms that exhibit acute phases, and others remain in a chronic condition. Regardless of the clinical picture, it must be kept in mind that no matter where the stimulus may arise, the sensation of pain is conducted only by those nerve fibers affected by the mechanical or chemical factors involved.
Two important factors must be considered in problems of faulty body mechanics —structural tension and nerve pressure or irritation:
Pain may be slight or excruciating depending on the severity of tension within structures containing nerve endings sensitive to stress such as found in overstretching muscles, tendons, ligaments, or capsules, especially those of and adjacent to joints. Piriformis, gluteus muscle attachments to the iliac crests, tensor fascia lata, and the lumbago syndromes are examples of nerve irritation associated with abnormal muscle, fascia, and tendon tautness and stress.
Pain may also result from nerve pressure or irritation, or pressure on nerve roots, trunks, branches, or endings from some adjacent structure such as bone, cartilage, fascia, scar tissue, taut muscles, or swelling from congestion, edema, or a mass. Examples of nerve root pressure pain are osseous encroachments of a subluxation or tunnel syndrome, facet syndrome, enlarged capsular ligament, or protruded intervertebral disc. In a root lesion, pain radiates to the periphery, is usually deep seated, and is directly related to muscle tension enhanced by any movement that would cause stretch or contraction of the involved muscle(s).
Isolating the lesion site is often aided by noting the distribution of pain along the course of the involved nerve and the areas of cutaneous sensory disturbance. The pain may be localized below the site of involvement or it may be widespread as a result of referred or reflex pain. Excessive motor fiber stimulation results in pathologic, involuntary, and painful muscle spasm. This may be the result of toxic irritation of the anterior horn cells; encroachment irritation of the nerve root; irritation, stretching, or pressure on a nerve trunk or plexus; irritation or pressure on peripheral nerve branches; muscle spasm secondary to trauma of an adjacent structure; primary muscle spasm from direct irritation or trauma; or psychogenic muscle spasm.
PERTINENT PHYSIOLOGIC REACTIONS TO CHRONIC POSTURAL FAULTS
An injured person rarely resembles the textbook stereotype. No two people react in an identical manner to actual or potential loss of body balance. All vary somewhat in the accommodation process according to one’s structural and functional needs, the momentary potential for redistributing body mass, and the visual efficiency necessary to guide correct adjustments. Isolated muscle weakness should be suspected especially in situations of head or pelvic tilt, trunk imbalance, scoliosis, and uneven gait or limp.
Tolerance. Poor weight-bearing because of disease, noxious reflexes, or just habit results in constant structural malalignment allowing a disproportionate amount of weight and muscle pull to be carried by some parts and not others. This alters the normal locomotion apparatus and functions of the internal organs as well. While these changes may develop insidiously, the resulting static abnormalities progress to pathologic changes in the body during standing, sitting, lying, and motion. They have a distinct effect on physical performance. They are tolerated for a short time, but sooner or later, serious, often subtle, maladjustments result when the body’s resources for compensation become exhausted. These factors total to predispose an individual to injury or hinder performance.
Endurance. An important factor in health care is that, with good postural body mechanics, balance is maintained with the least amount of muscular effort, thus encouraging longer endurance, with less strain on any one part. Locomotion can be made without wasted time or energy. Muscle pull in sustaining an erect carriage is more direct, thus avoiding strain. A natural balance is maintained between the iliopsoas group and the hip extensors, and a similar condition exists at the knee and ankle joints.
Effort. Energy requirements vary considerably with different postures. The rigid “military” posture requires about 20% more energy than the relaxed standing posture. In the rigid posture, blood pressure rises because of the muscle effort required. A completely relaxed standing position requires little more energy than that required for the sitting position.
Regional Effects. Postural faults can lead to a number of regional disorders. For example, a round-shouldered posture alters the glenohumeral articulating mechanism by depressing the overhanging acromion in front and rotating the dependent arm internally. Both of these conditions encourage cuff entrapment and attrition. Exaggerated cervical or lumbar lordosis decreases the size of the intervertebral foramina, frequently resulting in chronic radiculitis and degenerative changes. An exaggerated thoracic kyphosis decreases rib excursion and alters the functional motion of the shoulder girdle. These and many other postural disorders will be described further in subsequent chapters.
In spinal imbalance, there always appears to be some degree of intervertebral foramina insult present. Neuralgic pains in the thorax and legs are common. Less common, because it mimics visceral disease, is intercostal neuralgia. If originating in the cervical region and associated with hypertrophic changes, pain is often referred about the shoulders and down the arms, frequently being mistaken for angina pectoris. Similar neuralgic pains in the chest walls can be mistaken for pleurisy, pleural adhesions, or pulmonary lesions. Auscultation will serve in the differentiation.
A muscle in spasm or under strain from any cause (or an overstressed tendon or ligament) will become congested. This congestion always results in some degree of transudation and the conversion of fibrinogen into fibrin, which acts as a cobweb-like adhesion or interfascicular gluing that impedes fascial glide. As a result in muscles, tendons, and ligaments under strain, painful interfascicular constrictions occur, leading to the common algias associated with these structures.
Trigger Point Development
When vascularized tissue is subject to strain, changes take place with an invasion process resulting in possible fibrosis and calcific tendinitis or syndesmitis. Events occur in the myofascial planes at a point of major tensile stress leading to the development of “trigger points” and the resulting delta or spread effect. Muscles have their fascial encasements (epimesium, perimesium, endomesium); and, because muscles lie and move on others, the myofascial planes are described. The amount of fasciculi involved in the all-or-none contraction effort determines muscle tone and strength of muscle contraction. Furthermore, a muscle usually does more work at one point of its composite than at another.
Circulatory disturbances are rarely absent in gross postural faults. A low diaphragm results in venous congestion in its failure to assist blood returning to the heart. Sagging viscera stretch mesenteric vessels and narrow their lumina. Thus, circulatory symptoms may manifest throughout the body. For instance, medical researchers have recorded the relief of eyestrain and mild myopia in children by postural correction alone. They explain this as a relief of venous congestion in the head. In extreme cases, impaired circulatory inefficiency may be sufficient to produce a marked fall in blood pressure and loss of consciousness. This is said to be the result of general muscle relaxation with pooling of blood in the venous reservoirs, especially in the abdomen, thus reducing the practical blood volume. More often it causes only dyspnea and weakness, sometimes accompanied by palpitation. Precordial pain resembling angina pectoris is sometimes associated.
Faulty postural mechanics may cause the liver to rotate anteriorly and to the right. Traction is thereby exerted on the common duct and in some cases seriously interferes with biliary drainage. Ptosis of the kidneys, especially the left kidney, results in traction on the renal veins that may obstruct venous outflow to the point of causing passive congestion and albuminuria.
SPECIAL CONSIDERATIONS IN FEMALE ATHLETICS
Girls and women are now taking an increasing role in sports as various taboos and culturally imposed restrictions give way. While women have long been active in such sports as tennis and golf, they have recently increased their participation in such violent activities as wrestling, boxing, football, and demolition derbies.
To ensure optimal endurance and performance, adequate iron is necessary in he diet to carry oxygen to the cells. Iron deficiency is the most common nutritional fault in American females. A female loses from 5 to 45 mg of iron per day during menstruation. Thus, most female athletes require diet supplements and frequent monitoring of blood-iron content.
Relatively few studies dealing specifically with women in the training environment have been done. Gender differences in heart size, muscle mass, relative hemoglobin content of blood, oxygen consumption, anthropometric measurements, and body composition have been noted. Pollock/Wilmore list some studies that conclude that the performance of postpuberty female runners is similar to that of males when males ran with trunk weights equal to the percent fat of weight-matched women. We must keep in mind that the essential fat of the female cannot be eliminated by diet or training; thus, it becomes a biologic justification for separate standards and expectations.
Growth, Development, and Function
The capacity for physical activity during childhood is equal for both sexes. Strength, cardiovascular endurance, and motor skills exhibit few differences between the sexes to the age of 12 years. After adolescence, however, males develop faster physically, which allows for greater power and potential, but the capacity to develop motor skills remains about equal. Contrary to common opinion, women have achieved much greater muscle strength without an appreciable change in muscle bulk. Weight-lifting, with proper technique, will not necessarily cause undue hypertrophy.
The ratio of lean body mass to fat is one of the most obvious physical differences. Males typically have greater bone strength and density, greater muscle bulk and broadness in the shoulder area, and greater subcutaneous fat in the upper half of the body. At maturity, females are generally shorter in height, have more flexibility in their joints, have more delicate ligaments and tendons, have more subcutaneous fat in the hips and lower body regions, have less erythrocyte and hemoglobin mass, and exhibit a greater degree of pelvic tilt and obliquity. The female elbow offers a greater carrying angle and tendency toward cubitus valgus, and the female has smaller lungs, heart, liver, and kidneys than the male. Schroeder reports that female joints are more subject to injury in sports requiring an expulsive effort, sudden stopping, sudden checking of speed and turns, and landing in jumps.
Laubach compared basic strength abilities of men and women and reported that (1) lower extremity strength measurements in females range 57%—86% of males, averaging 71.9%; (2) upper extremity strength measurements in females range 35%—79% of that of males, averaging 55.8%; and (3) trunk strength measurements for females range from 37%—70% of males, averaging 63.8%). Pollock/Wilmore report that females average only 36.9% of bench-press strength and 73.4% of leg-press strength of that of males. But when expressed relative to fat-free body weight by removing the influence of body fat, females have only 53.4% of bench-press strength but 106.0% of leg-press strength of males. Such statistics are of general interest but are of minor concern clinically where we are dealing with unique individuals who are determined not to be “average.”
Female skin is more delicate than that of the male. Many dermatologic problems can be prevented if conditioning and participation progresses slowly enough to allow the skin to accommodate to the acquired demands of excessive exposure to perspiration, dirt, and bumps. During menstruation, large and bulky external sanitary napkins may irritate inner thighs during prolonged vigorous competition to the extent that a severe dermatitis develops.
Hair and fingernails also present special consideration. In many sports, hair must be either cut short or pulled out of the way of vision through tight braiding pulled into buns or ponytails. This traction, however, has occasionally caused some degree of hair loss and balding. Traumatized fingernails may result in nail breaking and splitting leading to secondary infection.
Temperature patterns occur in the menstruating female reflecting the effects of ovulation. There is a fall in morning temperature just before menstruation that continues at this level until the midpoint between adjacent periods. In about 24—36 hours before ovulation, the morning temperature rises and stays at a somewhat higher level until just before the next menses.
Strenuous Activity During Menstruation
With exception of an athlete experiencing unusual discomfort or excessive flow, there is no physiologic reason why training or competition should be avoided during menstruation. Most Olympic sportswomen do not interrupt training during menstruation, although the type of training and the intensity of training may be modified. About one out of four women sometimes interrupt training, and only one out of 20 does not train during menstruation. Although the majority of females prefer tampon protection during some phase of menstrual bleeding, the controversy about “toxic shock syndrome” deserves caution and suggests frequent changes. Caution must also be given with diaphragms continually worn and to intrauterine devices that might complicate an abdominal blow.
The female athlete usually exhibits less colic, less premenstrual headaches and tension, and greater regularity than the nonathlete. Physical exercise appears to be a distinct aid in the treatment of dysmenorrhea. Neither the menarche nor conditions for future pregnancy are disturbed by active participation in sports, and no detrimental long-range gynecologic effects from vigorous physical activity have been determined. However, according to Corwin, many female athletes report disruption or even cessation of their periods during intensive training. This is related to lowering the percentage of body fat, which has a direct effect on hormonal levels and the menstrual cycle.
There is no doubt that the influence of menstruation on athletic performance is a highly individualized effect. The female athlete who is distinctly disadvantaged by the physiologic function of menstruation can have her menstrual cycle medically adjusted so that competition will occur at the optimum time of her cycle, but this is not usually advisable. Eagles cautions against the numerous, and often serious, side effects from hormone therapy such as the potential for emboli formation following small foot fractures and the visual changes some females experience while on this type of medication. Headaches and fluid retention are other common complaints detected from cycle alteration.
The Breasts and Genital Organs
A metal breast protector is necessary in contact sports and in some noncontact sports such as volleyball to prevent contusions and pain. Breast injury may lead to a localized hematoma producing a region of fat necrosis characterized by a firm and painless lump that develops several weeks or months after the accident. This is unlikely differentiated from breast cancer except by biopsy.
Haycock et al have shown that lack of an adequate supportive bra can cause discomfort as well as injury to the breast when walking and running. Their controlled-study data suggest that women without proper breast support experience trauma to the breasts and supporting ligaments, especially when the breasts are large or pendulous. Thus, the need for a properly engineered athletic bra is obvious. A sports bra should cover the breasts, prevent slapping or lateral shifting during activity, and offer enough support, without undue restriction or abrasiveness, that there are no signs of ache or tenderness after activity. Metal parts, seams, and allergenic effects may present problems.
The activity itself and the size of the breasts, along with the tone of the supporting muscles and ligaments, determines whether a special athletic bra, a regular bra, or no bra is adequate. In modern dance or swimming for instance, the no-bra situation may occur when the participants are small breasted because the stretch material in leotards and swim suits (plus water support) provides adequate support.
The most common direct genital injuries of women are those involving vulva lacerations and hematomas (eg, in vaults, hurdles). Forceful douching occurs in inexperienced water skiers, which can result in serious gynecologic problems. Prevention can be had by wearing rubber pants.
Temperature Responses in Sportswomen
Because a woman has fewer functional sweat glands, body temperature in the female rises 2 or 3 degrees higher than that of the male before the cooling process of perspiration becomes significant. Thus, acute heat stress is a greater concern of female athletes. However, studies show that during prolonged activity in normal or hot weather women have less change in body temperature as compared to the male. While males sweat more, females cool quicker after physical activity in hot weather. Women appear to adjust their perspiration rate more efficiently to the required loss of heat. This suggests that females present more efficiency in body temperature regulation and have a greater cardiovascular component of thermoregulation.
Except with a poor obstetric history, there is no evidence that a normal pregnancy will be threatened by cautious exercise. Of all athletics, swimming appears to be the best physical activity for the expectant mother. On the other hand, there is evidence that physical fitness regimens during pregnancy contributes to ease of labor and postpartum light exercise assists the process of involution. Following delivery, intense competition is usually contraindicated for several months, especially if the mother is breast feeding.
Corwin advises that pregnant women should avoid increasing body temperature especially during the 1st and 2nd trimesters. Prolonged training in environments of high humidity and heat (along with the practice of using hot tubs, saunas, and Jacuzzi baths) can be responsible for raising body temperature for longer than 10 minutes. This can cause irreversible neurologic damage to the fetus. The personnel of spas and health clubs involved with the pregnant women should be aware of this.
A BASIC CLINICAL TEMPLATE
Injuries can be classified into 13 types: abrasions, contusions, strains, ruptures, sprains, subluxations, dislocations, fractures, incisions, lacerations, penetrations, perforations, and punctures. This manual will not detail the management of burns or injuries requiring referral for operative correction, suturing, or restricted chemotherapy.
Except for the most minor injuries, traumatized neuromusculoskeletal tissues are benefited by alert restorative rehabilitation procedures. The more serious the injury, the more prolonged is and the greater the need for professionally guided rehabilitation. The first step in rehabilitation is to explain to the patient that rehabilitation is just as important as the initial care of the injury.
The goal is not only to restore the injured part to normal activity or as near normal as possible in the shortest possible time but also to prevent posttraumatic deterioration. It is an individualized process that requires patient dedication. The author recognizes that it is easier to write about comprehensive planning than to motivate some patients to follow prescriptions after pain has subsided.
Most authorities would agree with Harrelson when he lists the goals of rehabilitation as:
(1) decreased pain;
(2) decreased inflammatory response to trauma;
(3) return of full pain-free active joint ROM;
(4) decreased effusion;
(5) return of muscle strength, power, and endurance; and
(6) regain of full asymptomatic functional activities at the preinjury level (or better).
One should keep in mind, however, that the goal of decreasing the inflammatory and effusion response does not mean to eliminate it. These responses are necessary to spur natural repair and regeneration processes. Unfortunately, these natural responses are often manifested to a greater degree than need. Thus, control of the mechanisms, not their obliteration, is the clinical directive. Healing is also influenced by the age, health, psychic, and nutritional status of the victim.
The protocols of clinical chiropractic are based on logic in harmony with nature. For example, we know that a small skin cut which normally heals in a few days takes months to heal in a completely sterile environment (eg, within a sterile bubble). This suggests that common airborne particles, bacteria, air currents, etc, act as stimulants to the healing process. It does not mean that secondary infection should be invited.
Basic Effects of Trauma
No injury is static: it continues to produce harmful effects on the injured person until either the injury or the person is defeated. As these effects are similar, the response to injury is also both systemic and local. It is for this reason that injuries and their effects must be evaluated from the standpoint that the whole person is injured and not from the view that an otherwise well-off person is afflicted with a local disability or that only a part of the total system is affected.
Since the effects of injury and the body’s efforts to defeat them are constantly changing, the doctor cannot rely on one observation or one outstanding symptom in evaluating the condition of the patient, especially one seriously injured. Repeated observations must be made and indications of the patient’s circulatory condition, neural expression, temperature, blood pressure, pulse, respiration, color, strength, vitality, and emotional status must all be considered to obtain as clear a picture as possible of the patient’s holistic condition and what treatment may be required at the moment the particular observation is made.
Managing Patient Discomfort
The triune of pain, tenderness, and local swelling is the doctor’s primary index for evaluating the progress of recovery. An anesthetized joint will never reveal that overstress was suffered. Without the warning signal of pain, the physician has no guideline for controlling the rehabilitative program. Thus, a compromise must be made between patient comfort and rehabilitation control.
Though extensive and prolonged immobilization assures a less painful recovery in most instances, it always carries with it related fibrosis and atrophy. On the other hand, quickly but logically initiated and gradual rehabilitation speeds the reduction of swelling and tenderness, and minimizes fibrosis and atrophy.
Enforced inactivity following major surgery leaves an indurated scar of thick fibrous tissue that remains tight and uncomfortable for a long time after surgery. Likewise, major joint and skeletal injury inevitably result in overabundant scar tissue from necessary immobilization. Even minor disorders treated with long-term immobilization develop large scar masses which permanently restrict function. On the other hand, uncomplicated surgery, wounds, and sprains followed by ambulation in a few days result in a cicatrix that is not tight, but rather soft and pliable.
Until recent years, the standard treatment for a sprained ankle was 3 days in a plaster boot, followed by 3—4 days of radiant heat and whirlpool baths, and then crutches for another week, all totaling about 2 weeks of therapy. The result was an individual exhibiting a distinct limp for 2—4 weeks and an indurated leather-like ankle where motion was restricted in all normal arcs. It was not uncommon to take several months before the ankle was considered functionally normal. Today the procedure and results are much different. For instance, several years ago the Athletic Department of Yale University found that the same type of injury put on a regimen of straps and cold packs for 1 or 2 days, supported walking the 2nd day, and jogging to tolerance the 4th day will exhibit a normal-looking ankle on the 5th or 6th day with subsiding tenderness (localized only) and no evidence of edema. With external support, the athlete is able to return to competition. It would appear to be a worthy objective within and without athletics, if not mandatory, to carefully control rehabilitation toward full return of function with minimal scar tissue and thus minimal fixation (motion restriction).
Work vs Athletic Injuries
Work injuries are similar to athletic injuries with the exceptions related to the usually better conditioned athlete. Work injuries frequently comprise prolonged microtrauma; athletic injuries frequently involve recurrence of sharp acute trauma. Injuries suffered at work or during competition vary from minor to severe. A severe knee injury from a harsh clip in football may be more or less severe than that suffered from a worker falling from a platform or struck by a moving machine. The care of the athlete can be complicated by parents, coaches, the press, game schedules, and player motivation. The care of the worker can be complicated by employers, union representatives, workers’ compensation conventions, attorneys, and worker motivation.
TEMPLATE OF CLINICAL MANAGEMENT ELECTIVES
Each of the following chapters includes a clinical template. Clinical templates form the customary basis of case management in each of the healing arts. Such templates are deduced from established general protocols. They should be regarded as a pattern for thought or an area mapped for consideration. They should never be used as a recipe book offering “this for that” solutions. They are not unyielding instructions or parameters having strict boundaries. Rather, they should be viewed as general directives that invariably have exceptions and invite modifications to meet the needs of the specific patient and unique conditions at hand. A doctor is judged by his or her clinical judgment, not on the use of a particular template, protocol, or philosophy. The phrase clinical protocol, as used in this manual, refers to a standard, an orderly set of procedures, or a generally accepted assemblage of efficient clinical rules.
Neither templates nor protocols should be used to encircle thought or chain rational creativity. They invite a certain course of action but do not demand that a specific path be taken. They may outline customary procedures, but they should not deny the possibility of inventive necessity. It is likely that 200 years from now, physicians will look back at the clinical practices of today with the same wonder as we look back at the accepted protocols of bleeding, induced vomiting, and avoidance of bathing that were considered ideal standards of practice 2 centuries ago.
With the above caveats in mind, the reader will find consideration of the following guidelines highly rewarding in the rehabilitative therapy.
The Physiology of Connective Tissue Healing
The first response to trauma is a local reflex vasoconstriction that decreases blood flow and oxygen supply to the area. Area cells are disrupted by the injury or die of the hypoxia. Cell death or degeneration releases potent enzymes inducing vascular changes. Notably, histamine release increases capillary permeability allowing the escape of plasma and blood proteins and cells into interstitial spaces. The quantity of colloids increases concurrently in the surrounding tissues, thus reversing their normal effect by pulling more fluid into interstitial spaces rather than back into the capillaries. These processes are recognized as early posttraumatic swelling.
Second-phase reaction initiates the repair process, which is simply explained by Knight and Hettinga. It is explained that during the initial vasoconstriction the reduced blood flow allows white blood cells to migrate to the margin of area vessels and adhere to their walls, eventually migrating into interstitial spaces. Once there, the white cells begin to remove foreign matter (extrogenous particles and debris from dead cells) by phagocytosis. The first white cells at the scene are neutrophils that have a hunger for bacteria. Macrophages then arrive and phagocytize neutrophil carcasses, cellular debris, fibrin, red cells, and other wreckage that may impair the healing process. Unfortunately, destroyed neutrophils release proteolytic enzymes into the inflammatory fluid of the area. These enzymes hasten hydrolysis of proteins into simpler substances and readily attack joint tissue. Thus, although this is the natural response of ridding the body of foreign and toxic substances, a lengthened continuation of this response can severely damage joint structures.
Once bleeding stops, some degree of hematoma is formed and resolution begins to organize thrombi to form richly vasculated granulation tissue. Nature’s goal is now one of cleanup (by macrophages) and repair, often occurring simultaneously. For repair to take place, enough of the hematoma must be removed to allow ingrowth of new tissue. Thus, the size of the hematoma or amount of exudate is directly related to total healing time. If the hematoma can be minimized, healing begins earlier to reduce total healing time.
Joint components react uniquely to trauma. Injured synovium stimulates the proliferation of surface cells, an increase in vacularity, and gradual subsynovial fibrosis. Prolonged mechanical irritation produces chronic synovial inflammation characterized by a reversal of normal synovial cell ratios. Fibrocartilage lesions are also accompanied by increased synovial effusion. As the synovial membranes changes, so does the content of synovial fluid —decreased viscosity, decreased concentration of hyaluronic acid, fibrin infiltration, and possibly hemarthrosis. In synovitis, synovial cells are destroyed. White blood cells ingest cellular debris, lysomes, and proteolytic enzymes, and then die in the transudate. This, in turn, releases the proteolytic enzymes and produces a vicious inflammatory cycle perpetuating the synovitis and establishing a sequel of progressing sclerotic changes.
Articular cartilage is especially susceptible to enzymatic degradation. Proteoglycan is a protein aggregate that helps to establish the resiliency and resistance to biomechanical deformation of articular cartilage. When the proteoglycan content of articular cartilage diminishes, Sledge reports that collagen fibers become highly susceptible to mechanical damage; the cartilage softens, fissures, and erodes; denuded bone is exposed; and osteoarthritis and/or degenerative joint disease is instituted. When the matrix fails because of the release of noxious enzymes, degradation by-products and proteoglycan are carried in synovial fluid to the synovial membrane to establish a reactive synovitis encouraged by prolonged effusion that also injures the joint capsule and properties of articular cartilage. Again, a vicious cycle can be established.
Management Protocols Following Trauma
The optimal procedure is to anticipate each step in the healing process and provide the opportunity for natural processes to express themselves offering aid only when necessary. This is not to say that if a variation in the process is seen at one of the normal stages of healing that treatment should not be enhanced accordingly. For example, increased local swelling and tenderness during a late stage strongly suggest an infectious process.
1. Stage of Acute Inflammation and Active Congestion
This is the stage of fresh tissue damage and reaction occurring immediately after strains, ruptures, sprains, and burns. Early cryotherapy is usually applied in the form of cold packs, vapocoolant sprays, ice massage, or cold immersions for the vasoconstrictive effect in controlling swelling, hematoma size, and pain. The prudent use of galvanism also has a vasoconstrictive effect. Nontraumatic mobilization, cryotherapy, and vasopneumatic compression can do much in reducing excessive effusion.
The goal is to control the natural healing process, not to inhibit it. Any form of induced stimulation during the early portion of this stage should be avoided. The injury itself is all the local stimulation necessary for a maximum response. More harm can be done by overtreating at this early stage than doing nothing.
Scratches and small skin tears associated with abrasions, scrapes, contusions, and similar bruises should be douched with tepid distilled water to flush foreign matter, sprayed or doused with a general disinfectant such as isopropyl alcohol, and covered with a sterile pad or gauze for protection and to discourage secondary infection. If edema or bleeding is determined or imminent, cold, rest, elevation, and a compression bandage should be applied. Remote meridian or another type of reflex therapy may be beneficial in controlling pain, swelling, and shock.
Generally, the injured part should initially be protected and rested to prevent further injury or irritation by use of a compress, bedrest, a sling, crutches, a cane, a foam or padded appliance, shoelift, or another form of support should be considered to safeguard the healing processes. If motion of the injured part should be restricted, it may be temporarily immobilized by a pressure bandage, strap, rigid appliance, brace, or cast.
The major goals soon after injury are to control pain and reduce swelling by vasoconstriction, compression, and elevation; to prevent further irritation, inflammation, and secondary infection by disinfection, protection, and rest; and to enhance healing mechanisms. Thus, common electives at this stage include:
Disinfection of open skin (eg, scratches, abrasions, etc)
Indirect therapy (reflex therapy)
Iontophoresis or phonophoresis
Mild pulsed ultrasound
Pulsed alternating currect (3—5 Hz)
Rest and Support
Following an acute musculoskeletal injury, especially during the first 24—48 hours, it may be necessary to treat the patient once or several times each day until the acute pain subsides. In some patients with severe articular injuries, mild multiple treatments and concentrated attention combined with bed rest is often the regimen of choice.
By virtue of the increased vascularity in an athlete’s well-conditioned musculature enhanced during exercise, interstitial hemorrhage following tear, sprain, or fracture tends to be profuse. While rest, ice, compression, and elevation (RICE) are standards in the treatment of acute injury of any individual, this factor of increased vascularity in an athlete underscores the need for the immediate application of RICE.
2. Stage of Passive Congestion
This stage develops the framework for natural reparative mechanisms to establish a network of fibrin and fibroblasts that begins the reparative process. Like the first stage of healing, it is characterized by swelling and local tenderness. Local heat and redness are often prominent, and the tenderness is more diffuse.
After 24—48 hours, pulsed ultrasound or cryokinetics (initially with passive exercise) is often indicated for its effect on mobilizing tissue and tissue fluid, on membrane permeability, and on dispersing accumulations of fluid and metabolic by-products and posttrauma cellular debris. Ultrasound helps to increase gaseous exchange in local tissues, disperse fluids, liquefy gels, softens tissues, increase membrane permeability, and provide mild heat and massage at the cellular level. Articular fixations in the area of involvement can be treated reflexively at this time.
To reduce stubborn stasis late in this stage by enhancing venous and lymphatic drainage, alternating applications of mild superficial heat and cold, light nonpercussion vibrotherapy, cryokinetics (passive exercise initially) and/or surging alternating current are generally beneficial at this stage. These procedures also tend to free coagulates, disperse accumulations, discourage adhesion formation, and enhance the tone of local nerves, muscles, and vessels.
The major goals in this second stage are to control residual pain and swelling, provide rest and protection, prevent stasis, disperse coagulates and gels, enhance circulation and drainage, maintain muscle tone, and discourage adhesion formation. Thus, common electives include:
Indirect therapy (reflex therapy)
Alternating superficial heat and cold
Protect lesion (padding)
Light nonpercussion vibrotherapy
Passive exercise of adjacent joints
Mild surging alternating current
Mild pulsed ultrasound
Cryokinetics (passive exercise)
Once the stage of likely recurrent bleeding has passed, a gradual rehabilitation program can be initiated to encourage the inflammatory reaction of resolution to pass quickly —thus reducing subsequent fibrous thickening of tissues. This program may be accelerated once the stage of fibrous thickening, noted through inspection and palpation, is exhibited. A great deal of atrophy, muscle weakness, and fibrous induration can be eliminated by applying progressive rehabilitation as soon as possible. Naturally, timing must be coordinated with the type of injury; ie, bone injuries often require longer support and rehabilitation procedures than do less severe soft-tissue injuries. However, once bone heals, it is usually stronger; once soft-tissue heals, it is usually less pliable and prone to reinjury.
3. Stage of Consolidation and/or Formation of Fibrinous Coagulant
During this stage, the formation of tissue repair is well established. The status is characterized by fibrous deposition and a chronic inflammatory reaction featuring a distinct reduction in local redness, heat, and tenderness if the part is rested. The incidence of recurrent bleeding progressively reduces as this stage develops.
Local moist moderate heat produces mild vasodilatation, increases membrane permeability, and enhances cellular nutrition by encouraging blood flow through the area. Moderate active range-of-motion exercises, alternating traction, and sinusoidal current tend to free coagulants and early adhesions, and tone local nerves and other soft tissues. Ultrasound applied during this stage has the same effect as that explained above. Articular fixations can usually be effectively mobilized without undue pain by adjustive (manual or mechanical) technics late in this stage.
The major goals here are the same as in Stage 2 plus enhancing muscle tone and involved tissue integrity and safeguarding against factors that may interfere with natural healing processes. Thus, common electives include:
Mild articular adjustment technics
Moist superficial heat
Cryokinetics (active exercise)
Moderate active range-of-motion exercises
Mild alternating traction
Sinusoidal alternating current
Mild transverse friction massage
Mild proprioceptive neuromuscular facilitation techniques
Professional care during healing requires repeated inspection and external support: (1) Periodic and regular appraisal can usually be made simply through inspection, palpation, function studies, and patient reports. When dealing with many traumatic injuries, one becomes astute in seeing and feeling the various stages of healing. (2)-Continuous support during the resolution stage should be provided by external measures without impairing the natural healing process. The common means are through tapes, bandages, splints, foam-type braces, etc.
After the acute stage of an injury has passed, attention should be given to more microscopic considerations. In the typical soft-tissue injury, external signs disappear within 2 weeks but the tissues involved may not be ready for athletic stress or heavy manual labor. Invariably, the greater the bleeding, the more acute and diffuse the inflammatory stage, and greater induration and fibrous thickening can be anticipated if not well managed.
Treatment for musculoskeletal complaints after the acute pain has subsided need not be spaced as close together as during the acute stage. Therapy is usually administered on a daily basis, then every other day, and eventually to about once per week. If pain persists after 10—15 visits, it is advisable to completely re-examine the patient and re-evaluate the initial diagnosis, seek consultation, or refer the patient for further specialized evaluation before therapy is continued.
4. Stage of Fibroblastic Activity and Potential Fibrosis
This stage is often called the “toughening phase.” Nature responds to injury by attempting to make the part stronger, splinted, or both. The chronic inflammatory reaction and degree of tenderness subside. Palpable thickening and induration in the area of reaction can be palpated.
Physicians not well schooled in traumatology may dismiss the patient at this stage because of resolution of entering complaints. However, the disadvantageous effects of this stage are the formation of disadvantageous scar tissue, shortened soft tissues leading to contractures, muscle weakness, and reduced joint mobility likely in more than one range of motion. It is at this stage when the skill of the chiropractor can do much to prevent disability or the predisposition to reinjury.
Causes for sharp pain should be corrected by now, but some residual tenderness likely remains. The major goals are to defeat any tendency for the formation of binding adhesions, taut scar tissue, and area fibrosis and to prevent atrophy. Thus, common electives are:
Articular adjustment technics
Local vigorous vibromassage
Transverse friction massage
Active range-of-motion exercises without weight bearing
Motorized alternating traction
Sinusoidal and pulsed muscle stimulation
Proprioceptive neuromuscular facilitation techniques
5. Stage of Reconditioning
As healing becomes more complete, treatment should be directed to developing strength, tone, and length in the injured muscles, tendons, and ligaments. Therapy during this stage is frequently scheduled once (possibly twice) a week and is usually combined with a specific exercise program that is given to the patient (by demonstration/explanation and writing) to apply at home.
At this stage, the sedentary individual will believe that the injury is completely healed because pain is absent during daily activities. Joint motion appears unrestricted unless challenged. For those involved in physical labor or strenuous sports, however, the healed tissues must be reconditioned to bear the intensity of the demands required. Thus, common electives are:
Direct articular therapy for chronic fixations
Progressive remedial exercise
Isometric static resistance
Isotonic with static resistance
Isotonic with varied resistance
Clinical practice in this area shows there are some unique disabilities found in competitive athletics that are rarely, if ever, encountered in general practice. Each sport requires a different type of history taking and examination emphasis; and each age group (children, adolescents, adults) presents individual problems. Preadolescent participation in sports offers unique risks and professional challenges. Likewise, an increasing number of senior citizens maintain a degree of fitness through tennis, golf, bowling, jogging, volleyball, and other sports that are not without risk. These factors are added to the usual variances seen in general practice such as degree of maturation, body type, effects of past illnesses and surgery, congenital abnormalities, gender variances, and so forth. As a rule, athletic rehabilitation must be carried beyond the usual range considered to be full function. Last, but far from least, is the particular athlete’s motivation and career aspirations that must be carefully appraised in terms of fitness and the patient’s short-term and long-range goals.
GENERAL DIRECTION IN MANAGING THE CHRONIC MUSCULOSKELETAL INJURY
Many chronic joint disorders seen in a chiropractic office present with two underlying periarticular muscle-ligament conditions: one or more muscle groups that are in a weakened state and a shortened and spastic condition of their antagonists. It is presumed that this functional imbalance, which leads to both physiologic and biomechanical overstress, is the primary cause of most articular disorders. Thus, adjunctive therapy in articular disorders should be directed to the involved joint(s) to correct this imbalance by strengthening certain muscles and ligaments, and stretching others. If not, the effects of therapy are likely to be effective only short term and recurrence of the problem (either locally or somewhere else in the kinematic chain) can usually be expected. If this hypothesis is often true, then the clinician can expect to find weak extensors associated with shortened and tight flexors, or vice versa, and weak abductors often associated with short-tight adductors, and vice versa.
These syndromes are common in many low-back pain cases where we find weakened abdominals associated with short-spastic deep lumbosacral extensors. While light palpation may indicate normal tone of the superficial erectors, deep palpation will invariably reveal hard-inflexible tissues. Observation from the side will often reveal in a sedentary patient a pot-bellied individual, an extremely sharp lumbosacral angle (due to an anteriorly rotated pelvis), and a relatively flattened lumbar and thoracic spine above. This picture does not fit the overconcern in most textbooks with lumbar hyperlordosis and thoracic hyperkyphosis. An imbalance syndrome in the extremities such as in the shoulder, elbow, wrist, knee, and ankle is much more subtle. Yet, careful examination will demonstrate its presence. For example, it is rare to find a meniscus disorder of the knee not associated with a weak quadriceps (especially a vastus medialis) and short-tight hamstrings. Likewise, it is rare to find a case of shin splints not associated with weak anterior muscles and taut calf muscles.
PRIMARY OBJECTIVES OF CASE MANAGEMENT
A large percentage of traumatic joint injuries can be avoided with proper conditioning, training, and practice. After injury, the following three points are the general aims of good case management.
Reduce and Absorb Swelling. Early cold, compression, elevation, and rest will do much to avoid the hazards of excessive swelling. Heat, massage, and exercise are contraindicated in the early stages, but beneficial in the later stages. Aspiration is contraindicated unless necessary for diagnosis or relief of severe pressure. To prevent capsular stretch from chronic effusion, local compression, elevation, contrast baths, and muscle activity are beneficial after 48 hours. Normal joint movement and tendon function cannot be achieved until periarticular swelling has been absorbed
Minimize Deformity and Wasting. An attempt must be made to normalize existing deformity, mechanical obstruction, and articular irregularities so that normal joint motion and configuration can be achieved. Joint stability must be achieved by conservative measures (eg, manipulation, physiotherapy, proprioceptive neuromuscular reeducation) or surgical and postoperative rehabilitative methods. Progressively increased exercises are necessary to minimize muscle wasting which rapidly follows joint trauma. A protective reflex muscle spasm may interfere with early rehabilitation. It is best treated with cold and cryokinetics.
Normalize Joint Movements and Function. Progressively increased remedial exercises of a well-supported joint help to restore normal joint motion. Support should not restrict motion in an unaffected plane. Once the joint’s full range of normal motion is obtained painlessly, strength-developing and skill exercises can be carefully incorporated with emphasis upon rhythm to avoid tissue breakdown.
THE NEED FOR ADEQUATE CONDITIONING
To develop good physical performance and prevent injury, conditioning programs should have four major components: (1) warm-up and stretching, (2) the development of muscular strength, (3) the development of joint flexibility, and (4) the development of endurance (both somatic muscular and cardiorespiratory). Experience has shown that conditioning is one of the most important ways to prevent injuries by strengthening tissues, keeping the joints flexible, improving physiologic tone, reducing excessive weight, and reducing fatigue. A well-conditioned person will have greater endurance, strength, and stamina.
An important factor in preventing injuries is the development of an appropriate level of physical fitness. Haycock feels that “conditioning is the equivalent of physical fitness”. To be “fit” is to be equal to the demands, whether it be work or play. Yet the attending physician should keep in mind that to be physically fit for one occupation, sport, or position does not imply adequate fitness for another. In athletics, for example, certain sports require greater levels of fitness of different anatomic parts, and this must also be realized. A marathoner will traditionally have poor upper body development as compared with a discus thrower who will have superior upper-body fitness.
It should be obvious to any clinician that different patients, injuries, and working conditions require different forms of rehabilitative “work hardening.” Work hardening is a term used in industrial medicine to refer to preparing an injured worker to a level of productive physical competence to return to work. Thus, it is goal specific, job directed, and program intensive (structured timeframe). Common procedures include structural and functional profiling, psychophysical modeling, goal definition, vocational rehabilitation, and ergonomic analysis.
Conditioning in Sports
To maintain acquired conditioning in athletics, each team member and prospective member should be provided with a regimen for preseason conditioning, and each player should be required to adequately warm-up before each competition or practice. As a general rule, at least 3 weeks of progressive practice should be held before the first competition. During the off season, two or three moderate workouts a week is usually enough to prevent much deterioration.
When an athlete is physically capable of performing a sport with optimal efficiency, he or she can meet both physiologic and biomechanical demands placed upon the body. This is true not only for typical performance demands but also for critical situations. A low level of physical fitness leads to fatigue that tends to impair the conditioned reflexes involved in physical skills. However, skill alone will not protect against the effects of overexertion if activity is carried beyond the limit of one’s level of physical fitness. Conditioning enhances flexibility, agility, speed, endurance, and strength. These are safeguards having positive benefits to one’s level of general fitness and performance.
Initial Conditioning: Warm-up and Stretching
As a ground work in athletic training or before any strenuous physical labor, a progressive warm-up period is a requisite. It consists of the entire body being put through stretching or flexibility exercises, and then of specific body parts essential to the sport and position. The benefits of adequate warm-up are also important before engaging in any stressful physical activity in the workplace or during leisure recreation.
The value of calisthenics in athletics has long been debated from a physiologic standpoint, and the final answer is still not known. The weight of evidence is empirical. However, we do know that properly designed and performed exercises call into action little-used muscle groups, strengthen them reasonably, and contribute to flexibility. Repetition increases muscle tone and enhances cardiovascular efficiency.
The length of a warm-up period varies with the individual and anticipated demands. Usually, it is said to be sufficient when perspiration arises. Warm-up should never result in fatigue, but it should present a renewed sense of joint “freedom”. Careful supervision should be maintained during the warm-up to prevent the eager athlete from overdoing and then becoming discouraged, sore, or strained. Acclimatization to a change in environment or altitude, temperature changes, and humidity changes also influence an athlete’s performance. The well-trained athlete generally adapts faster than one out of condition.
CLINICAL CONSIDERATIONS IN SOFT-TISSUE REHABILITATION
Clinicians are obligated to seek answers to many questions concerning human dynamics for it is impossible to separate structure from function. This requires knowledge of how the nervous system integrates proprioceptive input and coordinates activity of the musculoskeletal system so that each unit involved contributes its function properly. Thus, a primary concern within health care in its quest to maintain physical fitness and optimal reserves is the integration of neurophysiologic and biomechanical information.
The term “remobilization” in medical literature generally refers to conditioning regimens following weeks in immobilization such as a plaster cast. Chiropractors realize, however, that a potentially active joint that is not moved through its normal ranges of motion in daily activities by sedentary people or an active joint restricted by the effects of posttrauma fibrosis presents with the same picture. In other words, “why” a joint is not moved is not pertinent clinically. The processors of deterioration do not differentiate among the reasons for insufficient use.
The chiropractic profession has pioneered the art of articular remobilization in spinal and extraspinal joints. Joint mobility allows force to be transmitted through a greater range of motion. Passive exercise and remobilization techniques stimulate all types of mechanoreceptors of a joint (refer to Table 1.14). This is necessary to ignite impulses at least at the afferent part of the normal circuit. By mimicking joint movement by a passive force, the object is to spur the “memory” of this normal path in the spinal cord governing active reflex and higher CNS actions. Without proper mechanoreceptor input, trophic efferent impulses cease and bone, muscle, tendons, articular cartilage, capsules, and ligaments degenerate.
The neurologic circuit benefits from remobilization are only part of the picture. Recent joint research has done much to prove what chiropractors have learned empirically for many decades. Harrelson gives much support that joint tissues respond favorably to mechanical stimuli and that structural modifications are noted soon after exercise. Levick shows that interarticular motion also enhances transsynovial nutrient flow. Akeson and colleagues found that fibroblasts and chondrocytes interpret physical forces to influence their rate and synthesis, and extracellular degradation of connective-tissue matrix components is similarly controlled.
Donatelli/Owens-Burkhart supply evidence that movement maintains joint lubrication and critical fiber distance within the matrix and ensures an orderly deposition of collagen fibrils. They also state that forceful manipulation that breaks intracapsular fibro-fatty adhesions may be necessary to restore a full range of motion. Zarins' studies concluded that muscle regeneration begins within 3—5 days after initiating a reconditioning program and that both slow-twitch and fast-twitch muscle fibers can recover completely. When passive mobilization is assisted by the patient to some degree to produce a contraction, the results reflect Tucker and associates findings that protein synthesis responds quickly to major changes in muscle contraction by a rapid increase in synthesis.
However, mobilization is not the complete answer for it does not stimulate the deep-pressure compression-type mechanoreceptors. Hall shows that even with mobilization, deterioration will continue (especially in articular cartilage) until weight-bearing is allowed. Although ligament strength depletes with immobilization, mobilization has no significant effect on building ligament or tendon strength. This requires endurance-type exercise. Several authorities report that it can take from 1 to 3 years for a Grade III sprain to heal to its preinjury status, depending on the extent of overstress and the history of repeated trauma.
Although the degree to which joint flexibility can be influenced by training is controversial, there is no doubt that latent potential should be developed to its optimal, but not extreme, limits in certain sports and occupations. However, mobilization should never be carried beyond its anatomical limit. While some pain may be self-justified in pursuits of endurance development, it is never justified in terms of joint flexibility.
Since forceful passive mobilizing exercises may create damage, active mobilizing exercises are preferred. Exceptions to this are proprioceptive neuromuscular facilitation techniques, which consist of warming muscle groups before stretching by applying a strong isometric effort at the initial point of full stretch as a partner offers light resistance. With this technique, described later in this chapter, the pertinent muscles appear to accept further stretch because of partner assistance and the active contraction of muscles on the opposite side of the joint. Such isometric “priming” usually shows that the joint in question can be moved to a further end-position within the range of comfort.
The Anatomical Movers
Posttraumatic muscle rehabilitation is most efficient when specifics are known, but properly analyzing the anatomical movers at the point of performance has been a difficult task until recently. Chun developed a method that, in biomechanical terms, depends on the principle that a body segment moves along the direction of the resultant of the applied separate forces. In other words, the segment must move along the direction of muscle tension, passive tissue resistances, and external forces applied on the segment such as gravity, elasticity of the equipment used, friction, muscular tension of opponents, etc. Generally, the direction of the segmental motion and the external forces is known. Thus, the direction of muscle tension can be determined, as well as the main muscles responsible for the movement.
Chun states there are usually three situations in which the determination of the principle movers of human motion are possible:
1. The direction of segmental motion would be classified as opposite to the direction of the external forces (ie, gravity, etc). This indicates that the movers are located on the same anatomical side as that of the segmental motion.
2. Slow moving segmental actions occur in the same direction as that of the external forces. Consequently, the movers will be located on the opposite side of the segmental motion.
3. Rapid segmental movements also occur in the same direction as that of the external forces. The movers now represent muscles lying on the same side of the segmental motion.
Keeping these three points in mind during the prescription of mobilizing or strengthening exercises will greatly enhance the attainment of clinical goals.
Exercise Common Sense vs Technology
Within the last 20 years, exercise and its role in physical fitness has advanced from a trade to a science. An early product of the mass of data acquired has been the development of “body-building” apparatus. In recent years, however, we learned that many assumptions have been erroneous.
This text will not emphasize the use of sophisticated exercise equipment. The first reason is that most in common use are expensive and too specific for the type injuries generally seen and for the common patient. Prolonged specificity in muscle action is not natural.
Compare outdoor bicycling with use of a stationary bicycle. The fixed apparatus is fine for exercising hips in pure flexion and extension and stimulating activity of the hamstrings and calves and to a lesser degree the quadriceps and glutei. However, the plane of action is fixed —and this is not comprehensive. In riding a mobile bicycle, one must maintain balance, swerve to miss a stone in the path, bend laterally when turning, constantly shift one’s center of gravity, etc. One often must pedal uphill, downhill, and around corners and obstacles. This requires use of more than the large muscles of the thigh and leg. It also mandates use of the oblique abductors and adductors of the hip, knee, and ankle, and almost all large and small muscles of the trunk and upper extremities to a considerable degree. This is natural exercise (alternating isotonic, isometric, and stretching) and promises greater benefit in building healthy soft-tissue tone and strength.
The second reason is that the use of apparatus is extremely boring except to the type of person who enjoys monotonous activity such as working on an assembly line or pulling the lever of a drill press all day. For most people, using an exercise machine or lifting weights is a bore. Spending a morning digging, planting, weeding, chopping, mowing, building something, or painting is fun in comparison to an hour at the “fitness center.” Watch how many people “workout” after the bell has rung! Walking a golf course, playing a friendly game of tennis, or swimming are usually welcomed activities. Taking a hike with a loved one is fun; walking a treadmill is boring for most of us. Boring activity is resented and soon discarded.
Professional athletes motivated by the promise of a million-dollar contract and stardom, of course, are exceptional. They dance, grunt, and sweat to a different drummer.
Recent studies also show that (1) exercise bouts at 60% of maximum are more beneficial than regimens at 80% of maximum, (2) whole body exercise is more beneficial to fitness and excess fat loss than exercise of a part, and (3) pulse taking to acquired a certain level is a waste of time because some people show little change regardless of effort within normal ranges.
General Rules of Exercise with Weights
Following are some general rules in prescribing and supervising therapeutic exercise that have been gleaned from several authorities.
Attire. Clothing, nonrestrictive underwear, socks, and shoes appropriate for exercise should be worn.
Conditioning. A warm-up period of brief jogging and general stretching exercises should precede each weight-moving session. A postexercise cool-down period of progressively lightened exercise is equally as important.
Posture. Ideal posture should be strived for when exercising.
Style. A load should be moved in a smooth manner from a prestretched position and briefly halted in the position of full muscle contraction. Jerking motions should be avoided.
Speed. Speed should be moderate, not too fast or too slow. Negative work should take about twice the time as positive work.
ROM. Range of motion should be as great and as varied as possible in the routine.
Loading. The load should be heavy enough to require a maximum intensity of contraction (to the point of failure) after several (8—12) repetitions.
Timing. A high-intensity session every other day is just as effective as a daily session. It also offers the benefit of interval recovery.
Sequence. Large muscles should be worked first, small muscles last.
Neuromuscular Re-Education. The rehabilitating patient should be allowed to perform as normal function as possible in daily activities without interfering with the healing process.
Proprioceptive Neuromuscular Facilitation Techniques
The techniques that fall under the heading of proprioceptive neuromuscular facilitation (PNF) techniques are special stretching maneuvers designed to enhance neuromuscular responses through proprioceptor stimulation. The goal is to reduce sensory activity through spinal reflexes to relax muscles to be stretched. Knott/Voss, Moore/Hutton, and Sullivan and associates have done much to perfect these techniques, which are based on Sherrington’s principle of reciprocal innervation; ie, relaxation of a muscle being stretched (the agonist) through voluntary concentric contraction of its antagonist, but PNF should not be applied until hypermobility (joint instability) and acute inflammation has been corrected or until fractures have healed. It is contraindicated in the presence of bone disease (eg, malignancy, advanced osteoporosis, ossified RA joint).
PNF is beneficial in cases of joint adhesions, spasms, contractures, deranged articular cartilage, taut capsules, and various end-feel abnormalities related to soft-tissue fixation (fibrosis) effects. It is an excellent method to distract impacted tissues and enhance articular lubrication.
Before PNF is performed, the patient should be in a comfortable relaxed position with the involved joint in a loose-packed position. The part should be thoroughly examined before any manipulation is attempted. Rings and other jewelry should be removed from the part to be stretched. Three common PNF techniques are the contract-relax, hold-relax, and slow-reversal hold-relax. In each of these techniques, firm stabilization must be provided, movements are made in a smooth manner, and motion is halted before pain is induced. Pain initiates a protective spasm. Whenever possible, a loose-packed joint should be maintained by applying distraction with the stabilizing hand.
Contract-Relax Technique. The body part to be stretched is passively moved into the agonist pattern to the end of the physiologic ROM. At this point, the subject isotonically contracts the involved muscles into the antagonistic pattern against the strong manual resistance of the doctor or therapist. After relaxation occurs, the body part (eg, limb) is again moved passively into as much ROM as possible. This maneuver is repeated several times and then followed by active exercise. Thus, the purpose is to increase joint ROM in an agonistic pattern by using consecutive isotonic antagonistic contractions.
Hold-Relax Technique. This procedure is similar to the contract-relax method described above but motion is not allowed on isometric contraction. This is beneficial when spasm and pain accompany restricted joint mobility. The subject is instructed to gradually increase the intensity of each successive contraction. Thus, the purpose is to initiate isometric contraction of shortened muscles against complete resistance of the doctor or therapist.
Slow-Reversal Hold-Relax Technique. In this procedure, the body part is slowly moved several times into an agonistic pattern to the point of painless block and then passively returned to the neutral position. Thus, like the hold-relax maneuver, this technique applies the reciprocal innervation principle. Following several passive stretches, isometric contraction is initiated, relaxation occurs, and then more passive stretch is applied.
Applied Oscillation. Once the basic techniques of PNF have been mastered, manual oscillations (vibration-like movements) can be added when the part is near its physiologic limit. Small-amplitude oscillation near the point of end-feel or large-amplitude oscillation well within the functional ROM (never at its limit) are extremely helpful in joints limited by pain. Small-amplitude oscillation at the end of joint-play, large-amplitude oscillation stopping at the physiologic limit, and a short high-velocity chiropractic thrust stopping at the anatomical limit are beneficial in stretching painless restrictions. The effect of oscillation is to dynamically fire mechanoreceptors to decrease muscle tension. Also, the fast-conducting fibers are stimulated to block impulses from the small pain-conducting fibers, according to the Gate Theory. Wright/Johns and Kaltenborn describe the neuromechanisms involved.
Conditioning and Posttraumatic Exercise Regimens
Terminology of Strength. Strength has many definitions. A general one states it as the maximum force that can be exerted by a muscle. In discussing strength, however, the terminology used is often confusing. The phrase isometric (equal in length) strength refers to muscle activity occurring without muscle shortening. Isotonic (equal in tone) strength means muscle activity with shortening of the muscle. Both of these general terms are misnomers in that there is a degree of length change in isometrics due to tendon stretching, and normal tone is influenced in isotonics by altered mechanical advantage and resistance.
Acquisition of Strength. Strength is acquired through training requiring repetition against increasing resistance. Thus, it is the effect of all-out effort against resistance. It is specific to a muscle or muscle group and specific to that angle at which the exercise occurs. Thus, to be strong at every angle, training must be throughout the range of joint motion. As motion requires synchronized body parts, all parts must be trained to be strong and have adequate endurance.
From a general viewpoint, new or lost strength can be acquired in three ways:
1. Isometrically by exercises done against resistance in a manner that body movement or joint angle are restricted (eg, pushing against a wall). Muscle involved maintains a fixed length, with tension generated equal to the resistance encountered. Isometric exercise sometimes offers a short cut to goals of equivalent repetitive drudgery, but it is inefficient in building strength at multiple joint angles. In the early phase of rehabilitation, it may be the only type of exercise permitted and always is preferable to no exercise at all.
2. Isokinetically by exercises of a constant velocity against resistance that adapts to the angle of a joint (eg, Orthotron or Cybex II equipment). Isokinetic exercise uses variable resistance in which the speed of motion is fixed but the resistance varies to accommodate the input force (eg, manual resistance, Cybex, Biodex equipment). These exercises are used primarily to rehabilitate to the point of normal strength, after which other forms of exercise are used. In isokinetic exercise, work is done at a set speed with resistance matching the input of force at that speed. As input changes, resistance changes to match the input but speed remains constant. A person’s muscular resistance is met with a proportional amount of resistance through full agonist and then antagonist activity.
3. Isotonically by exercises against resistance in a manner that body movements are allowed (eg, weights and weight machines, spring or friction devices). In pure isotonic exercise, muscle length changes causing or resisting a change in joint angle and resistance remains constant while velocity is inversely proportional to load. Both eccentric and concentric contractions can be achieved. Common nonequipment (unaided) exercise regimens for developing muscle strength and endurance include sit-ups, bar chinning, cross-country jogging, push-ups, spinal extensions, rope climbing, and half-knee bends. Dynamic exercise may be (a) isotonic in which fixed weight is moved through a ROM (eg, ankle weights); (b) variable resistance in which resistance varies in a fixed ration through a full ROM (eg, Nautilus, Eagle equipment).
Positive vs Negative Isotonics. Isotonic exercise can be positive or negative. In a positive (concentric) contraction, muscle tension develops, muscle length shortens, and a resistance is overcome. In a negative (eccentric) contraction, muscle tension develops, muscle length increases, and a resistance is relieved. Thus, when a weight is lifted, positive work is accomplished; when a weight is lowered, negative work is fulfilled. A common example of positive and negative exercise is in chinning a bar, which requires positive strength, and then slowly lowering the body (load), which requires negative strength.
Positive work requires twice as much oxygen (but often half the time) than that of negative work. Negative work has little effect on cardiovascular conditioning, but it has shown to be far superior in strength development. For an unknown reason, muscle soreness is more profound after a bout of negative exercise than positive exercise. This likely originated the “no pain, no gain” epithet.
Isometrics. Muller showed that one isometric contraction (slightly more for the well-trained athlete) of 40%—60% of maximum held for a few seconds each day would result in the maximum possible increase of muscle strength. From this study, while slightly modified, renewed interest in the Charles Atlas type of “dynamic tension” exercises, in addition to aerobic isotonic exercises, has become widespread within the sports world.
A distinct advantage of isometric exercise is to early prevent or retard atrophy resulting from necessary immobilization (eg, fracture, whiplash). A disadvantage of purely isometric exercises is that benefits are confined to a range of motion of only 20° to either side of the training angle at which contraction is performed.
There are many types of exercise and each has its particular goal therapeutically. See Table 1.24. Regardless of the type of exercises and regimens used, careful consideration must be made of the total situation of the particular labor or competition involved. There is always the question in athletics of how much training is enough, as overtraining can dull an otherwise sharpened performance.
This consists of stretching and moving a joint through its various ROMs by an external force. Passive exercise is unvolitional as far as the subject is concerned; ie, it manipulates local tissues without input from the high CNS centers. It is highly valuable initially in cases of paralysis or severe weakens. Because it sets up sensory bombardment to the spinal cord if the afferent neurons are intact (and hopefully to the long ascending tracts), it is helpful in attempting to re-establish an impaired neuromuscular circuit. Mechanoreceptor stimulation also appears to have an enhancing effect on connective-tissue healing, which may be related to the fact that exercise is the best preventive for osteoporosis.
Passive exercise may be applied manually or mechanically, and theoretically the affect should be the same. Nevertheless, there is much we can only speculate about the benefits and mechanisms of “therapeutic touch” from human to human. Two types of passive exercise can be used, unforced or forced, depending n the circumstances and goal involved. Harrelson and scores of others recommend painless unforced exercise to maintain joint mobility. Forced, possibly uncomfortable, passive exercise is used to nudge motion beyond the range of abnormally restricted motion.
Muscle Training by Resistance Exercise Equipment
A goal in weight training for physical conditioning or rehabilitation is to work the muscle at maximum efficiency throughout the joint's range of movement. This goal, reported Ariel and associates, necessitates proper assignment of force, displacement, velocity, and when desired, time, acceleration, and the amount of work and power. To do this, it is necessary to assess the individual’s biomechanical changes and then to develop a resistance and velocity intensity that will accommodate those changes in a functional manner. This means that the variations in resistance intensity and velocity must be precisely and wisely incorporated into a resistive mechanism. It is also essential that the operation of such a mechanism is not adversely affected by improper machine design.
The benefits of exercise machines have not met their publicity. A principle of biomechanics states that inertial forces affect the motion and magnitude of the muscle movement. The smaller the inertial forces produced by the exercise machine’s moving parts, the greater the muscular involvement. Most all gravity-dependent exercise machines are subject to inertial forces and apply resistance in one direction only. Thus, only the agonist muscle group is exercised and the training is not automatically followed by a correspondingly balanced antagonist muscle activity.
Exercise equipment using springs, torsion bars, etc, is able to overcome the inertia problem to some extent and can partially overcome the unidirectional force restriction. However, the problems of safety, nonlinear resistance, and the nonadaptability of the machine to an individual’s force characteristics are still serious drawbacks. For this reason, most authorities consider them unacceptable.
One type of machine in common use operates on a constant velocity principle where the resistance is changed in direct relationship to the forces acting on the moving bar. This equipment, however, operates on an open loop mechanism that does not allow feedback control of the exercise while it is in progress and the velocities cannot be changed in a manner that simulates ballistic human motion. Hydraulic mechanisms can overcome the inertial problem as well as the unidirectional problem. However, applications of such a mechanism are limited by a fixed flow rate that restricts the user to move at a limited number of preset velocities and, at any given moment, the user is unsure of just what his performing force or velocity actually is.
A computerized closed-loop feedback control exercise mechanism has been developed that can overcome these problems and provide the user with the flexibility and the adaptability to exercise at any resistance or velocity pattern throughout the range of movement. Such sophisticated equipment is often impractical within the typical family-oriented practice but it serves well in the orthopedic and sports-injury related practice. Far less sophisticated means can be used in most instances.
Home Exercise Prescriptions
Because time and convenience is limited, treatment cannot be restricted to the office environment. Nutritional counsel and prescribed home exercises, for example, are extremely beneficial in both musculoskeletal and many visceral disorders. To be effective in enhancing a patient’s rehabilitation, exercise must obviously be conducted with sufficient warm-up, frequency, duration, and intensity, and these factors must be based on the individual patient’s current functional and biomechanical status. Thus, explicit, motivational instruction and patient compliance are often basic factors in arriving at a successful outcome.
EVALUATING FUNCTIONAL PERFORMANCE
The body can adapt to withstand a wide variety of threatening environmental forces. This results in systems designed to work in harmony during ever-changing internal and external stimuli. The nervous system provides the necessary intricate coordination, and physiologic measurements offer us data on the essential factors involved in the integrated aspects of organic function. While voluminous data can be gathered, our major concern in rehabilitation involves those aimed at restoring and maintaining homeostasis.
Fitness is an attribute of the human organism at its best. The development of optimal physical fitness produces changes increasing physical capacity and produces changes in altered metabolism at the cellular level. A reduced level of fitness predisposes to injury, its extent, and modifies its healing at both its macroscopic and microscopic aspects.
The degree of vascularity of the capillary network between skeletal muscle fibers and in associated tissues depends greatly on the type of habitual exercise. The quantity of interstitial fat, most marked in atrophied muscle, is also determined by the degree of exercise. Lymph vessels are not found within voluntary muscle.
Because every sport and every physical activity demands a different combination of physiologic capabilities, an individual’s fitness must be specific for the task at hand. Even if the potential exists to develop certain capabilities, the decision to do so is a personal one.
The common human performance parameters are those of strength, endurance, flexibility, speed, coordination, balance, and agility. Body type could also be included here. Intelligence, creativity, and motivation are other parameters. Clinicians must keep in mind that the quality of one’s strength, power, flexibility, speed, coordination, balance, and agility are determined essentially by neuromuscular functions. The range of ability to perform motor activity is determined by three essential aspects: (1) neuromuscular function (eg, strength and skill), (2) energy output (eg, aerobic and anaerobic processes), and (3) psychologic factors (eg, motivation, perseverance). These aspects are involved in almost all types of physical labor, though emphasis varies.
Performance is the result of central and peripheral neuromuscular mechanisms, the energy yield of split compounds, and profound psychologic effects. The methods of estimating physical performance capacity can be classified into two major groups:
(1) physical fitness tests and
(2) physiologic tests. Typical examples of physical fitness tests in sports are sprints, endurance runs, high jumps, long jumps, and throwing.
Determination of maximum oxygen intake and of muscle strength comprise the common physiologic types of tests as in:
(1) determining the mechanical power developed on a bicycle ergometer or staircase;
(2) determining the time element necessary to run a specified distance;
(3) determining the duration of running on a treadmill at varying degrees of speed and grade; and
(4) determining the distance run in a specified period.
Most studies used to evaluate physical performance have been in the field of athletics. We can use this specialized information by applying it to the nonathletic patient as it involves daily activities. While the principles remain the same, a concern is to remember that
(1) the demands of the nonathlete are much less strenuous, and
(2) the factors considered in physical fitness are not equal in all people who could be judged highly fit.
Little can be done to modify body type as much of the variables found in body build and its individual physiology, especially in regard to oxygen intake, are genetically determined. While skill has an influence on efficiency, body type places a finite limit on physical achievement goals. It is granted that a great deal of practice time is allotted to the development of skill, but many aspects of skill are inherited (eg, receptor organ sensitivity). The potential “superstar” probably starts life with a peculiar advantage.
Because body type and receptor-organ sensitivity are essentially governed genetically, training cannot turn an antelope into an ox or vice versa. Depending on one’s genetic framework, training is an enhancement to potential expression. But many variables are not trainable. Skill is the result of practice, not training. Practice tends to develop timing, accuracy, and conditioned responses so that conscious faculties can be concentrated on competitive strategies rather than on physical activities during competition. The term “pressure practice” is practice under highly competitive game conditions (eg, an intersquad scrimmage).
ATHLETIC TRAINING AND PRACTICE
“Training” and “practice” have different goals in sports. Training refers to the improvement or maintenance of physical capacity such as systematic endurance or strength exercises. Normally, these are out of context with a particular sport. Practice means repeating specific skill-developing techniques used in a specific sport so that they may be executed at a higher level of performance. During practice, a swimmer might practice his push-off, a tennis player his forehand, a golfer his putting, etc. To complicate terminology, what would be called practice in one sport might be called training in another. For example, weight lifting is practice for the weight lifter, training for the football tackle. Running is practice for the track athlete, training for the boxer.
As available time is also a concern, the relative degree of emphasis between training and practice varies from sport to sport. Training is minimal in tennis and golf, practice is secondary to training in most explosive-strength sports, and most highly skilled team sports require a careful blend of training and practice.
Coordination, Balance and Agility
Coordination may be defined as the ability to integrate separate abilities into a complex task. Well-coordinated movement, usually involving the large muscles, requires alert timing between the nervous and muscular systems, as seen in bowling, gymnastics, badminton, throwing, jumping hurdles, handball, tennis, ice hockey, baseball, golf, or soccer. Balance is a necessary attribute when one’s base of support is reduced yet body position must be maintained. Ballet-like balance is required in such sports as tightrope walking, handstanding, surfing, karate, hockey, skiing, and to some varying degree in most ballplaying sports where movement is required in an “off-balance” position.
Agility, the ability to change positions in space, involves speed with the addition of a sudden change in direction or height such as in a defensive maneuver or a change in attack. The number of positional changes available is obviously almost endless, thus total agility is difficult to evaluate. Agility is demanded in hockey players, running backs, gymnasts, infielders, divers, boxers, karate enthusiasts, and wrestlers.
Mechanical Advantage and Bulk
Mechanical advantage and disadvantage have distinct relationships with performance. Pace varies with limb length, for example, thus long limbs are an advantage in running, especially in long distance events. A higher center of gravity is a disadvantage in that it takes extra postural effort to maintain balance (eg, gymnastics, skating), but it has its advantages in sports (eg, basketball) where increased height places one closer to the goal.
Body bulk has both its advantages and disadvantages. Muscle bulk, specially in contact sports, provides both force inertia and protection for bones and joints. Body weight is of less consideration in swimming sports because much weight is supported, it offers some buoyancy advantages, or it provides necessary insulation due to subcutaneous fat (eg, open-water swimming). In contrast, due to gravitational pull, a heavy bulk is a disadvantage in running sports as the weight must be raised at each pace. There are also disadvantages in that bulky hypertrophy increases viscous resistance to movement, produces problems from physical apposition, and increases the body mass to be moved. Thus, to avoid mass accumulation in an irrelevant part of the body, muscle training should be specific for the use desired, as indiscriminate muscle hypertrophy is likely to impair performance in endurance events.
Strength is nearly proportional to the quantity of body muscle. Muscle issue constitutes about 43% of body weight in the well-developed adult male and about 38% in the adult female. The average ratio between muscle strength and an individual’s weight has been computed to be about 26:6. Thus, the aggregate strength of the muscles of a 150-lb male is about 4,000 lbs. Since only a portion of all muscle can be employed for a specific task, only a small part of one’s total strength can be effectively used for a particular task.
As described previously, strength is developed in three manners: (1) isotonically by exercises against resistance in such a manner that body movements are allowed; (2) isometrically by exercises done against resistance in such a manner that body movements are restricted —sometimes offering a short cut to goals of equivalent repetitive drudgery; and (3) isokinetically, by exercises of a constant velocity against resistance that adapts to the angle of a joint. Isokinetic exercises are employed primarily to rehabilitate up to the point of normal strength, after which other forms of exercise are used.
Application. Weight lifting is quite helpful in enhancing strength and endurance when judiciously applied, but it has little effect on developing flexibility or cardiorespiratory endurance. With weights, sets of about a dozen repetitions per bout are typical. A “bout” is one exercise series or program. Training with weights has both its zealot adherents and opponents, and both are well-armed with empiric evidence.
Most athletic movements are isotonic rather than isometric, and most all sports present strength demands above those required for normal living. Boxing, wrestling, judo, football, hockey, soccer, lacrosse, and nearly all other contact sports require above-average strength output, as do certain noncontact sports such as mountain climbing, gymnastics, and rowing. Strength development programs (eg, weight lifting, exercise equipment) are now popular in a wide number of sports in which they were rarely considered in times past (eg, tennis, swimming). See Table 1.25.
Certain exercises should be discouraged. For instance, deep-knee bends and the duck-waddle, both used for many years with several sports, exert severe stress on the cruciate ligaments of the knee, far outweighing any benefit to the quadriceps muscles.
Guided Progression. Care must be taken in any exercise program for logical progression. Regardless of a patient’s enthusiasm, the beginning level should be comfortably below that which may cause injury. Progression at any stage should be to a comfortable point requiring moderate effort. Stress should be felt, but pain should not be. The rationale is for the patient to work to full capacity against an orderly ever-increasing resistance.
Progression means to permit a small but increasing overload to musculoskeletal tissues to spur adaptation of bones, tendons, muscles, ligaments, and capsules. Failure to increase demands will stymie further development. Imposing an increase in loading too quickly produces reinjury. The objective is to slightly overload, not overwhelm, the musculature. Correct procedure, state Wallis/Logan, is to balance these two extremes by applying the Specific Adaptation to Imposed Demands (SAID) principle. Wilmore says this implies that the body responds to a given orderly demand with a specific and predictable adaptation. More simply, function improves with use.
Harrelson points out that it is not a prerequisite that full pain-free active ranges of motion are attained before beginning active resistive exercise. The patient may begin isometric manual resistance or active resistive exercise in a limited range of motion as long as the healing process is not jeopardized. This is usually achieved by light-load high repetitions, not a few heavy-load repetitions.
An ideal program should be balanced and conducted on a daily basis with varying intensity on alternate days, depending on how often and when the athlete competes. An intense workout the day before competition or hard labor is usually not wise.
Types of Strength. For discussion, strength can be divided into dynamic (isotonic), explosive, and static (isometric) strength:
Dynamic strength is the ability to lift, move, and support body weight, calling on endurance when functions are strenuously repeated; ie, explosive movements repeated in rapid succession (eg, pull-ups, sprinting). Limits are imposed by speed resisting factors and the quantity and quality of energy-exchange factors. If extreme pain, breathlessness, or weakness comes at the end of an effort, a gain in active muscle strength will do much to improve performance.
Explosive strength is the ability to release maximum power in the fastest possible time (eg, standing long jump). Single violent efforts are commonly seen in sprinting, jumping, and throwing where speed factors are combined with force/velocity features of active muscle. Response is determined by mechanical leverage (influenced by body type), immediate energy resources from tissue chemical coupling (influenced by glycogen and mineral ion levels), the quantity of actin and myosin filaments per fiber (influenced by training hypertrophy), and the number of fibers activated (influenced by learning experiences). The performance result of these forces is determined largely by the degree of dynamic viscosity.
Static strength, a separate factor of physical fitness, is exertion of a maximum force for a brief period of time against a difficult to move object (eg, handgrip or arm-pull dynamometer). The importance of static strength is brought out in such activities as weight lifting. Such strength depends on the total number of active muscle fibers involved in a specific activity; ie, the functional (gross muscle less fat and connective tissue) cross-section of the muscle exerting the force, under control of the nervous system, with some assistance from the type of contraction and mechanical advantage in play. Lessening of central inhibition and greater relaxation of antagonists also play a part in the performance effect. Limits are imposed by exhaustion, motivation, Valsalva effects, pain, and quickly diminishing endurance. Muscles required to contract against increasing resistance become progressively stronger and usually, but not inevitably, hypertrophied; ie, women need not fear that weight lifting with good style will bring gross overdevelopment.
Effects of Strength on Circulation. Either progressing central or local fatigue adversely affects skill: diminished skill is commonly associated with approaching exhaustion. As muscle perfusion is greater in a strong muscle as compared with that of a weak muscle, fatigue, to a great extent, is due to inadequate perfusion. However, the overt signs of pallor and the energy-wasting poor coordination, confusion, and staggering gait are to be blamed on inadequate blood flow to the posture-regulating center. Strength also has an effect on recovery in that strength tends to minimize the microtrauma secondary to oxygen lack and local weakness.
General Health. There is a close correlation to one’s degree of strength and endurance and one’s degree of health because of the relationship to a greater capacity for physical work and the lessened functional response to the challenges of stress. In this regard, the absence of disease would not indicate health.
Power, the rate of doing work, is determined by the rate at which energy can be released within muscle. While the type of contraction (ie, isometric, eccentric, or concentric), resistance, duration, quantity of repetitions, and number of exercise bouts are important in any exercise program, the most important factor appears to be that the contraction force developed by a muscle must be close to maximum if improved change is to be expected.
It has been well established that low-repetition high-resistance exercises develop power; high-repetition low-resistance exercises develop endurance. Many authorities believe that strength is the only training variable in enhancing the speed of muscle contraction and that tissue viscosity is relatively constant. This is only true, however, when strengthening actions mimic movements used in customary activities.
Endurance is the capacity to maintain strenuous activity of a large number of muscle groups for a duration sufficient to prolonged resistance to progressing fatigue and oxygen demands. It is essentially oxygen dependent and a manifestation of cardiovascular and respiratory function (both aerobic and anaerobic capacity).
The word “endurance” is generally used to denote the ability of skeletal muscle to continue contractions relative to contraction length (time), contraction quantity (per unit of time), and contraction quality (force). During vigorous muscle effort, the endurance factor is determined by the initial glycogen content of muscle fibers (influenced by diet and training).
Endurance increases as the result of enhanced muscle hypertrophy, glycogen reserves, myoglobin, and increased vasculature. Local endurance is an effect of muscle strength. We witness this in the power of serves in a long tennis match and the final paces of the runner. In such instances, repetitions of isotonic overload exercises enhance local endurance. Both quantity of movements and the time duration involved are reflections of endurance; eg, the number of push-ups or pull-ups, time to run a mile. Endurance exhibits in a variety of ways in sports, especially gymnastics, crew, cross-country skiing, mountain climbing, wrestling, marathon runs, and swims.
Circuit Training. Circuit training is frequently used to develop endurance and strength both locally and generally in athletes. A series of exercises (eg, 8—10) is done in sequence. A battery of stretching curls, push-ups, sit-ups, pull-ups, and shuttle runs may be completed. These exercises are added to those primarily designed for a specific activity. During the first circuit program, each participant is judged on each exercise for the maximum number of repetitions. This maximum may be determined either by time or by the point of exhaustion. The score obtained is divided by three to arrive at the individual’s training rate for each exercise. At subsequent sessions, the participant completes three circuits of the prescribed exercises as fast as possible at the training rate. As training progresses, the time necessary to complete the three circuits will gradually decrease, then adjustments can be made by increasing the number of repetitions. An alternative method to continually retesting the maximum level is to set three progressively difficult grades of performance, but this largely ignores individual differences.
Cardiovascular-Respiratory Training. Circuit training can be modified to be appropriate for even youth and the elderly showing signs of dysfunctional cardiovascular—respiratory efficiency. Careful monitoring and supervision are mandatory to avoid overstress. With progression keyed to adaptive changes, such training can lead to increased respiratory volume, increased blood volume and cardiac output, improved heart rate and stroke volume, and an increase in total hemoglobin. Shands also reports benefits in improved blood supply to active musculature have also been noted.
Speed is highly correlated with muscle power and difficult to isolate. Speed (fastness) can refer to running time or reaction time. It can refer to the legs of a racer, the fists of a boxer, the arms of a goalie, the eyes of a skeet shooter. As inertia is proportional to mass, total speed considers three aspects: time/distance in initiating body movement (explosive force of active muscles); time/distance rate of acceleration to maximum; and time/distance loss of acceleration as the event is prolonged. During the last stage of a run, the reducing metabolic energy must cope with continuing resistances in air flow, tissue viscosity, surface friction, and other energy losses.
Great speed is obviously essential in runners, tennis players, and football backs and ends. Like a heavy truck, it is difficult for a bulky body frame to accelerate quickly to maximum speed. The ideal physique of a sprinter would be one with powerful legs and little weight elsewhere. In sprinting, performance is enhanced by a preliminary warm-up that raises intramuscular temperature. A slight increase in temperature enhances muscle-tissue viscosity and use of energy resources influencing muscle contraction.
Reaction Speed. Reaction speed is determined by the interval between when stimuli are received by receptor organs (eg, eyes, ears, hands, soles) and when the muscles react. A fast reaction time is necessary for high efficiency in such events as table tennis, dashes, and boxing.
Plyometrics are exercises that link speed of motion and strength to cause an explosive reactive-type motion. They are helpful in developing speed, power, and locomotor skill. This is achieved by maximizing the myotactic (stretch) reflex. Muscles are fully stretched by eccentric contractions immediately before a concentric contraction. The greater the stretch on the muscle from its resting length, the greater the load the concentric contraction can overcome.
Application is commonly done with large rubber bands (eg, Thera-Bands) or surgical tubing. The subject muscles are stretched against the resistance of the band or tube, then the patient moves the part or limb as fast as possible through all normal ranges of motion.
Such drills, states Harrelson, were once confined to off-season strength training programs but have now become part of therapeutic rehabilitation in the late stages. Application two or three times weekly is sufficient when combined with other regimens. Judicious use of plyometrics is important because overuse injuries easily occur when supervision is not alert.
While performance assessment is often studied in an isolated compartmentalized fashion (eg, strength, endurance, aerobic-anaerobic capacity, etc) by the exercise physiologist, care must be taken to avoid oversimplified specific-muscle training that does not enhance overall performance. For example, the development of isometric strength does not assure an improvement in dynamic performance. Multiple intrinsic and extrinsic factors and adaptations affect performance on any one day. A “star” is more than the sum of his parts.
Physical performance during youth is greatly determined by body size, body type, the degree of maturation of the nervous system, and the degree of sexual maturation (more important in males than females). Added to this under conditions of good nutrition, the body of both the immature and mature thrives on use, and use encourages adaptation to maintain a functional reserve of about 25% greater than demand.
FACTORS UNDERLYING PHYSIOLOGIC TESTS FOR PHYSICAL FITNESS
The day-to-day variability in oxygen consumption in most physical actions is about 5%, and differences of 10% of this percentage among individuals can be expected. Energy costs vary greatly in different sports; eg, for a 150-lb player, 4.4 kcal/minute in archery, 9.1 kcal/minute in field hockey, 13.3 kcal/minute in judo, and 18.6 kcal/minute in squash, Energy output also varies in the same sport depending on such factors as intensity of competition, neuromuscular skill level, position demands, performance level, age, body type, atmospheric conditions, and field conditions. In exercise physiology, however, it has been shown to be valid to measure energy expenditure of muscle tissue in terms of oxygen consumption in liters/minute but not valid to convert such data into energy units of watts or kilocalories/minute.
Metabolic capacity, maximum oxygen-intake capacity, and maximum oxygen-debt capacity are the current priority concerns of exercise physiologists.
1. Metabolic capacity determines the amount of activity possible for approximately 2—3 hours through the maximum quantity of energy-yielding substrates available from body reserves during maximum aerobic demands.
2. Maximum oxygen-intake capacity (aerobic power) determines the amount of activity possible for approximately 15—30 minutes through coordinated circulatory and respiratory adjustments producing the maximum amount of tissue oxygen.
3. Maximum oxygen-debt capacity (anaerobic power) determines the amount of activity possible with all-out effort for approximately 50 seconds through anaerobic release mechanisms.
When muscular effort must be prolonged longer than a minute, performance becomes increasingly dependent upon the demands of holistic homeostasis and not just that of active tissues. Basically, this involves oxygen supply, carbon dioxide removal, heat balance, and the replenishment of nutrients.
To maintain health, stored resources (potential energy) must be kept in balance with power expenditures (kinetic energy). While carbohydrate and fat are normally oxidized almost completely in the human body, protein is not. Protein derivatives of uric acid, urea, and creatinine are excreted in the urine. In addition, not all food ingested is absorbed; that is, 97% of carbohydrate, 95% of fat, and 92% of protein ingested is absorbed, and these numbers do not consider the “coarseness” of foodstuffs such as coarse corn meal or roughly ground whole grains.
Metabolic Rate. Metabolic rate is directly proportional to gross body weight. Such factors as lean body mass, age, diet, sex, height, surface area, and race do not have a significant influence on metabolic rate during physical activity. The greater the energy demands, the higher the requirement for oxygen consumption. Total energy is the result of the basal (waking state) metabolic rate plus the energy necessary for work. This offers a ratio that can be used as an index to measure exercise intensity and performance efficiency. In a given period of time, energy output intensity is directly related to mechanical performance, measured by oxygen consumption in a specified period. In this sense, oxygen consumption can be considered a reflection of metabolic power.
Metabolic Capacity. Metabolic capacity is directly related to performance capacity, reflecting the quantity of energy-yielding nutrients available (2—3 hours) from body reserves under aerobic conditions. Thus, one’s maximum aerobic power and metabolic capacity are closely related, yet there are many individual differences. Besides metabolic capacity, other indices may be used such as those of glycogen storage, cardiac output, and water-balance efficiency.
To produce necessary energy, the body uses an aerobic (oxygen) pathway and an anaerobic (nonoxygen) pathway. To maintain life, the primary factor is the continuous and adequate flow of oxygen. Restricted oxygen flow quickly manifests in function deterioration as seen clinically following infarcts and strokes, underscoring why so much emphasis is placed on oxygen demands during physical, psychologic, and environmental stress. Life signs and the degree of life are routinely evaluated from detectable arterial pulsation, breathing quantity and quality and rhythm, temperature, and reflexes —all of which are related to oxygen flow.
When oxygen demands exceed supply (oxygen debt) during and following prolonged exertion, lactic acid accumulates within muscle tissue and encourages fatigue. The greater the exercise intensity, the greater the lactic acid accumulation. Following maximum exercise, it may take an hour or longer to attain resting levels. Oxygen debt must be repaid rapidly such as through hyperpnea.
Short bursts of effort primarily using explosive strength requiring less than 120 seconds are considered anaerobic activities. Because blood, circulation, respiration, and all the other factors contributing to human function during effort cannot be produced on a moment’s notice, nature provides certain limited anaerobic mechanisms to meet the metabolic demands of active cells. Even with minimal work intensity, there is a period of oxygen deficiency that disturbs homeostasis and sets in motion a call for restoration at a higher metabolic level.
Both aerobic and anaerobic mechanisms determine an individual’s performance capacity, but anaerobic activity is maintained only for a short time. An anaerobic state exists when oxygen is not used to produce energy and when glucose and glycogen reserves are used. The greater the intensity of the effort, the greater the anaerobic energy contribution. This can be measured by the amount of oxygen intake during the recovery period, usually attaining its peak (maximum oxygen debt) in about 50 seconds after intense exercise begins. If performance demands are great enough to exceed maximum oxygen transport capabilities, performance proceeds only until anaerobic energy stores become exhausted.
An index of work capacity is mechanical power of an anaerobic nature. Common tests are (1) running staircases, as the energy requirement for maintaining speed in running a specified distance depends on mechanical performance during the period and (2) using a bicycle ergometer, where the mechanical work is calculated by recording through a photoelectric circuit the number of wheel revolutions. Activity examples also include weight lifting, throwing, 100-yard dash, 100-meter freestyle swim, a basketball fast break, or running bases in baseball.
Interval training was developed because of problems associated with lactic acid buildup. Workouts interspersed with rest periods diminish a large accumulation of lactic acid and delay fatigue. Sessions require strict administration. It consists of repetitive efforts in which distance is set and pace is timed with established intervals for recovery between efforts. Long runs increase aerobic capacity, and fast, short runs increase anaerobic power and strength. As conditioning progresses, the time is shortened, the number of runs is increased, and the number of rest intervals is decreased.
The interval pattern of effort and rest for a specific amount of work and time critically determines the rise of excessive lactate levels, which, as previously explained, is a major cause of fatigue. In long-term events, it is important for an individual to keep high energy demands met by anti lactic acid reserves and try to tactically have the competition exceed their reserves.
Pace and recovery time is usually determined by pulse rate rather than time. Some authorities state that heart rate must be 60% of the available range from rest to the maximum attainable (eg, 140+ beats/minute during running) to develop a rate decrease of the working heart. Thus, they claim, an athlete’s pulse below 140/minute indicates a need for a faster run or swim. Once pulse rate decreases to a desired level, rest intervals are ended. Such conclusions, however, fail to consider many unique individual factors.
The Pulmonary Apparatus
The level of oxygen saturation greatly determines the oxygen-carrying capacity of the blood, and oxygen saturation depends on factors determining the quality and quantity of oxygen diffusion in the lungs. These factors include:
(1) the quality of pulmonary blood flow and neuromuscular mechanisms,
(2) the lung area available for the diffusing process,
(3) the time duration in which blood receives alveolar-capillary exposure,
(4) the thickness of the alveolar-capillary membrane,
(5) the alveolar air and pulmonary capillaries oxygen pressure differential, and
(6) respiratory frequency, which is often linked in the athlete with the rhythm of movement. It therefore becomes apparent that the quality of oxygen transport is contingent on the blood, the cardiovascular system, and the pulmonary-respiratory system.
Ventilation. Lung function is evaluated by physiologists by measuring pulmonary residual volume and vital capacity —the components of total lung volume. As an index to breathing capacity, vital capacity is calculated from the maximum amount of air exhaled after a maximum inhalation. About 20% of vital capacity is used during rest. About 70% might be used during prolonged exercise. Up to a quarter of external ventilation is “wasted” in pulmonary “dead space” due to the incomplete mixing of alveolar and airway air, enhanced by an athlete’s or a laborer’s typically diminished respiratory rate.
Ventilation efficiency is assisted as tidal volume increases with decreased respiratory frequency for a given total ventilation. More commonly, ventilation efficiency is judged by the quantity of air inhaled or exhaled in relation to the amount of oxygen absorbed. Such measurements must take into consideration varying atmospheric conditions and individual metabolic needs. Because adequate oxygen is essential for life, both oxygen demands and oxygen consumption must be considered.
Lactic Formation and “Choked” Performance. It has been described that during heavy exercise lactic acid accumulates within muscle as a result of oxygen demands exceeding oxygen supply. Choking of performance because of excessive competition or poor pacing may lead to early anaerobic demands on metabolism. The result is lactate accumulation, witnessed as a premature distressing hyperventilation. Local muscle weakness may also induce premature breathlessness.
Hyperventilation from premature lactate accumulation can cause a person to exceed normal ventilation adjustments where oxygen delivered to the circulation is less than the corresponding demand for oxygen consumption. It is thus important for an athlete to avoid lactate accumulation until late in activity. If local muscle weakness is the cause, the situation can be corrected by strengthening exercises so the athlete can operate nearer aerobic power before lactate accumulates sufficiently. Marathon runners usually operate just under their lactate threshold until the final sprint.
Second Wind. A “second wind” is considered an opposite reaction to that found with choked performance. While early lactate accumulation may be the result of physiologic forces (eg, cardiorespiratory maladjustment), with prolonged activity systemic blood pressure rises, movement pace is steadied, ventilation diminishes, and the respiratory muscles become “warmed-up”, which reduces respiratory resistance and awareness of breathing, and the level of circulating lactate is lowered. Other mechanisms may also be involved.
Diffusing Capacity. Many well-conditioned athletes, especially swimmers and other endurance-related participants, exhibit a large pulmonary diffusing capacity (larger pulmonary surface) that enhances oxygen transfer. These athletes also exhibit an increased ratio of oxygen intake to lung ventilation per minute, which decreases as exhaustion approaches. However, even with maximum effort, the equilibrium of pulmonary gases between the blood stream and alveolar spaces is fairly complete. Thus, a gain in diffusing capacity offers little benefit except for swimmers who deliberately hold their breath or for athletes performing at high altitudes.
Carbon-Dioxide Homeostasis. Both low and high levels of carbon dioxide affect normal tissue function. Excessive carbon dioxide elimination may be encountered in high altitudes, witnessed by intermittent ventilation and symptoms of mountain sickness; ie, dyspnea, headache, blood pressure and pulse rate changes, and neurologic disorders due to maladjustment to reduced oxygen pressure at high altitudes. Accumulation of carbon dioxide is unusual except for the scuba diver due to the increased rate of carbon dioxide production, the decreased maximum voluntary ventilation, the added external dead weight, and the possible inefficiency of the carbon dioxide-absorbing canisters.
The Circulatory System
Blood transports oxygen, energy subtrates, and metabolic wastes. It also serves a vital role in temperature regulation. Reduced blood volume, reduced red cells, and reduced hemoglobin lower the body’s capacity for aerobic activity. Each tissue has a range of functional response with definite limits of adaptation. In this sense, blood oxygen transport capability is limited by its capacity to carry oxygen (ie, hemoglobin content and oxygen saturation). An individual’s pulmonary blood flow, lung diffusing capacity, rate of oxygen removal, and total hemoglobin all have a close relationship with maximum oxygen intake. Total hemoglobin determines the potential arterial capacity to transport oxygen. For example, low hemoglobin levels in an athlete are often attributed to increased cell destruction, as shown by increases in circulating haptoglobins from increased rates in blood flow or extrinsic trauma (eg, runner’s feet, boxer’s abdomen). Dietary habits are more significant than the minute amounts of iron lost in perspiration.
Cardiac Output. Blood oxygen transport also depends on cardiac output. While evaluation of cardiac output during exertion is helpful in diagnosis, stroke volume is difficult to determine directly. Cardiac output increases with work intensity and is directly related to the quantity of oxygen intake: maximum heart output parallels maximum oxygen intake. Such factors as heat exposure and/or dehydration influence stroke volume and change the relationship between heart rate and stroke volume that alters the relationship between oxygen consumption and heart rate. Cardiac output effectiveness is also determined by relative circulatory distribution among active muscles, viscera, and skin. The maximum limits of stroke volume are determined by the type of exercise and body posture. For example, in comparison to a runner or swimmer who uses most of the body, a cyclist, in not using his upper extremities for propulsion, often pools a large amount of blood within upper extremity veins. The consequence of this is a reduced stroke volume in the cyclist.
Oxygen Pulse. During exertion, cardiac stroke volume increases and the active cells take more oxygen from arterial blood. Both of these factors increase oxygen delivery to cells. The term “oxygen pulse” refers to the quantity of oxygen removed from the blood during each pulse. It is measured in a specified period by dividing oxygen intake by heart rate. Oxygen pulse increases during exertion, reaching its typical maximum of from 11 to 17 ml at about 135 pulses per minute and decreasing after further cardiac acceleration.
Heart Rate. Heart rate is closely correlated with maximum oxygen intake. Typically, heart rate is parallel with performance intensity, but maximum cardiac rate decreases with advancing age. There is a linear relationship between heart rate and metabolic rate. Due to the wide variance in individual balance between sympathetic and vagal drives to the cardiac pacemaker, the resting heart rate of the endurance-trained athlete may reach lows of 30 per minute. The maximum sustained heart rate during competition is about 185-195 per minute or less. In activities of high stress and isometric exertion (eg, skiing), peak heart rates of 250 per minute or more may be briefly encountered.
Blood and Pulse Pressures. Blood pressure and pulse pressure also have a lose relationship with maximum oxygen intake. To meet oxygen demands during prolonged exertion, the blood quantity in the muscles and the blood flow within the lungs must be increased. By increasing the force of heart muscle contraction, systolic blood pressure is raised as heart rate increases. This increase is minimized in the well-trained athlete. This is attributed to decreased peripheral resistance because of vasodilatation.
Pulse pressure, the difference between systolic and diastolic pressures, offers an index to the efficiency of cardiac contraction and stroke volume. Difficulties in the exchange of oxygen and carbon dioxide in active tissues are rarely anticipated except in specific types of events. For example, an overland cyclist may complain of pain and weakness in leg muscles during hill ascents. This is apparently caused by local circulatory obstruction resulting from vigorous quadriceps contractions. However, if activity can be continued in spite of the pain, increased systemic blood pressure tends to overcome the local vascular occlusion. This phenomenon is thought to be a manifestation of the heart failing to develop an immediate and adequate increase in blood pressure.
EXCLUSION CRITERIA FOR POTENTIALLY HARMFUL ACTIVITY
While the scope of this book cannot include all possible types of dysfunction and pathologic structural disorders that would exclude an individual from a specific activity, certain guidelines can be used to support the physician’s decision. The base for discussion here is the athlete, but a person involved in strenuous physical labor would be just as appropriate.
1. Whatever the circumstances and pressures, no athlete should be allowed to risk permanent injury. An athlete is either capable from a health standpoint or not.
2. An athlete should be allowed to participate in the sport of his or her choice if practice and competition can be without danger to self or squad.
3. As all sports contain some risk, one sport or level of competition (intramural vs varsity) should not be considered safer than another in itself. Impartiality must be constantly held. However, the risk of a disability must be differentiated between one sport or position, and the demands involved, and another sport or position. For instance, ankle weakness may be viewed differently in a running sport than in polo.
4. Before any screening, evaluation, diagnostic, or therapeutic procedure is used, informed consent must be given.
A physician wins no friends when he must disqualify a motivated athlete or a willing worker who depends on a particular job for his livelihood. Yet, any acute or chronic disease process is reason for disqualification until health is attained. A weakened player is not the equal of a healthy player, and the risk of injury is far higher.
Self-limiting infections require only temporary exclusion. While competition during mild coryza may be permitted, fever is a strict reason for exclusion. A low-grade tonsillitis or dental sepsis may result in poor performance and greater risk. As a guide, the “step test” is often used for signaling if an athlete is ready to return to active competition after an infection.
The player steps on and off an 18-inch platform at a rate of 30 times per minute. The examiner records the player’s pulse rate at 30 seconds, 1 minute, 2 minutes, and 3 minutes after the exercise. The following formula is then applied:
Duration of exercise in seconds x 100
2 x sum of any 3 pulse counts during recovery