Professional Responsibilities

As primary-care physicians, our responsibilities to the patient go far beyond the procedures of finding spinal subluxations and treating them. We are also responsible for the examinations necessary to differentiate whether a particular patient is a chiropractic patient. We must apply the standard procedures of examination, analysis, and diagnostic differentiation that are accepted by the scientific community. These are taught by accredited chiropractic colleges, and they must be done in such a manner that our peers would derive a like conclusion.

Initial examination findings, progress records, adjunctive evaluations, and other judgments must be recorded in a credible manner. And therapy must be commensurate with the condition as it is differentiated by examination findings.


Basics of Clinical Evaluation

Before conducting the actual procedures of clinical evaluation, it is well to be reminded that the signs, symptoms, functional alterations, and morphologic changes revealed by our examinations are often evidence of the existence of a subluxation syndrome. The recognition of these changes and the tracing of the neurologic components active in creating them constitute the basic procedures necessary to understand the pathophysiologic processes involved. Admittedly, direct environmental physical, chemical, or psychologic factors may be present that require differentiation. In some cases, irreversible pathology, particularly in the geriatric case, may have developed. Differentiation of the chiropractic patient must be made from those possibly requiring the services of another school of healing.

Standard procedures of physical, orthopedic, neurologic, laboratory, and radiographic examinations must be used and enhanced by the incorporation of traditional chiropractic examination procedures.

      Physical Examination

The general accent during screening should be on problems involving pain, disability, and the status of the

(1) head, ears, nose, mouth, throat, eyes, fundus, intraglobe pressure, cervical lymph nodes;
(2) heart, blood pressure, vascular tone, pulse rate and rhythm;
(3) chest and lungs, cardiopulmonary sounds, air volume, expectorant, respiratory rate and rhythm;
(4) abdomen, fluids, masses, distention, adhesions, bowel habits, stool, digestive complaints;
(5) urinary frequency, amount, difficulty, blood, control;
(6) female genitals, menses, menopausal changes, hot flashes, fatigue. nervousness, breast and vaginal findings;
(7) male genital findings;
(8) rectal (visual, digital) and proctoscopic findings;
(9) sensory changes and reflexes;
(10) joint range of motion;
(11) regional strength; and
(12) gait.

      Orthopedic and Neurologic Examinations

Degenerative changes occur in the spine that may appear on a x-ray film as errors of position or motion. However, these may be well adapted to and therefore not an active clinical subluxation syndrome. Orthopedic and neurologic findings must be correlated to such structural changes in order to make a clinical judgment of the significance of the radiographic manifestations. Minor positional and dynamic changes if accompanied by other features of a subluxation make these changes more significant. Conversely, particularly in the elderly, positional errors unaccompanied by neurologic or neurovascular manifestations as evidenced by the absence of other signs and symptoms must be challenged. They may be well compensated and not of clinical significance.

Spinal Inspection.   As we observe the patient in a standing, sitting, or recumbent position, we may see various structural or functional distortions in the spine. Although exaggerations of curvatures such as scoliosis, lordosis, or kyphosis are biomechanically significant, they may not be at the root of the patient's complaint. See Figure 2.1.

In considering the geriatric patient, some spinal distortions may be present from degenerative changes in the spine or from old compression fractures. Such changes may be well adapted and, therefore, not an active source of the neurologic interference of a primary subluxation syndrome. Otherwise abnormal gait, stance, and movements may be normal to a particular patient due to compensation. Functional scoliotic curves that improve with flexion or other motions should be differentiated from fixed structural changes. It is important that these findings, as well as all others, be recorded so that the written case history documents the final diagnosis and confirms it as the logical conclusion.

Palpation and Motion Studies.   Soft-tissue tone and texture are apparent on palpation, and areas of subjective tenderness should be appraised. If stimulation produces reflex pain in another area, this should be noted. Swelling, bogginess, hypertonicity, spasm, as well as flaccid areas, atrophic tissues, and similar findings should be evaluated and recorded. These changes may be the result of direct trauma or disease or the result of a subluxation syndrome. Therefore, all findings should be correlated and traced to the neurologic origin of such responses.

Descriptions of positional changes should be explained in terms of motion. Subsequent chapters of this text that concern roentgenology will enlarge on this type of description. Although this terminology is applied more often to descriptions as visualized on a x-ray film, palpation (static and dynamic) may reveal the same changes.

Positional disrelationships as well as errors of motion can best be analyzed as the segment in question is put through various ranges of motion. Failure of normal articular motion in one or more planes (viz, flexion, extension, rotation, lateral bending) indicate a fixation type of subluxation; excessive motion, a hyperkinetic subluxation. Fixed misalignment as palpated in a static position can be made more or less evident on motion palpation.

Where there is a loss or excess of motion that can be measured, it should be done and recorded in degrees by use of a goniometer or similar device. Unfortunately, this is often difficult in the spine, and the individual segmental motion errors that are best perceived by motion palpation cannot always be measured in degrees. However, their existence should be noted, evaluated, and recorded. They may be confirmed, of course, on local stress x-ray studies of the spine.

Muscle and Ligament Testing.   Certain tests have functions that are valuable depending on the condition being evaluated.

Strains.   Muscle and tendon strains and inflammatory reactions become painful when the muscle must contract, with or without joint motion. When the joint is actively moved, pain increases in the involved tissues. When the patient resists counterpressure of the segments controlled by these muscles, the pain is increased. Deep pressure on the involved muscles or tendons is also painful. Spasm and myofibrosis without undue inflammation may be tender on palpation; but on exercise, they are less painful than a strain or inflammatory reaction.

Sprains.   Overstress of ligaments is characterized by pain on motion. The pain is maximal during active motion and minimal when passive resistance is applied. Pressure on involved ligaments causes pain in the acute stage; in chronic sprain, pressure produces less tenderness. However, in either case, hypermobility or joint instability, as a form of subluxation, may be present with consequent proprioception nerve irritation periodically initiating protective muscle spasm (splinting).

Muscle Weakness.   This also may be apparent on testing the strength of a muscle against counterpressure. Depending on which muscles are involved, the proper nerve pathway or reflexes to these muscles must be followed and evaluated to determine the cause of the neurologic interference. This cause may include neurologic diseases such as polio, central nervous system degenerations, peripheral nerve pressure, or other neurologic disorders. Peripheral nerve pressure is particularly common to an intervertebral disc syndrome or to other space-occupying lesions. In the elderly, overall strength may be poor and, therefore, we must qualify our findings. See Figure 2.2.

Measurements.   It is often important to measure the circumference of the arm, forearm, neck, thigh, leg and chest, if indicated. These should be measured at their greatest girth and recorded. A lesser measurement later may confirm the original presence of a swelling such as in a neck injury. In other cases, a lessening of size may confirm, with other findings, the atrophy that often accompanies nerve root pressure. This may be caused by disc protrusion, a space occupying mass, or some type of malpositioned motion-unit syndrome. Lack of the normal difference between the chest measurements during inhalation and exhalation may indicate a pulmonary disease or possibly ankylosing spondylitis.

Muscle strength and/or weakness as a by-product of a subluxation syndrome is an area that has much to offer in our total evaluation of these conditions. There also are a variety of other orthopedic tests indicative or suggestive of certain conditions. Because of the standardization and nearly uniform acceptance of these tests, they should be used. A partial listing is given in Chapter 3.

The clinical analysis and differential evaluation procedures used to ascertain whether a subluxation is present and of importance depends on the training and judgment of the examining doctor. Such analyses and procedures are usually based on the presence of some findings previously described, but not necessarily all. Some criteria indicating the presence of a subluxation require such an excess of examination time and equipment that they may be considered clinically superfluous under average circumstances. Roentgenologic procedures should be limited to those that are clinically necessary so overexposure is avoided. And, of course, all subluxations do not show all classic features.

It must be particularly stressed that degenerative changes may occur in the spine that appear on a x-ray film as errors of position or motion. However, these may be well adapted to and, therefore, not an active subluxation syndrome. Orthopedic and neurologic findings must be correlated to these structural changes to make a clinical judgment of the significance of this radiographic manifestation. Minor positional changes, if accompanied by other features of a subluxation, make these changes more significant. Conversely, and particularly in the elderly, positional errors unaccompanied by neurologic manifestations, as evidenced by the absence of other signs and symptoms, must be judged according to their clinical relevance.


Common Chiropractic Clinical Orthopedic and Neurologic Examinations

We now proceed to the more common chiropractic clinical examinations that may indicate a subluxation syndrome. For this description, these examinations are singularly developed; in actual practice, the procedures are usually more of a composite, as the condition evaluated would warrant. Thus, the clinical sequence may be different from that used here.

As we observe the patient in a standing, sitting, or recumbent position, we may see various distortions in the spine. Although exaggerations of the spinal curves are significant, we are primarily interested in the subluxated segment(s) of origin. That is, specific kinematic errors of vertebrae. These may often be visualized as a sudden demarcation from normal position and motion.

The quality of fixation or limited motion common to many subluxations may vary from minor degrees to complete failure of movement. The error in the function of the motor unit, as well as excessive motion, can be determined as the spine is put through normal ranges of motion. Individual segmental variation is difficult to record objectively. However, sectional motion can be appraised by various methods such as the distance the patient can flex to the floor with the arms extended. Rotational and lateral flexion ability can be appraised by what percentage of normal is present. A goniometer can be used to measure lateral bending and rotation of the cervical spine. Degrees of sectional movements can therefore be objectively measured and recorded for future evaluation. These degrees of abnormal motion may also be evident in certain roentgenographic studies such as the cervical-lateral in neutral, flexion, and extension positions.

In the following section, some common subluxations are described with their attendant mechanical features and consequent distortional effect on the spine.

      Examples

Features of anatomical right short leg with compensatory scoliosis.   Here, landmarks include the crest of the ilium, the sacral dimple, the gluteal fold, and particularly the apex of the greater trochanter --which are all lower on the right than on the left. The compensatory scoliosis is well balanced with the shoulders and head fairly level and over the pelvis. The sectional lumbar scoliosis is convex on the right with the bodies of the vertebra rotated anteriorly to the left, shown by the ability to rotate the lumbar spine further to the left that to the right.

As the spine is flexed into the Adams position, it tends to straighten, which indicates a functional scoliosis due to muscular asymmetry. Symptoms may not be present in the pelvis but express elsewhere in the spine. Complaints often arise at the apex of a compensatory sectional scoliosis where motor units are overly stressed due to resulting muscle and/or ligament overstress; therefore, symptoms of spasm, local pain and tenderness, radiating neuralgias, and other signs of inflammation may manifest. In time, this overstress may lead to degenerative joint disease.

Right posterior-inferior and left anterior-superior sacroiliac distortion.   We see a similar picture in this example. That is, the crest of the ilium, the sacral dimple, and the gluteal fold are lower on the right than on the left. However, the apex of the right trochanter is not, and the right posterior superior iliac spine is more prominent than on the left. Some of these features indicate a sacroiliac subluxation as a cause of pelvic unleveling and the compensatory scoliosis rather than the cause being a deficient lower extremity.

The major subluxated sacroiliac articulation may exhibit such features as marked joint tenderness, muscular hypertonicity in the pelvic muscles, reflex patterns of pain, and particularly a greater effort in flexing the thigh on the side of the subluxated innominate. This can be shown by having the patient attempt to raise one lower extremity and then the other; while he lays supine and the pelvis is stabilized by pressure on the anterior crests of the innominates. The extremity that is the more painful or shows the greatest effort at flexion usually indicates the side of symptomatic sacroiliac subluxation.

Level pelvis with L5 laterally flexed to the right.   In this example, L5 is laterally flexed to the right, the pelvis is level, but there is a marked lateral bending of the lumbar spine to the right with a sectional lumbar scoliosis starting at the fifth lumbar segment. Since lateral flexion is nearly always accompanied by some degree of vertebral rotation, and vice versa, these segments also may be misaligned in a hyperrotary manner to the left or right.

Though these composite planes of misalignment may be visualized by observation and verified by static roentgenography, they can also be shown by motion studies. For example, if L5 flexes laterally to the right further than to the left, it is in lateral flexion malposition to the right. If it rotates further anteriorly on that side as opposed to the left, it is also hyperrotary to the right. However, if it laterally flexes to the right, but rotates further anteriorly to the left, it would be hyperrotated to the left.

Note that a lateral flexion subluxation to the right with hyperrotary malposition to the right produces a sectional scoliosis with the convexity on the right and, also, vertebral body rotation to the right (the classic Lovett positive scoliosis) with the spinous processes moving toward the convex side. On the other hand, a lateral flexion to the right with hyperrotary malposition to the left will cause a sectional scoliosis with the convexity on the right and vertebral body rotation to the left (classic Lovett negative scoliosis). These individual segmental composite planes of malposition are best appraised by dynamic palpation of the subluxated segment as the spine is put through various positions of motion.

Left lateral flexion of T7 with hyperrotation to the left and a sectional thoracic scoliosis.   In this example, T7 is laterally flexed to the left and hyperrotated to the left. Therefore, the spine below this segment is vertical, and T8 is level. T7 is not level; it laterally flexes further to the left than the right, and the sectional scoliosis that it produces is convex on the left, shown by a high left scapula and shoulder. This compensatory scoliosis is rotated anteriorly to the left. Therefore, it rotates easier to the left than to the right and laterally flexes to the right easier than to the left, particularly at the apex of this compensatory scoliosis.

Any malpositioning of a spinal segment may be evaluated using the principles in these examples for they are based on the phenomenon that a subluxated vertebra moves easier into its planes of malposition and resists movement into planes of normal positioning. Flexion and extension malposition also exhibit this principle. In this example, C5 is in flexion; therefore, the space between the spinous process of C5 and C6 will be wide, C5 will flex with ease, but extension will be limited and be more obvious above or below the flexed segment.

Extension of L5 postural shift with limited flexion and ease of extension.   Another example is the common extension subluxation of L5 on the sacrum with the typical consequent facet over-riding and syndrome. Here, the lumbar spine is in extension and body weight is shifted posteriorly. On motion, L5 does not flex well and the segments above may flex excessively.

However, extension is more marked than normal and the segments above may show less ability to extend individually.

Muscle and Ligament Testing

Muscle and ligament testing has various functions, which are all valuable depending on the condition being evaluated. Muscle and tendon strains and inflammatory reactions are made painful when the involved muscle(s) must contract, with or without joint motion. With support, they may be less painful. When the patient resists counterpressure of the segments controlled by the involved muscles, the associated pain is increased. Deep pressure on the involved muscles or tendons is also painful. Spastic muscles or myofibrosis, without undue inflammation, may be tender on palpation; but on effort, they are less painful than a common strain or inflammatory reaction. Note that spasm, myofibrosis, and atrophy or other degenerative changes may be the result of a neurologic reaction initiated by a subluxation or the irritation of its attendant proprioceptive mechanism rather than be the consequence of direct tissue damage.

      Examples

Cervical strain.   If there is a strain of the lateral cervical muscles, the muscles would be painful on deep pressure and active lateral bending against resistance would be painful. However, supported passive movement produces little discomfort. In cases of spasm or myofibrositis, the involved muscles are tender on deep pressure. However, active or passive movement as well as isometric contraction will not produce undue pain as this usually depends on the degree of inflammation present.

Cervical sprain with subluxation.   Overstress of ligaments is characterized by pain on motion. The pain is present when the joint is moved whether it be active or passive; ie, with or without support. Isometric contraction of the muscles (ie, without motion) may not be painful, particularly when the joint is supported to prevent the slight ligamentous motion in the initial stabilizing period before muscle contraction. Digital pressure on the ligaments causes pain in the acute stage; in chronic sprain, pressure may produce less pain. In either case, however, hypermobility or joint instability, as a form of subluxation, may be present and the consequent proprioception fiber irritation may initiate protective "splinting" periodically.

Cervical sprain without subluxation.   Using the cervical spine again as an example, sprain would be painful on either active or passive motion. The involved muscles will be sensitive to pressure and tend to become spastic to protect (immobilize) the cervical spine. Pressure directly on the ligaments involved, if possible, will be painful. However, isometric muscle contraction would elicit little pain providing the involved vertebrae are adequately supported so they do not move. Many articulations and their attendant soft tissues may be evaluated using these principles.

Professional health care makes many demands in observation, data recording, communication, and therapeutic skill. Quality case management is the result of accurate observation, thorough analysis and synthesis of information, and appropriate action. Good records safeguard the quality of these functions.

Awareness of the root(s) of the patient's problems is the first step in rational health care. The second step is to have comprehensive records of the patient's problems, the care administered, and monitored progress. Therefore, more is needed besides a memory of the patient's complaints. Total recall from visit to visit of existing problems and their ramifications over a period of weeks or months is difficult to imagine.

Examination procedures and data recording should never be performed without alert attention to detail. In today's society, it is a rare practitioner who at some date will not find himself on the witness stand where he must be prepared to defend his professional judgment and actions.


Objectives

Clarity and honesty are good goals in both written and oral communications. Good decisions are the result of accurate and complete facts being at hand from which a logical course of action can be planned. Experience shows that a successful practice is determined to a great extent by the quality of the doctor's data gathering and retrieval systems.

Essentially, the case record is a compilation of data concerning patient care. It should present a well-organized and carefully documented report of the patient's progressive health status. The patient's complaint and other subjective data must be supported by objective physical findings and data from other diagnostic tests.

As many cases involve third parties, it is important to record all data in acceptable terminology. All healing professions, as well as their specialties, enjoy jargon that computers are unable to interpret. Thus, any terms that fall outside standardized nomenclature can result in loss of time, effort, and income.


Proper Recording

Each practitioner must maintain adequate records for both professional and legal reasons to

(1) enhance continuity of patient care,
(2) document the quality of the care given,
(3) justify payment for services rendered,
(4) serve as a defense against malpractice suits, and
(5) function as a basis for submitting reports to appropriate third-party agencies.

Clinical records deal with the health-care aspects of the practice. The entering patient data form, the patient history form, the case history and examination form, case progress records, clinical laboratory reports, and x-ray reports are examples. Administration records concern the business side of the practice; eg, ledgers, practice analyses.


Entering Patient Data

As a new patient enters the typical chiropractic office, he or she is greeted, seated comfortably, handed a clip board to which has been attached a card or slip, and requested to record some basic information. Much of this information is for administrative purposes such as the patient's address and telephone number, employer's name and address, and referral and insurance data. Some data such as date of birth, chief complaint, number and ages of children, and occupation are of a clinical nature and likely will be transferred to other records.

After the entering data are obtained, the next step is to obtain a record of the patient's health history. An assistant may be responsible for the initial gathering of this information that allows recording when symptoms first appeared, how long the disorder has existed, what the patient has previously done about the condition, and other facts helpful in case evaluation that will be explored in detail later.


Types of History Recording

The type of information collected generally concerns the patient's chief and minor complaints; the patient's medical, surgical, obstetrical histories; and family, social, and accident histories. Other points recorded are of past patient illnesses, operations, miscarriages, births, drug or food sensitivities, congenital difficulties, past medical and chiropractic care and the results obtained. The family history concerns the health status of siblings and parents, offering possible clues to hereditary influences. The social history of a patient relates to where the patient lives, marital status, number and ages of children, type of work and work environment, smoking and drinking habits, activity excesses and inhibitions. The history of accidents and their effects are recorded. The doctor will later explore in detail during consultation with the patient each point recorded by an assistant

The two most common methods used in gathering a case history are programmed questionnaires and direct questioning. A screening device such as a printed form does not minimize the doctor's role in taking the history. It is only an efficient means of supplying general data and serving as reference points from which the doctor will investigate further so that the time saved in asking standard questions can be used in more critical aspects of case evaluation.

To save patient and office time, some doctors use a personal history form that requires only a simple "Yes" or "No" answer that can be checked or encircled by the patient. These forms are usually designed so that a group of questions refers to a particular body system. Such questionnaires give the doctor an opportunity to review basic data prior to seeing the patient so that he may formulate some fundamental questions in his mind prior to patient consultation. The patient should be assured that all information will remain in confidence. It is obvious that a patient that is severely ill should not be confronted with a printed form.

Some doctors feel that a questionnaire should be presented to a patient only after the initial history has been obtained and rapport has been established between doctor and patient. Any approach must be designed to the patient, the problem at hand, and office policy.

The importance of a case history is directly proportional to its completeness and accuracy. Thus, in questioning a patient, the doctor must accomplish two tasks:

(1) convince the patient of the importance of the interview and questioning, and
(2) establish the sequence and relationship of events up to the present illness. If the first task is not accomplished, the second cannot be achieved. As the history develops, the doctor must begin to formulate tentative ideas about likely diagnoses.

The examination begins with a review of the recorded initial data. During consultation, the doctor further investigates this information, probing deeper and wider, and arrives at an initial judgment of what examination procedures are best suited for the particular patient and complaints involved. When the patient interview is completed, the doctor proposes the type of examination necessary; and on patient agreement, the examination will proceed. After examination, the doctor records the results of the physical examination, spinal analysis, laboratory findings, and other data necessary to profile the patient's condition. Both normal and abnormal findings should be recorded.

This whole process may be achieved in a matter of minutes in simple acute cases. In a severe chronic condition of an obscure nature, the process may take from several days to several weeks before a working diagnosis and prognosis are arrived at.


History and Examination Forms

Professional printing houses have a large selection of case history forms to choose from, but some doctors prefer to design their own to meet personal goals and specifications. Other doctors do not desire a restricted format, but prefer, rather, to develop customized clinical records through dictation that is later typed. When a printed form is used, all spaces must be filled else it may appear that an oversight has occurred.


Progress Records

Once patients' conditions are recorded as they enter the practice, progress, changes in treatment, or changes to previously given instructions should be noted after each visit. Progress notations constitute a permanent record of what was done and offer chronological patient status. While the patient's history indicates the patient's status at the time of the initial visit, progress records documents the patient's state of health at subsequent points in time.

The case record (patient chart) serves as the basis of all intra- and inter-office communications. The continuing case record (progress report) identifies

(1) who the patient is,
(2) what care or procedures were given and on what date,
(3) who provided the care,
(4) where the care was given,
(5) and how the patient responded to the care given. Records document what humans may forget.

The Chief Complaint and Present Illness

The chief complaint is a brief statement, preferably in the patient's own words, concerning his or her reasons for seeing the doctor. It also portrays the patient's sense of priorities about his problems. The chief complaint is the presenting symptom or major problem for which the patient is seeking help. It is the response to such questions as "What seems to be the matter?" or "How can we help you?"

The term "present illness" is actually a relic of the past in which a patient saw a physician for a single illness. Years ago, patients rarely sought relief for chronic, multiple, interacting problems as they do today. Thus, "active problems" would be a better descriptor --but "present illness" is commonly used today with a modern interpretation.

      Chief Complaint

Once the chief problem has been defined, encourage the patient to offer more details. After this explanation, you can direct specific questions to profile the patient's problem in greater detail. Probing deeply into the patient's chief complaint frequently uncovers problems that were predestined in years past and could have been avoided or minimized if an efficient case history had been obtained at that time. Thus, the doctor's role should be as preventive as it is therapeutic.

If the patient is in pain, limit his questions at this time by asking something to the effect, "What's bothering you the most?" In most instances of pain, it is practical to concentrate on the acute condition during the first visit. Keep in mind that the patient's symptoms represent only what the patient feels to be wrong and what the patient is concerned with. You may find a severe problem that is asymptomatic, but this should not be an excuse to minimize what the patient is concerned.

      Present Illness

If the patient is not in pain, seek what else has been troubling the patient. The goal is to encourage the patient to relate all his problems so that a description of the present illness can be made. It is also well to have the patient describe his symptoms on subsequent visits. It takes time to build trust and openness --and almost impossible to obtain a thorough case history in the first visit. Retelling invariably adds facts not previously revealed or recently remembered. If the patient has been involved in trauma, shock, or a crisis (febrile or emotional) it is not unusual for a degree of amnesia or faulty recall to exist.

Be confident at the end of the interview that the emotional and factual substance of the interview was satisfactory and that the patient has been open and truthful. If not, the information is probably incomplete or misleading.

At this time, you should have a list of the patient's problems: some that are likely related to the chief complaint and others that are probably not. Clinical judgment will determine priority considerations. The quality of this judgment is determined largely by

(1) how thoroughly the beginning and course of the problem is understood,
(2) where the problem is and its radiation,
(3) the problem's quantity and quality,
(4) what circumstances aggravate or aid the problem, and
(5) what manifestations are associated. The answers to these questions should be recorded for each complaint.

Avoid tendencies to jump to conclusions based on a few facts. The interpretation of history, physical, and laboratory findings may be faulty; eg,

(1) the patient may not be perfectly open and honest during the interview;
(2) symptoms, being subjective, are a mixture of emotional and physiologic factors;
(3) physical findings may be misleading; or
(4) laboratory tests are not always accurate. All standard diagnostic procedures are helpful, none are perfect.

Patient Profile

The patient profile is the opening statement in the patient's record. It usually has a brief narrative about the patient's way of life:

(1) life history, including usual day's activities and education,
(2) marital status,
(3) occupation,
(4) finances,
(5) personality,
(6) habits,
(7) hobbies and special interests,
(8) religion, and last but not least,
(9) habitual posture.

The purpose of the patient profile is for the doctor to form a picture of the patient's present life-style such as home, work, and recreational activities to see, first, if anything therein may be the cause of or contributing to the patient's health status, and, second, to gain insight into the impact of the patient's problems on his daily activities.

These factors, singularly or combined, may be a contributor of stress leading to lowered resistance and disease. The life history may disclose certain socioeconomic burdens or recent relocation frustrations. Marital status may suggest a marital incompatibility or a divorce maladjustment. Religion may have an influence on diet, on fears behind anxiety, or on guilt behind depression. Financial strain may be contributing abnormal tension within a personality that is habitually "high strung" without the added pressures of money worries. Habits in diet, sleeping, or exercise may be a factor. Habits and addictions to tobacco, alcohol, diet fads, laxatives, and drugs may be causative or contributing factors. The patient's occupational history may reveal peer or superior friction, postural strains, or chemical or physical work hazards.


Patient History

The complete patient history consists of the

(1) presenting symptom,
(2)present illness,
(3) personal history, including past sicknesses, hospitalizations, medications,
(4) family history,
(5) accident history, and
(6) a systems review. The aim is to have an accurate office record of, understanding of, and appreciation for these factors.

As defined, a presenting symptom is the chief complaint: the major problem for which the patient has sought relief. A detailed description of the patient's current problem developed chronologically is the "present illness." Every symptom and sign has a beginning and a course of development that may be progressive or fluctuating. Since symptoms and signs are products of the body that produced them, each body creates symptoms and signs in a unique way, and each personality adapts to them in a unique way.


Personal History

To assess the patient's personal health history, questions should probe childhood diseases, major illnesses, operations, pregnancies (deliveries and abortions), allergies (airborne, contact, medications, food), serious accidents, and immunizations and reactions to such.

      Prior Sicknesses

A patient's recount of hospitalizations may give clues to active conditions. Surgery conducted several years previously may cause adhesion troubles today. Record dates of surgery, hospitalizations, length of confinement, and known complications.

Chronic diseases may be superimposed on an acute condition. For example, infections hamper diabetes control, a sudden rise in blood pressure may bring out a cardiac weakness, an acute abdominal strain may interfere with a compensated lordosis, sneezing may aggravate a chronic spinal disorder, or poorly adapted emotional overstress may exhibit in one or more conversion symptoms.

      Medical Care

Current medications direct attention to problems presently being treated or controlled. Remember that medications interact with other drugs and certain ingested vitamin and minerals. Some patients do not know the name of the medications they are taking or why they are taking them. If this occurs, note the prescriptions and look up the drugs actions and side effects. Determine if the patient is following the instructions on the bottles or tubes.

Question the use of nonprescription drugs. Overuse of aspirin, for example, is a common cause of gastritis, especially compounded with alcohol intake. Many drugs interfere with gastric pH, enzyme quality, normal renal excretion, intestinal bacteria, and normal blood chemistries. Drugs may also confuse the significance of certain signs and symptoms; eg, a black tarry stool may be the result of bismuth powders or an iron tonic rather than a sign of upper GI bleeding.


Family History

Hereditary factors are common in the background of diabetes, renal disease, hypertension, mental illness, heart disease, cancer, and allergies. Questions should be aimed toward the health status of grandparents, parents, and siblings. Age and cause of death are important information. Ascertain if one or more members of the family is or has experienced symptoms similar to those presented by the patient.


Accident History

A comprehensive accident history is important to an accurate patient history. In detail, discuss the where, when, and how each accident or severe strain occurred. Determine the care administered, the scope and degree of trauma, the diagnostic tests taken, and the care administered. Allopathic whiplash cases, for example, are sometimes dismissed on the relief of pain. Joint stiffness and fixation often result because of the compensatory connective tissue effects of overmobilization --similar to traumatic arthritis effects. Proper chiropractic care would prevent this: if not completely, then to a large extent.

Following an automobile accident, for example, it is important to know from which side the force came, the position of the patient at the time of impact and after. Was a seat belt or shoulder harness fastened? Did the patient's head strike anything? Was there unconsciousness? What were the immediate symptoms? What were later manifestations? These and many more similar questions should be deeply probed.


Systems Review

A physical examination cannot be conducted with the proper curiosity and direction unless a proper case history has been developed. When the case history is complete, the doctor should have a fairly good idea which one of four important pathophysiologic groups the patient's problems fall:

(1) a functional disorder (pathophysiologic disease without visible pathology);
(2)an organic disease (with or without overt pathology),
(3) a neurosis or psychosis; or
(4) a psychosomatic or somatopsychic disturbance. It is often difficult to differentiate between functional and organic illness. In functional disorders, there is undoubtedly a degree of chemical and intracellular alterations preceding gross structural (organic) manifestations.

Body Size and Proportions

Growth and development normally involve both an increase in size and changes in proportion. We readily recognize that a child is not a miniature adult proportionately. Growth and proportion effects are common features of genetic determinants, hormone balance, connective-tissue health, and nutritional considerations.

      Hormonal Influences

The pituitary growth hormone affects somatic growth. Thyroid hormone promotes linear growth and has a direct influence on cartilage ossification, epiphyseal maturation, and thus on skeletal proportions. During youth, an overproduction of androgen stunts growth and an underproduction removes checks on linear growth. In adolescence, however, androgens stimulate growth and muscular development and are responsible for the development of secondary sexual characteristics. Sex hormones influence epiphyseal maturation. If the growth plates in the long bones close too early, longitudinal growth is halted. Thus, several hormones influence body size and proportion.

      Nutritional Influences

Nutrition, either beneficial or detrimental, also has a distinct effect on growth and development due to its influence upon hormone and connective tissue quality. Connective tissue development determines one's appearance to a large extent. Genetics, hormone balance, and nutrition manifest themselves in connective tissue quality as seen in bone, cartilage, collagen, elastin, muscle, and fat.

      Evaluation

Abnormal development bilaterally also offers diagnostic clues. With slight variations, the body should be essentially symmetrical and balanced around its center of gravity. Discrepancies in the size or shape of paired parts are readily observed when one is different from its mate. It is of obvious importance to determine which part is abnormal in size or shape and which is normal. Yet it is often difficult to judge discrepancies from normal when paired parts are equally abnormal or subnormal and the degree is subtle.

A comparison of the state of one part with its partner is a relative thing. We often hear someone refer to another as having large ears or eyes, but they may appear large relative to a small skull. We commonly refer to an anatomical or functional "short leg" in chiropractic and rarely refer to an anatomical or functional "long leg."

The evaluation of body size and proportion is made by inspection, mensuration, and palpation during the physical examination. Note maturity and size of features; overall sexual development relative to age; skin color; asymmetry of paired parts; posture; biomechanics; and gait.

Mensuration.   One basic mensuration technique is as follows:

(1) Measure the lower body segment by recording the distance from the symphysis pubis to the floor.
(2) Measure the upper segment by recording the distance from the symphysis pubis to the highest point on the crown.
(3) Measure arm span by recording the distance from the laterally outstretched fingertip to the sternal notch.

These three measurements are normally equal after 10 years of age. The above measurements are made with the patient standing upright. It is also helpful to measure the circumference of the head, thorax, abdomen, thighs, arms, and obviously asymmetrical parts.

Trunk:Limb Ratio.   The trunk is normally longer than the limbs during early youth. With age, the extremities grow faster than the trunk until the limbs and trunk become the same length at near the age of 10 years and remain so throughout adulthood. It is an abnormal sign when the trunk is longer than the limbs after the age of 10 and usually indicates hypothyroidism or is seen in certain chondrodystrophies. If the trunk is shorter than the limbs after the age of 10, gonadal hormone deficiency can be suspected to have failed to check long-bone epiphyseal closing at the proper age. Abnormal ratios may be slight, yet they are distinct diagnostic clues. Minor degrees of atrophy are determined by measuring the circumference at corresponding levels of each arm, forearm, thigh, and leg. Take care that the limbs are in a state of relaxation.

Fat Distribution.   The distribution of fat also offers distinct diagnostic clues. Fat normally tends to form centripetally in the visceral areas and centrifugally in the extremities. Typical males have more muscle than fat, and their center of gravity is through the shoulders. Typical females, on the other hand, have more fat than muscle, and their center of gravity is in the hips. The "baby fat" of childhood may be an indication of immaturity in the apparent adult. Fatty appearing legs and ankles, however, may actually be edema exhibited from protein depletion, caused by either malnutrition or failure of the liver to synthesize ingested protein.

Specific diseases often present a characteristic fat distribution. Abnormal fat distribution is an important sign in adiposis dolorosa and adrenal cortical hyperfunction:

• Adiposis dolorosa is characterized by an accumulation of subcutaneous lumps of fat that is extremely painful to the touch. Such patient's must be helped with great gentleness.
  
  

• Adrenal cortical hyperfunction (Cushing's syndrome) features an obese trunk and face associated with limb wasting; facial fat produces a plump, rounded "moon face" demeanor. An accumulation of fat over the thoracic spine and especially in the supraclavicular fossae is called a "buffalo hump." Other characteristics include hypertension, thin skin that is easily bruised, abdominal striae pigmentation, and excessive facial blood offering a "blushing" appearance. When these signs are found, it is almost diagnostic of the disease.

Wasting.   A severe loss of fat and muscle bulk (wasting) is a common sign of most chronic debilitating diseases. Striking localized signs commonly appear in the face and abdomen. Loss of cheek fat and fat around the temples give the zygomatic arches a prominent "gaunt look." Abdominal skin hangs in loose folds. The skin of the upper arms also hangs in loose folds, and the axillae hollow from tissue loss. A hollowing of the supraclavicular fossae is an early sign. Wasting in children is called kwashiorkor; wasting in adults, cachexia.

Atrophy and Hypertrophy.   Atrophy and hypertrophy have a distinct effect upon symmetry. Abnormal biomechanics, bone, muscle, fat, or connective tissue may affect symmetry, and the abnormal distribution or tone of normal tissues may affect symmetry. In chiropractic especially, the examination of symmetry is important as it influences biomechanics and spinal balance, postural stress, and functional tone.

Atrophy and hypertrophy also have diagnostic significance:

Atrophy.   The term atrophy refers to localized wasting, a reduction in part size. A reduction in innervation, blood supply quality or quantity, or exercise to a limb, for example, produces atrophy, Generally, if a limb is the same length as its partner, it is likely that bone is not involved and the condition has occurred after bone maturity. If limb length is reduced, it is probable that the condition began before bone maturity such as seen in poliomyelitis, congenital deformities, birth trauma, dwarfism, rickets, and progeria. Typical exceptions to this rule would be osteoporosis and osteitis, which show a reduction or malformation of bone in the adult long after bone maturity. When limb atrophy is segmental, peripheral nerve loss is probable. For example, atrophy of the lateral interosseous muscles and the hypothenar eminence is seen in ulnar nerve palsy. Muscle atrophy is often the result of a dystrophy --a disorder due to defective or faulty cellular nutrition.

Hypertrophy.   Enlargement or overgrowth of a part due to increase in size of its components (eg, connective tissue) is called hypertrophy. There are few known causes of hypertrophy except that which is a result of excessive exercise of the part; eg, compensatory ventricular hypertrophy of the myocardium is seen in a number of cardiovascular conditions. Two unusual types of hypertrophy leading to asymmetry are hemihypertrophy and polyostotic fibrous dysplasia. Hemihypertrophy features enlargement of one side of the head and body. The overgrowth affects all organs and tissues on the affected side. This syndrome is often related to various congenital anomalies and early tumor. In its early stage, a slight limp and unilateral facial prominence may be noted. Polyostotic fibrous dysplasia (Albright's syndrome) is characterized by bone swelling and deformity, especially of the face; structural weakness; "coffee-stain" skin lesions; and early sexual development in females.

Gait

There are various modes of walking peculiar to certain disease that are important diagnostic signs. The range of movements in the lower extremities assists in recognizing specific diseases and helps the examiner determine postural changes resulting from an unnatural gait. A shortened leg gives a characteristic limp. A stiff knee causes the affected limb to swing outward while walking. Intermittent claudication or limping is observed in chronic peripheral vascular diseases (eg, endarteritis) because muscles in action require more blood than muscles at rest.

The normal walking cycle has two phases:

(1) a stance phase when the foot is on the ground; and

(2) a swing phase when the foot is moving forward. The stance phase is subdivided into

(a) heel-strike,
(b) foot-flat,
(c) midstance, and
(d) toe push-off.

The swing phase is subdivided into

(a) acceleration,
(b) midswing, and
(c) deceleration --depending on the intent. See Figure 2.3.

More than half the walking cycle is used in the stance phase. As this phase is the weight-bearing phase requiring the greatest stress, most problems become apparent in its analysis. Observing a gait deformity and noting what phase it occurs contributes diagnostic clues. Most stance-phase problems are the result of pain and feature an antalgic gait where the patient spends as little time on the affected extremity as possible.

During inspection, have the subject sit in a chair, arise, and then walk across the room if you have not had an opportunity to witness this previously. Note how the patient rises from the chair to the standing position. Observe the necessary base of support: how far the knees are apart and how far the forward foot is from the back foot. If the chair has arms, note how the hands are used in arising from sitting to standing to assist weak knees, weak hip extensors, or to maintain stability, balance, and coordination.

As the patient walks, observe any deviations from a normal gait. Normally, the head and trunk are vertical, step length is even, and the arms swing freely and alternate with the leg swing. The foot should be near a right angle to the leg and the knee is extended but not locked at heel-strike. The trunk should be vertical at stance. At push-off, the foot should be firmly flexed with the toes hyperextended. The foot should easily clear the floor during the swing phase.

As the body advances, note smoothness of the body's vertical oscillation. A pathology may express itself in increased vertical oscillation and disrupt the normally smooth pattern. During the stance phase, note heel-strike, foot-flat, midstance, and toe push-off of each extremity. During the swing phase, note acceleration, midswing, and deceleration of each extremity. Normal gait presents smooth function without any sign of impairment or affectation of parts of the body.

Compare patient's gait with normal walking base width, lateral shift of pelvis, and hip rotation:

1.   Note walking base width. From heel to heel, this should not be more than 4 inches. If wider, dizziness, unsteadiness from a cerebellar problem, or numbness of a foot's plantar surface may be the cause for the wider base.

2.   A slight lateral shift of the pelvis and hip to the weight-bearing side is normal to center the weight over the hip. Lateral shifting is accentuated in gluteus medius weakness.

3.   When one hip is in the stance phase and serves as the fulcrum for rotation, the other hip in the swing phase should rotate about 40° forward. This normal hip rotation is not seen in patients suffering a stiff or painful hip.

A limp may be a sign of disease or of malfunction or both. A common limp is caused by a poor-fitting shoe, a corn, plantar wart, or bunion. Any articular malfunction from the spine to the foot may result in a limp. Muscle weakness or spasm, fascial contraction, fracture, a torn ligament or tendon, bone disease, or a neurologic disorder may be cause for a limp. An uncomplicated limp can usually be traced to a knee, ankle, or foot dysfunction or deformity, a hip disorder, or a sacroiliac or lumbar lesion. A limp also may be in compensation to another condition such as a sprained ankle, injured knee, old fracture malunion or hip surgery. However, most limps seen are "guarded" limps; ie, walking in a manner to protect or relieve stress on an area.

A guarded limp may point to a specific musculoskeletal or visceral disorder. For example, walking in a stooped position with one hand supporting the back is a frequent sign of a lumbar lesion. A female gait exhibiting rigid buttocks is a sign of a uterus retroflexed or prolapsed, or of a lumbosacral lesion. Walking on the toes is seen in cases of lumbosacral or cervical lesions. A gait presenting lateral bending may be caused by a pericardial or a pleural friction rub, a sacroiliac lesion, a shoulder condition, an affection of the brachial plexus, or a lesion in the upper thoracic spine. A ram-rod gait signals a thoracic lesion(s).

When a difference in leg length is suspected, measurements should be taken in both the standing and the prone positions to determine if the "shortening" is the result of structural or functional factors. With the patient standing, measure the distances from the anterior superior iliac spines (ASISs) to the inner malleoli with a steel tape. Measure from the notch just below the ASIS to the depression just below the internal malleolus. Record these measurements and measure again with the patient prone on a flat examining table. Before taking the prone measurements, use light traction on each extremity to eliminate any induced pelvic tilt. If measurements are taken only in the prone position, a unilateral fallen arch, foot pronation, knock knee, hyperextended knee, tibial torsion, pelvic subluxation, specific muscle weakness or tautness will be reduced and offer a false impression. These functional disorders will be more obvious in the weight-bearing standing position.


Several pathologic gaits deserve definition:

1.   In the ataxic gait, named because it occurs in locomotor ataxia, the patient walks in a stooped posture with the eyes looking at the feet. The foot is raised unusually high, thrown forward with force, and brought to the ground flat-footedly with a stamp. When in the air and before being lowered, the foot wavers as if there is a degree of uncertainty in bringing it down. The patient walks with his feet wide apart and is constantly looking at them. This is done to supplement the loss of proprioception. It is sometimes called the tabetic gait and characteristic of a lesion in the dorsal ganglia, dorsal roots, or posterior columns of the cord; rarely in higher levels. The ataxia is increased when the eyes are closed or when the patient must walk in a darkened room. The gait is seen in tabes dorsalis, pernicious anemia, and other disorders involving proprioceptive pathways.

2.   In an apraxic gait, motor power is present but the "memory" of how to use the power is lacking or diminished. Steps are small, slow, and uncertain, and the patient must be urged or assisted to initiate progress. The gait is typical of frontal lobe lesions or bilateral lesions of the corticospinal tract in the internal capsule, cerebral peduncles, or high brainstem.

3.   A cerebellar gait resembles the actions of an intoxicated person. The patient walks with the feet wide apart, takes short steps, and sways to and fro so that progression in a straight line is almost impossible. The gait is found in tumor of the cerebellum and disease of the semicircular canals. It may suggest chronic use of alcohol or other drugs (jake legs) or neurosyphilis. The gait resembles that of a person trying to walk on a rolling ship, constantly trying to maintain equilibrium with little success. Cerebellar lesions are invariably associated with vertigo. When the cause is a unilateral lesion, deviation is to the involved side because of the hypotonia.

4.   A propulsive gait, also called festination, is characteristic of paralysis agitans or Parkinson's disease. The body and head lean far forward, and the subject walks with short, hurried, shuffling steps making it appear as if he is being pushed from the rear and about to fall. Progression is slow at first, and then increases rapidly. It is difficult for the patient to stop suddenly or to turn a corner. The hurried "sissy" tottle of parkinsonism is due to the forward tilt of the trunk in the attitude of a stoop and the attempt of the patient to maintain balance.

5.   A senile gait is caused by shortening and loss of elasticity of ligaments and tendons, and a stiffening of cartilage, muscle, and fascia because of degenerative aging processes. Steps are short, shuffling, and assumed in a stooped position if osteoporosis is present and causing a marked dorsal kyphosis.

6.   A spastic gait is common in upper motor neuron diseases that have a spastic paralysis of the extensor muscles. This gait is characteristic of spinal paralysis, lateral sclerosis, and some other forms of myelitis and anterior tract or brain damage. The legs are firmly extended, the foot is dragged along in a shuffling manner with the toes scraping upon the ground to permit one foot to pass the other, and the pelvis is tilted slightly. The upper extremity is flexed while the lower extremity is extended. Sometimes the adductors contract causing the legs to cross (scissors gait), and the knees often rub each other. This is seen in Little's disease, a congenital spastic stiffness of the limbs, a form of cerebral spastic palsy resulting from agenesis of the pyramidal tracts. There is a unilateral spastic gait in spastic hemiplegia in which the pelvis is tilted and the leg is swung around in front of the other with the toes often scraping the ground; sometimes referred to as a "mowing" gait. The most common cause is hemiplegia due to cerebrovascular disease, but any condition that produces an upper motor neuron lesion can produce the gait.

7.   A steppage gait is a prancing, high-stepping, foot-drop gait. The gait resembles that of a person walking in tall grass, hence its name. The gait is especially suspect of tertiary syphilis. It is often found in infantile paralysis, multiple neuritis, peroneal nerve injury, and arsenic poisoning paralysis, The flexor muscles of the foot are so flaccid that the toes hang downward when the foot is raised from the floor. To prevent the toes from dragging on the floor or catching upon objects, the foot is raised high and brought to the floor forcibly before the toes can drop; thus, the foot strikes the floor heel first.

8.   The waddling gait occurs when there is extreme muscular weakness in the thigh and hip muscles as commonly found in pseudohypertrophic muscular paralysis and muscular atrophy or dystrophy. It is also seen in bilateral hip dislocation. When walking, the subject swings from side to side in a very noticeable manner; thus, it is often referred to as the goose gait. The shoulders are thrown back, the lower section of the spine is hyperlordotic, the pelvis is tilted greatly, and while in this state, the leg is brought around and placed on the floor.

Pain and Related Symptoms

Many diseases begin either with pain or have pain as a prominent symptom at some time during their course. Thus, a correct diagnosis can hardly be made without an intensive study of the symptomatic expressions of pain, To have any sensation (eg, pain, temperature, sight, touch, smell, proprioception, hearing, taste), it is first necessary that the sense-receptive organs are intact, the sense-conveying organs normal, the sense-interpreting centers active, and the associative memory centers (consciousness) intact. Any type of sense-receptive organ will register pain when irritated or hyperstimulated, and any somatic, visceral, or mental stimuli that are inimical to the well-being of the organism will provoke pain.

The sensation of pain has three general components:

(1) reception of the pain stimulus by the pain receptors and conduction of impulses by sensory nerves,
(2) perception of pain in the higher brain centers, and
(3) reactions to the pain such as physical, emotional, and psychologic responses.

The acuity of pain sensation interpreted depends greatly on the degree and clarity of consciousness possessed by a particular individual; ie, the greater the degree of mentality, the greater degree of estimating and interpretive capacity of the individual. Other factors determining pain sensitivity are ethnic dispositions, temperament, general integrity of the nervous system, attitude and circumstance, age, and factors affecting one's pain threshold.

One's pain threshold may be lowered by

(1) chronic fatigue from spinal distortions, neuromuscular strains, and overwork;
(2) psychogenic stress from worry, frustration, guilt, and anxiety; and
(3) subclinical toxic irritations from catabolic accumulations, elimination deficiencies, dietary indiscretions, and nutritional deficiencies.

On the other hand, the pain threshold may be increased by a state of physical and mental well-being free from fatigue or stress. It is also increased in high levels of stress (eg, battle).


Classifications of Pain

Pain may be viewed according to

(1) time of occurrence, as in posttherapy pain;
(2) duration or length of time experienced, as in acute or chronic pain;
(3) intensity, such as in mild pain or severe pain;
(4) causative agent, as in self-inflicted pain or spontaneous pain;
(5) mode of transmission, as in referred or projected pain;
(6) ease of transmission, as in inhibited or facilitated pain;
(7) location, as in superficial, deep, or central pain;
(8) source, as in gallbladder or sacroiliac pain;
(9) manner experienced, as in sharp, burning, or dull pain; or
(10) general causation, as in organic, pretended, or psychogenic pain.

From another viewpoint, pain can be classified into the two general divisions of subjective pain and objective pain:

(1) Subjective pains are those having no organic cause; rather, they arise through a mental process. Subjective pain can be subdivided into emotional pains, hysterical pains, habit pains, and occupational pains.
(2) Objective pains are those arising from some foreign agent or condition that is abnormal to the area in which it is excited.

Objective pain can be divided into central objective pain and peripheral objective pain. Central pain is pain for which no peripheral cause exists at the time the pain is perceived by the patient. Peripheral objective pain may be either intrinsic or extrinsic. Examples of intrinsic pain are the parenchymatous type that arise from inflammation, masses, colic contractions, or displacements. Examples of extrinsic pain are those that register from pressure on nerves or nerve terminals such as new growths, entrapments, swollen organs, tensed tendons, stretched ligaments, and contracted muscles.

Peripheral pain can be divided into superficial pain and deep pain syndromes. Superficial pain usually has a prickling or burning quality and usually has a sudden onset. It is relatively uncomplicated because it is directly perceived and can be readily localized. Associated symptoms may include hyperalgesia, paresthesia, analgesia, tickling, itching, brisk movements, rapid pulse, and a sense of invigoration. Nausea is rarely, if ever, associated. The quality of pain is a sharp, bright sensation felt superficially, Its duration is typically shorter than that for deep pain, and localization tends to be more precise than that for deep pain. Pain produced by external pressure results from trigger points, traumatic lesions of sensitive subdermal tissue, or the development of a toxic accumulation or deep-seated inflammatory irritation.

Deep pain originates in structures far below the surface, Three varieties occur:

(1) true visceral (splanchnic) and deep somatic pain, which is felt at the point of noxious stimulation and may or may not be associated with referred pain;
(2) referred pain, which is pain experienced at a site other than the area of stimulation; and
(3) pain from secondary skeletal muscle contraction.

True visceral pain comes from a diseased organ. Deep somatic pain is characterized by its segmental distribution and originates from a lesion of vertebra, muscle, or other neuromuscular origin. Referred pain is projected from a viscus or other structure deep to the surface of the body. Secondary skeletal muscle contraction causes pain from spread of excitation within the spinal cord. Associated symptoms of deep pain are mainly those of autonomic response as sweating, nausea, vomiting, and at times low blood pressure, bradycardia, syncope, faintness, hyperalgesia, tenderness, and perhaps shock or abdominal muscular rigidity. The quality of pain is primarily dull, aching, but it may be boring, crushing, throbbing, or cramping. Its duration is often quite long, Localization is often diffuse over a fairly broad area.

Some authorities divide the overt and covert signs and symptoms of pain into two groups: those essentially of sympathetic or parasympathetic origin:

Pain sympathetic in origin.     This pain occurs when the vital functions are excessively stimulated. A basically sympathetic response occurs with pain from low to moderate intensity or superficial pain. Observable signs and symptoms include pallor, elevated blood pressure, dilated pupils, skeletal muscle tension, and increased respiratory and heart rates.


Pain parasympathetic in origin.     This pain occurs when vital functions are excessively depressed. A basically parasympathetic response arises with pain of severe intensity or deep pain. Observable signs and symptoms include pallor associated with decreased blood pressure, contracted pupils, nausea and vomiting, weakness and fainting, prostration, and possible loss of consciousness.

Tenderness.     A frequently encountered associated sensory symptom is tenderness, which may be defined as pain upon pressure. Some conditions cause tenderness when pressure is exerted, but no abnormal sensation is felt when there is no pressure.

Paresthesia.     Besides pain and tenderness, another type of abnormal sensation is paresthesia: perverted sensations or uncomfortable sensations not amounting to pain. The most common paresthesias are sensations of weight (pressure), bearing down, fullness, coldness, faintness, itching, girdle sensation, numbness, tingling, precordial constriction, and weakness.

Temperature

Body temperature results from the balance between heat generation and heat loss, determined by the set point of the temperature-regulating center of the hypothalamus. Temperature is highest at the center of the body, diminishing toward the periphery. When temperatures rise above the set point, the body compensates through peripheral vasodilation, sweating, and hyperventilation to enhance heat loss. When temperatures fall below the set point, the body compensates by increasing the metabolic rate, tensing the muscles, and shivering to promote heat generation. It must be determined if the cause of abnormal body temperature is a dysfunction of heat production, heat loss, or of the hypothalamic thermostat.

Temperature Ranges.   Average human oral temperature is 98.6°F (37°C) with daily variations from 97°F around 4 am to 99.6°F near 6 pm, plus or minus 1°F. In fever, this variation is often exaggerated. In the elderly and in miliary tuberculosis, the daily variations may be reversed. Normal functions as emotional excitement, exercise, digestion, ovulation, pregnancy, or being in a hot room may result in a slight temperature rise. The rectal and vaginal temperatures are about 1°F higher than oral, and axillary or groin temperature is about 1°F lower than oral temperature. Pulse rate increases about 10 beats per minute for every 1°F rise in temperature. Respiratory rate increases 2 or 3 per minute for each degree of temperature rise.

Hyperthermia.   Any form of hypermetabolic condition can create a fever through increased heat production. Interference with sweating also interferes with normal heat loss. The most common cause of fever, however, is a change in set point of the hypothalamic thermostat. For an unknown reason, infections and inflammatory processes cause the hypothalamic temperature center to become less sensitive to heat. A rise in temperature is commonly associated with such disease processes as infection, cancer, and autoimmune disorders.

Features of Simple Fever.   Simple (mild--moderate) fever may present symptoms of a hot dry skin, flushed face, dry mouth with excessive thirst, malaise, lassitude and languor, anorexia, nausea and vomiting, costiveness of the bowels, scanty highly colored urine, weakness, headache and backache, increased pulse rate, quickened respiration, and frequently herpes simplex. There may be cerebral symptoms in high fever of delirium, stupor, or coma, and a suppression of body secretions. Fever or feverish conditions are attended by a relative preceding sensation of chilliness or by a chill with rigors.

Classes of Fever.   Body temperature between 99°F and 100°F is spoken of as feverishness; a temperature between 100°F and 101°F as slight fever (hyperthermia); 101°F to 103°F, moderate fever; 104°F and 105°F, high fever. A temperature above 106°F (hyperpyrexia) is considered a grave symptom.

Hypothermia.   Subnormal body temperature results from poor heat production or a thermostat abnormality, very rarely from exposure to cold unless alcohol or drugs are in the body. Hypothermia is produced whenever the central nervous system is depressed from drugs, primary brain disease, or toxins that alter the internal thermostat.

A temperature below 98°F (hypothermia) is a common occurrence immediately after the fall of fever by crisis and also observed in shock and collapse. A subnormal morning temperature with a persistent rise during the afternoon is highly suggestive of tuberculosis. In malnutrition, valvular heart disease, myxedema, diabetes, cancer, comatose patients, drug intoxication, metabolic acidosis, and epilepsy, a large number of cases will show subnormal temperatures.

Respiratory Rate and Rhythm

Respiration consists of the exchange of oxygen and carbon dioxide between the atmosphere and the body cells, including inspiration and expiration, diffusion of oxygen from alveoli to the blood and of carbon dioxide from the blood to the alveoli, along with the transport of oxygen to the body cells and carbon dioxide from the cells.

Normal respiratory rate at birth is 44 per minute. At the 5th year, it is 26 per minute; and in the adult, it levels off near 18 per minute. A rate increase or decrease from this at rest is considered abnormal as are variations in depth, regularity, and effort. The ratio of the pulse to respiration is 4 to 1 in the adult.

Note the type of breathing (thoracic or abdominal), degree of respiratory expansion, signs of respiratory bulging or retraction, respiratory rhythm, or signs of dyspnea. Signs noted during inspiration and expiration such as abnormal rate or depth of breathing may point to serious impairment in the control system from a defect in the brain, pulmonary apparatus, blood flow, or blood pH balance. Besides breathing rate and depth, determine the type of respiration (thoracic or abdominal), degree of chest expansion, type of respiratory rhythm, and note if signs of dyspnea exist. See Figure 2.4.

Respiratory Control.   Control centers for respiratory rate and rhythm are located in the brain, certain blood vessels and sinuses, in the pulmonary apparatus, and in muscles and joints. Brain centers (essentially medullary) are sensitive to carbon dioxide tension or blood pH changes; peripheral sensors control through pressure and stretch receptors sensitive to blood pressure fluctuations and oxygen tension. They control by increasing ventilation such as seen in pain, emotional states, anxiety and apprehension. The respiratory centers are highly responsive under all forms of mental stress. Thus, anger, joy, and excitement are associated with an increase in the respiratory rate. Very rapid respiration is often associated with hysteria.

Hypoventilation, a combination of shallow respirations and bradypnea, is usually associated with CNS disease, primary or metabolic. Underventilation results in decreased breathing rate and depth due to any factor reducing the sensitivity of the medullary centers such as from carbon dioxide retention or drugs. Intrinsic pulmonary disease and oxygen therapy may result in chronic hypercapnia leading to symptoms of lethargy, headache, disorientation, and ending in coma. On the other hand, anxiety, lung disease (eg, pneumonia, pulmonary emboli), or congestive heart failure may result in hyperventilation. Overventilation is often associated with symptoms of respiratory alkalosis (eg, finger tingling, oral numbness, vertigo, syncope). Rapid deep respiration is often related to metabolic acidosis and aspirin poisoning.

Clinical Features of the Pulse

Both radial pulses should be felt simultaneously as a matter of habit so errors may be avoided in appreciating differences in the two pulses. When the tips of three fingers (never the thumb) are placed on an artery, note

(1) the rate of the pulse,
(2) the rhythm of the pulse,
(3) the amount of force necessary to obliterate it (compressibility),
(4) the size and shape of the pulse wave,
(5) the size and position of the artery, and
(6) the tension or firmness of the artery's walls.

Much information can be learned by comparing and associating pulse rate, pulse rhythm, pulse amplitude, contour of the jugular vein, and the 1st heart sound. Delay in one radial pulse when taken in connection with other signs may furnish decisive evidence of aneurysm of the aortic arch because arterial degeneration may betray its presence chiefly in the peripheral arteries.

      Pulse Rate

The typical pulse rate is about 72 per minute in the male and 80 in the female, with normal variations extending from 60 to 100 per minute in some patients. Pulse rate at birth averages about 130; and until the 3rd year, it is usually above 100. In some families, a slow pulse (60 or less) is hereditary; as may be a permanent pulse rate of 90 or more. Some young patients may exhibit sinus arrhythmia: a mild variation in rate of no clinical importance.

Pulse rate varies considerably from patient to patient and is normally increased in apprehension (eg, during examination) and during pain. Exercise, eating, and emotions markedly quicken the pulse. Increased vagal tone reduces both heart rate and blood pressure. Fever exhibiting a slow pulse (very unusual) is seen in some enteric infections in which there is an increase in vagal tone. A general rule in relating fever with tachycardia is that an increase of 10 beats per minute can be anticipated for every degree of temperature increase. A rate increase greater than this points toward an additional disease.

Reduced metabolic demands produce slow heart rates, while increased demands for oxygen, heart disease, increased circulating catecholamines, and a decreased blood volume result in tachycardia, as do common stimulants such as coffee, tea, cigarettes, and many drugs. A compensatory tachycardia results from any disorder that reduces the ability of the heart to pump blood.

      Pulse Rhythm

Beat-to-beat variations in pulse amplitude usually result from changes in left ventricular stroke volume into the central aorta initiating the pulse wave transmission to an unobstructed peripheral pulse. The pulse may be irregular in rhythm or force, but it is usually irregular in both respects. As a rule, irregularities in force are the most serious, whether occurring as alteration or in the absolute type of arrhythmia associated with auricular fibrillation. Intermittence or irregularity in rhythm by itself is much less ominous.

It may be generally stated that
(1) irregularity in the force of pulse beats is a serious sign if overexertion and temporary toxic influences (tobacco, coffee, etc) can be ruled out,
(2) it is far more serious when occurring with diseases of the aortic valve than in mitral disease, and
(3) it often occurs with sclerosis of the coronary arteries and myocardial weakening.

A regular pulse with a constant amplitude does not prove cardiac health. Atrial flutter and atrial tachycardia can be related to a pulse rate well within the normal range. A regular pulse rhythm and a constant pulse amplitude associated with a slow rate may represent several rhythms, as seen when a premature beat is unpalpable. Conversely, a regular pulse rhythm and a constant pulse amplitude related to a rapid rate may point toward sinus, atrial, junctional, or ventricular tachycardia.

      Vascular Tension

When arteries are contracted and small, the pulse wave corresponds; but if they are large and relaxed, only a moderate degree of power in the heart is needed to produce a high pulse wave. When tension remains constant, the size of the pulse wave depends on the heart's contraction. Conversely, when heart power remains constant, the size of the pulse wave depends on the degree of vascular tension. Vascular tension is estimated in the diastolic blood pressure reading; and once it is allowed for, the power of the heart's contractions can be estimated from the height of the pulse wave.

Pulse tension results from diastolic arterial pressure. The degree of contraction of the vascular muscles determines the size of the functional artery and to a great extent the pressure of the blood within it. But if the heart is acting feebly, there may be so little blood in the arteries that even when tightly contracted they do not subject the blood within them to any large amount of tension. Thus, to produce high tension, two factors are necessary: a degree of muscle power in the heart and arteries. To produce low tension, only arterial relaxation is necessary, and the heart may be either strong or weak.

Any anatomical change in the arterial walls (eg, arteriosclerosis) that chronically diminishes their elasticity is manifested in the peripheral arteries (especially the brachial) in the following forms:
(1) simple stiffening of the arteries without calcification,
(2) tortuosity of the arteries, and
(3) calcification. Simple stiffening without calcification is due to fibrous thickening of the intima and produces an arterial condition that is almost impossible to manually distinguish from high tension.

      Thrills and Bruits

It may be possible to palpate low-frequency thrills within a vessel wall that indicate a turbulent flow of blood within the vessel. Thrills may originate within the vessel being examined or be transmitted from a site proximal to the palpating finger. Palpable thrills and auscultated bruits are caused by any condition that disturbs normal laminar blood flow. In aortic insufficiency and hyperkinetic states, carotid pulsations may be striking. A carotid thrill is often noted in cases of aortic stenosis and situations where the carotid artery is partially occluded. Conversely, diminished or absent carotid and brachial pulsations may be present when the aortic arch or its major branches are involved in a diffuse process such as aortitis, aortic aneurysm, arteriosclerosis, or congenital anomalies.


Jugular Pulse

The action of the heart can also be appreciated by examination of the contour of the pulse of the jugular vein while auscultating the intensity of the 1st heart sound. The tricuspid valve normally opens when the right atrium contracts, and the pulse of the jugular vein coincides with this contraction. However, a large "booming" type jugular wave and intense 1st heart sound result if both the right atrium and right ventricle contract when the tricuspid is closed. This occurs because the shorter the ventricular "filling time" the more intense the 1st heart sound, and vice versa. A shortened ventricular filling time may be the result of a shortened cycle interval or an increased heart rate, or a combination of both. Such rhythm abnormalities may be occasional or frequent, depending on the underlying cause and its degree.


Blood Pressure

      Production Factors

Blood pressure results from two forces in the vascular system identified as the propelling and the resisting forces. The average adult heart contracts 75 times per minute, and each contraction forces about 3 ounces of blood into an already filled arterial system, inducing arterial wall stretching. The pressure produced by the intermittent contraction of the heart is the propelling force.

Measured blood pressure is the product of cardiac output times peripheral resistance. Any given elevation in pressure may be the result of high flow and low resistance or low flow and high resistance. The long-term determinant of blood pressure is fluid intake counterbalanced by fluid excretion. Short-term determinants include the baroreceptor-activated reflexes in the heart, aorta, and carotid sinuses, the kidney and adrenal angiotensin-aldosterone systems, and the intravascular and interstitial fluid shifts.

Four main factors increase systolic pressure in a natural way: exercise, emotions, stimulants, and food. Some things ingested (eg, coffee) are always stimulative, and all foods have a relative stimulative effect. Normal activity is a form of exercise; and all humanity is more or less emotional. These conditions raise the blood pressure by increasing the rate of the heart or slightly increasing the tension of the arteries. Their effect is temporary. Clinically abnormal blood pressure is always persistent. It does not vary greatly from day to day nor at different times in the day.

      Hypertension

Increased arterial tension throws added work on the heart and results in its hypertrophy. The action of the hypertrophied left ventricle is the cause of increased systolic pressure. This in itself is not dangerous since the hypertrophy is adaptive to increased peripheral resistance. Conditions that increase the peripheral resistance diminish the elasticity of the artery wall and thus destroy its integrity. In time, the weakened part yields and either stretches producing an aneurysm or ruptures permitting blood to escape.

In hypertension, arterial lumina are smaller and more force is required to stretch them. Hypertension may be caused by the action of toxic substances in the blood stream that irritate and injure the delicate nerve endings. Pain, intracranial pressure, meningitis, and encephalitis induce a rise in blood pressure due to hypertension. A hypertonic state of arteries or arterioles throughout the body constitutes a state of systemic hypertension that may occur exclusively from nerve irritation.

High blood pressure due to hypertension is commonly found in nephritis, but it also occurs in diabetes mellitus, increased intracranial pressure, toxic thyroid, angina pectoris, and impending uremia. When systolic pressure is persistently 180 or over, an impermeable kidney is suspect. The function of the kidney may become subnormal long before kidney structure begins to deteriorate. Thus, urine examinations will not disclose the nature of a failing kidney in its early stages.

In essential hypertension, an elevation in blood pressure may be the only abnormality that can be discovered. It affects either gender and people of all body types, but it predominates in those inclined to be fleshy. It is also more common among people who live under high tension (eg, occupational or emotional stress). The peripheral arteries in all parts of the body are contracted. These include those of the kidney, which may well occur in advance of vascular spasm elsewhere. Restriction of blood flow through the kidney impairs proper filtration of impurities and the elimination of toxic substances. Pioneer chiropractors felt interference with the flow of vasodilating impulses through the lower thoracic nerves is a chief cause. In advanced cases, the kidney is structurally damaged even if urinary pathology is absent.

      Arteriosclerosis

Arteriosclerosis may result from infections and toxic diseases, or it may be preceded by hypertension. The lumen of the artery is diminished by a thickening of its wall. This thickened wall may later be the site of cholesterol and calcareous deposits (atherosclerosis), which further destroy elasticity. Structural changes developing in the arterial system tend to spread to and involve the heart. This weakens the circulatory pump and thereby limits the extent to which the systolic pressure can be raised. High systolic pressures are occasionally encountered in arteriosclerosis, but more often the systolic pressure is less than 170. The continued development of fibroid, fatty, and other changes in heart muscle may permit blood pressure to become subnormal even in the presence of sclerosed arteries.

      Hypotension

Abnormally low blood pressure is due to a decrease in the resisting or propelling force, or both. It may be caused by a decrease in the amount of blood (eg, extensive hemorrhage). Profound anemia tends to produce fatty degeneration of the heart and blood vessels; consequently, it is a cause of low blood pressure. Low blood pressure is also associated with dilatation of the heart and chronic myocarditis (a generic term that includes both inflammatory and degenerative processes of the myocardium).

Several conditions tend to reduce diastolic pressure. Aortic aneurysm severely reduces diastolic pressure, but it may be associated with hypertrophy of the heart that raises systolic pressure. Aneurysm of the aortic arch between the innominate and left subclavian arteries is a common cause for a wide variation in the blood pressure of the two brachial arteries. Dysentery, hemorrhage, and large effusions into the serous cavities lower blood pressure by decreasing the volume of fluid in the circulation. The most common states giving extremely low blood pressure readings are shock, collapse, internal hemorrhage, and toxic paralysis of the vasomotor center. Wasting diseases lower blood pressure because of the weakening of the vital circulatory organs and dehydration of tissues.


Weight and Height

A patient's general appearance can offer an overview of endocrine function in many instances. This is because of the important role the endocrines play in growth and maturity processes where abnormal signs in size and shape are important. In appreciation of the vital signs, the endocrines are important in energy production, temperature regulation, pulse rate, blood pressure, and homeostasis.

Assessment of a patient's weight and height is important if the patient's general appearance leads one to suspect that a malfunction or structural disease process is being manifested. An obvious underweight patient directs the examiner to consider all the causes of weight loss. In symmetrical overweight, evaluate possible diabetes or hypoventilation; Cushing's syndrome if the weight distribution is asymmetrical. When an unusually tall and lanky frame is presented, Marfan's syndrome is suspect. Temporal or interosseous muscle wasting leads one to consider all causes of weight loss.

Weight change dues to an involuntary gain or loss of more than 7% in 1 year is often associated with polyphagia or anorexia:

1.   Weight change related to polyphagia refers to a weight gain of fat frequently associated with depression, a change in life-style, a nutritional deficiency, or a metabolic disturbance. Weight loss related to polyphagia is highly suspicious of diabetes mellitus or hyperthyroidism.

2.   Weight loss related to anorexia is associated with severe illnesses such as cancer, malabsorption, infection, anorexia nervosa, hepatitis, severe depression, and esophageal disease. However, even if there are anorexia and a decreased food intake associated with a serious systemic disease, there may be no weight loss because the loss of protoplasm weight may be compensated by an increase in interstitial fluid mass weight. In cirrhosis, severe muscle wasting is often balanced in terms of weight by associated ascites. In the average person, the pleural, peritoneal, and subcutaneous fluid spaces can easily hold from 5 to 11 pounds of fluid.

The Cranium and Face

Inspect size and shape of the cranium for signs of microcephalia, hydrocephalus, rickets, cretinism, Paget's disease of bone, myelomata, and cranial metastasis. Note bulging or depression of the fontanels. Check abnormal patterns of hair loss, skin lesions, signs of pediculi, scars, and bony nodes. Auscultate for cranial and orbital bruits.

Seek general signs in the face of dehydration, edema, cyanosis, jaundice, chloasma gravidarum, and skin lesions. Evaluate signs of anxiety, exophthalmic goiter, paralysis agitans, lower lid renal puffiness, mouth breathing, unilateral facial palsy, tongue protrusion, skin color, and abnormal movements of the head and face. Check lip color and for mouth lesions, scars, lumps, edema, telangiectasis, and hyperpigmentation.


The Nose and Sinuses

Externally inspect nasal shape, humps, broadness, unusual length, distortions and deformities, bridge depression, scars and pits, skin growths, drooping tips, discolorations, dilated vessels, and nostril size.

Internally inspect nasal patency. Look for septum deviation or other airway blockage that may obstruct a passage, signs of epistaxis, perforations resulting from chronic irritation or trauma, gummatous destruction, allergic congestion, or other abnormalities. See Figure 2.5. Note color of the nasal mucosa and judge whether the turbinates are normal, hypertrophic, or atrophic. If a nasal discharge is present, classify it as watery, mucous, mucopurulent, purulent, or bloody.

Palpate the bony and cartilaginous junctions of the nose, the roof of the orbit of the eye, the ascending processes of the maxillae, and the canine fossa. Transilluminate the sides of the nose for masses and the maxillary and frontal sinuses. Percuss the paranasal sinuses (maxillary and frontal) for tenderness.


The Nasopharynx and Laryngopharynx

Signs of inflammatory disease, neoplasms, polyps, cysts, and congenital defects may be found in the nasopharynx. Changes in voice resonance will usually be traced to an obstruction (inflammatory or neoplastic mass) in this area, as will hearing loss and otalgia from obstruction to the eustachian tube's orifice. Obstruction causes a negative middle-ear pressure leading to serum transudation into the middle-ear chamber.

Examine the nasopharynx with the aid of a warmed mirror directed up and behind the uvula. Look anteriorly from the nasopharynx into the nose, and note the posterior border of the nasal septum dividing into the two choanae. View the posterior tips of the middle and inferior turbinates, Rosenmueller's fossa, torus tubarius, and the salpingopharyngeal fold. Adenoidal tissue will be seen in the upper posterior wall of the nasopharynx. If this tissue is hypertrophied, the posterior aspect of the nasal passages will be obscured. The eustachian tubes will be seen laterally. Keep in mind that what you see in the mirror is a reverse image. A mass of lymphoid adenoid tissue (pharyngeal tonsil), present on the posterior wall up to the age of about 16 years, connects with the palatine and lingual tonsils by a band of lymphoid tissue extending down the lateral wall of the pharynx. Note the quantity and quality of the mucous blanket, and test the gag reflex.

Invert the mirror and inspect the laryngopharynx. The intrinsic muscles of the larynx can be observed as they act on the larynx's cartilaginous framework to relax, tense, adduct and abduct the local cords. The larynx can be brought up and backward to be visualized by asking the patient to say "ah" and "eee." Inspect the base of the tongue, the lingual tonsils, the epiglottic tubercle, aryepiglottic fold, the vestibular fold, the laryngeal sinus, the false and true vocal cords, and the cuneiform tubercle. The image in the mirror is up-side-down; ie, the epiglottis will appear on top and the posterior pharyngeal wall will appear at the bottom of the mirror.

Laryngitis.   In acute laryngitis, the local mucosa will appear red and edematous, the vocal cords will change from their normally pearly white color to a pale or bright red depending upon the severity of the disorder and its stage. The cords may be webbed with secretions, and coughing may have produced ecchymotic spots. Repeated infections, heavy smoking, mouth breathing, and overuse of the voice lead to chronic laryngitis featured by pale, boggy, congested cords that are webbed with secretions. Tubercular laryngitis presents pallor and ulceration of the laryngeal mucosa.

Hoarseness.   Hoarseness of at least over 2 weeks in duration is the chief reason for conducting a laryngopharynx examination. Besides laryngitis, hoarseness may be the result of partial paralysis from a unilateral recurrent laryngeal nerve lesion, larynx carcinoma, a benign tumor, or a congenital defect. Paralysis may be the product of trauma, an inflammatory disorder, neoplasm, CNS lesion, or vascular abnormality affecting the nerve. Hoarseness is often the first sign of larynx carcinoma and associated with throat pain, dysphagia, stridor, cervical adenopathy, thyroid cartilage widening, hemoptysis, and halitosis.

The Oropharynx

Evaluate the jaw muscles, mucosa of the cheek, teeth, occlusion, gums, salivary duct orifices, the palate, the floor of the mouth, the tongue, the tonsils, and the salivary glands. Inflammation, often bacterial, usually presents with edema, ulceration, and a purulent exudate. The color of oropharyngeal tissues will normally vary from pale pink to red.

The mouth, the "mirror of the body," frequently offers the earliest signs of many degenerative, nutritional, and metabolic diseases that sometimes appear many months prior to other manifestations. See Figure 2.6. Use a tongue blade to retract the lips and cheeks. Use a penlight or direct reflected light from the head mirror to the mouth recesses, inner cheeks, and lips. Inspect the tonsils and immediate pharynx area for signs of inflammation, ulceration, or swelling.

Move the protruded tongue laterally and inspect and gently palpate (use a finger cot) the dorsolateral border of the tongue for a mass (common site) with the cheek retracted with a blade. Judge the tongue for color, moistness, papillae condition, coat, ulceration and cancers, fissures, muscle movements, tremor, atrophy or hypertrophy, macroglossia, leukoplakia, and epithelial desquamation. Release the tongue and continue to palpate the floor of the mouth, cheeks, lips, and hard and soft palates with the opposite hand supporting the jaw. Have the patient touch the roof of his mouth with the tip of his tongue while his mouth is open. Inspect the undersurface of the tongue and the anterior surface of the mouth. Palpate the base of the tongue and the entire floor of the mouth. Lesions not observed are often found by palpation. Palpate the submandibular and cervical lymph nodes for adenopathy.

Teeth.     Evaluate teeth for form, occlusion, and hygiene. If mobile teeth are felt on palpation, it suggests advanced periodontal disease when trauma can be ruled out. Localized looseness is an early sign of primary or secondary neoplastic alveolar bone destruction, as is acquired malocclusion of the jaw. A blue-grey tooth is likely dead from an old infection. Five-pointed bicuspids (mulberry teeth) and notched incisors (Hutchinson's teeth) are characteristic of congenital syphilis. Hutchinson's "screw-driver" teeth appear late or a child may be born with them already erupted. A painful dental disorder may be isolated by lightly tapping the suspected tooth with a mirror handle. A tooth normally has a dull, limited sound on percussion; when ankylosed to the alveolar, it becomes more resonant.

Gums.     Check gums for bleeding, pigmentation along gum line, sponginess, gingivitis, hypertrophy, suppuration about the roots of teeth, alveolar abscess, epulis, and sordes. Evaluate the breath for characteristic odors of abscess, diabetes, uremia, or alcohol.

Mucous Membranes.     Inspect the mucous membranes for salivation quality, color abnormalities, swellings and cysts, ulcers, patches, spots, and other lesions. Inspect the submaxillary, sublingual, and parotid ducts and observe the amount of flow and appearance of the salivary secretion. The floor of the mouth may indicate sublingual gland retention cysts. Palpate the glands. A stone in the submaxillary duct will present obstruction symptoms and signs, especially after drinking something sour.

The Palate.     Inspect the shape and appearance of the hard palate. The function of the soft palate is tested by the pharyngeal reflex. The first trace of jaundice may be seen in the palate. Exostosis of the mandible will be seen and felt as a hard mass projecting inferiorly from the bone supporting the premolar teeth. A similar benign mass in the midline becomes more prominent with aging atrophy, especially when the natural teeth are gone. It is also a common (20%) congenital defect seen in the young. A malignancy is the first suspicion of any mass not in the midline. Sometimes malignancy of the posterior palatal vault will be revealed only by palpation and felt as a submucosal nodular swelling. A high-arched palate is characteristic of congenital defect and mouth breathers with nasal obstruction. Cysts in the anterior third of the palate are associated with the nasopalatine canal. In subacute bacterial endocarditis, the palate will commonly show evidence of microemboli appearing as tiny petechiae. Chronic irritation by nicotine may present a stomatitis characterized by elevated accessory salivary glands that have dilated red orifices.

The Uvula.     Note the size, color, length, and any deviation of the uvula. A swollen uvula, with transparent edema of its tip, often complicates a pharyngitis or any lesion with violent cough. Elongation of the uvula may bring it into contact with the tongue and excite cough by tickling. In viral pharyngitis, small vesicles surrounded by erythema will be seen.

The Sputum.     Examine the sputum and determine its composition, color, odor, and quality. Sputum is usually scanty in dry inflammations of the bronchial tubes, pleura, larynx, and in asthma. Sputum is abundant in chronic inflammation of the bronchial tubes, lungs, and larynx. Record the quality of sputum as watery, viscid, mucous, purulent, rusty, yellow or green. Distinguish between hemoptysis and hematemesis.

The Temporomandibular Joint

Jaw sprain is often the result of improper dentition or dislocation from trauma. Relative muscle strain, capsule and ligament sprain, muscle spasm, and soft-tissue swelling may be involved depending on the extent of injury. Poor occlusion leads to a chronic sprain or strain as does bruxism. Overstress results in pterygoid spasm and an asymmetric lateral motion of the jaw. Restricted joint motion is the result of muscle spasm, rheumatoid arthritis, osteoarthritis, joint ankylosis, scar tissue, trismus from spasm of the elevating muscles of mastication from any type of local inflammation, hysteria, tetanus, or congenital defect. TMJ dysfunction usually presents with a unilateral dull ache of gradual onset, pain aggravated by chewing, a joint click felt or heard, deviation of the jaw to one side, tenderness and muscle spasm, a nervous bruxism, and pain on opening and closing the mouth.

Evaluate active joint motion by having the patient open and close his mouth and observe the movement of the mandible from the front and sides. Motion rhythm should be smooth, the arc should be continuous and unbroken, and the mandible should open and close in a straight line symmetrically, with the teeth easily separating and joining. An awkward arc, restricted range of motion, and lateral deviation during motion suggest an abnormality.

Place the index finger of each hand in the patient's external auditory canals and apply pressure anteriorly while the patient opens and closes his mouth. Movement of the mandibular condyles will be felt on the fingertips. It should normally be smooth and equal on both sides. Then palpate the lateral aspects of the joints by placing the first and second fingers just anterior to the tragi, have the patient open and close his mouth, and note any abnormalities. A palpable crepitus suggests traumatic synovial swelling or meniscus damage, and a slight dislocation (painful) may be felt when the patient widely opens his mouth. If there is any doubt of the presence of crepitus, auscultate the joint for clicks or grating sounds.

The adult range of motion is usually normal if

(1) the examiner can insert three finger widths between the incisor teeth when the mouth is opened and
(2) the patient can jut his jaw forward and place his lower teeth in front of his upper teeth.

Continue by palpating the middle fibers of the temporalis muscles between the eye and the upper ear. Palpate the body portion of the masseter muscles. Palpate the external pterygoid muscle by having the patient open his mouth.

Place a gloved index finger posteriorly above the last molar, between the gum and the buccal mucosa, on the mandibular neck. The external pterygoid will normally be felt to tighten and relax as the patient opens and closes his mouth. The patient will report tenderness and pain during palpation if the muscle has been strained or is spastic. Palpate the internal pterygoid muscle intra- and extra-orally simultaneously. Palpate the mylohyoid muscle beneath the tongue. Check the related posterior cervical, sternomastoideus, and trapezius muscles for spasm and tenderness during examination of the neck and cervical spine.

Judge muscle strength by placing one hand on the patient's occiput to steady the patient's head and your other hand, palm up, under the patient's jaw. Ask the patient to open his mouth while applying resistance with your palm. The patient should be able to open his mouth against increasing resistance of your palm. If the patient is unable to close his mouth actively, try to close it passively.


The Ears

Inspect the lateral and medial surfaces of the auricle and the lateral mastoid process for abnormalities. Determine tenderness in the auricle by pulling it in all directions and in the tragus by pushing it. In mastoiditis, tenderness over the mastoid antrum is associated with the ear projecting farther from the head than normal. In palpating the antrum, bend the ear forward with one hand and insert the index finger of the other hand into the triangular depression between the mastoid process and the attachment of the ear on a level with the tragus.

An otoscope (or an ear speculum and head mirror) is used for examining the ear canal and tympanic membrane. First examine the external canal for signs of debris, inflammation, masses, discharge, foreign bodies, and patency. Next note the eardrum and its landmarks or the absence of landmarks such as the short process, handle, and tip of the malleus, and the light reflex. Note any healed or active perforations, scars, or distortions of the drum. Examine the drum for retraction of the pars flaccida or a fluid meniscus behind the drum or internal bubbles. Angle the speculum in all directions so that a view may be obtained of the entire drum, but the speculum should not be inserted past the cartilaginous exterior portion. Benign bony exostoses may be found in the external canal, but they have little diagnostic importance. Inspect for signs of inflammation, perforation, tumors or polyps, and cholesteatomas. See Figure 2.7.

Perform the general functional hearing tests to determine whether a defect of hearing is present, the general degree of the impairment, and the general location of the lesion; ie, whether the defect is in the conduction or perception apparatus. Common tests used are the Weber, Schwabach, Rinne, and Stenger tests.


The Eyes

Note the general facial expression and general eye features, then inspect for details of eye structures. The external structures of the eye are examined and recorded in the following order: the eyelids, orbit, conjunctiva, cornea, anterior chamber, iris, pupils, lens, and lacrimal ducts. Inspect and palpate the tear point at the medial end of each lid for function and size.

Examination of the eyes includes an evaluation of visual acuity, visual fields, color vision, ocular movements, external structures, pupillary responses, intraocular pressure, and the ocular fundus. By visual examination alone, many diseases may be identified. For example, direct inspection might reveal changes in the cornea, conjunctiva, iris and pupil that can be immediately related to well-known disorders. A hand magnifying lens is helpful in observing the smaller details of the external structures. A Snellen chart is usually used for screening visual acuity.

Evaluate the cornea and note scars, color, vascular congestion, deposits, and signs of inflammation. Observe the consistency and color of the iris, and note pupil irregularities and signs of inflammation. Inspect the iris and choroid for signs of congenital anomalies such as heterophthalmos, persistent pupillary membrane, coloboma of the iris or choroid, irideremia, dyscoria, hippus, or albinism. Use a penlight to inspect the depth of the anterior chamber, and check to see that there is no visible opacity (cataract).

Tests for visual fields, pupil reflexes, accommodation, pupillary constriction, extraocular movements, and the corneal reflex are conducted in relation to cranial nerve tests. Failure to move the eye voluntarily in any given direction indicates muscular incompetence caused by primary muscle disease or a neurogenic factor. Note parallel coordination and signs of strabismus or nystagmus.

The Eyelids.     Inspect the lids for edema, skin changes, and palpebral fissure difference. Note position of each lid relative to the anterior orbit and record the degree of ptosis. Check for entropion, ectropion, blepharitis, hordeolum, edema, and blepharospasm. Evaluate the degree of exophthalmos and the distance between orbits. Inspect for conjunctival edema, pallor, foreign bodies, petechiae, and vascular injection both on the anterior eyeball and posterior lid surfaces. Note pterygium, conjunctival congestion, bogginess and episcleritis, signs of pemphigus, and scleral tint. Note the degree of moisture on the inner lids.

Manually Screening Intraocular Pressure.     A crude method for determining potentially high intraocular pressure can be obtained by finger pressure. As the patient looks downward, place the tips of both index fingers on the upper led above the downturned cornea. One index finger presses against the eyeball while the other rests firmly on the globe; then the active finger relaxes slightly and the other finger indents the eyeball. This maneuver is alternated several times in a slow piston-like manner, with pressure applied directly toward the center of the eyeball. In this manner, a frank rise in pressure or an extremely soft globe may be perceived. However, if it is allowed in your state of practice to apply a local anesthetic for diagnostic purposes, tonometry to evaluate intraocular pressure is the far more accurate procedure.

Ophthalmoscopy.     With an ophthalmoscope, test the "red reflex" before examining the fundus. The fundus is examined in a definite sequence: optic disk, retinal vessels, and macula. Keep in mind that the fundus is the only place in the body where a cranial nerve and arterioles may be viewed without surgery. Inspect the fundus for retinal hemorrhages and signs of hypertension, arteriosclerosis, optic neuritis, optic atrophy, cranial trauma or tumor, and disease of the meninges.

The Anterior Neck

      Inspection

Inspect first for gross abnormalities and then for details. Check for scars, blisters, discolorations, skin texture and lesions, and pulsatile movements. Note congenital defects such as pterygium colli or congenital torticollis. Evaluate any parotid or submaxillary gland enlargement. Check for fixed or movable masses, and transilluminate if present. Have the patient swallow, and note the function of the cricoid cartilage area and possible superior movement of the thyroid gland. Check the trachea for midline alignment. If the thyroid is visible, note its size, shape, symmetry, and any sign of nodules. Venous thrombosis, mediastinal tumors, and inflammatory exudates may produce visible and palpable edema in the neck.

Observe abnormal shadows, neck contours, curvatures, and restricted movement. Note relationship of neck, head, and shoulders from an A-P, lateral, and rotational standpoint. Check head tilt, sway, carriage during rest and gait, and other abnormal postural expressions.

      Palpation

The neck should be palpated with the patient supine so that the muscles are relaxed and the head may be passively controlled. With the patient supine, the following landmarks should be noted: The C1 transverse process (the widest in the neck) lies between the angle of the jaw and the mastoid process, the hyoid bone is above the body of C3, the top of the thyroid cartilage (Adam's apple) is above the body of C4, the bottom of the thyroid cartilage is above the body of C5, and the first cricoid ring is above the body of C6. If abnormal nodes or masses are palpable, they should be recorded according to size in millimeters and number (single, multiple).

Palpate each sternocleidomastoideus muscle individually after passively rotating the patient's neck first toward one direction and then the other, opposite the muscle being examined. Check for possible strain (eg, trauma, postural hyperextension) from its origin on the sternum and clavicle to the mastoid process. Note any abnormal size, shape, tension, tenderness, or mass.

During palpation of the sternocleidomastoideus and cervical trapezius, there is an opportunity to palpate the lymph node chain that bilaterally extends along the anteromedial border of the muscles. The nodes are normally not palpable unless inflamed (eg, upper respiratory infection) or calcified.

The vertebral bodies can often be palpated from the anterior by pressing the index and middle fingers through an imaginary surgical approach to the neck between the carotid sheath and the sternocleidomastoideus laterally and the trachea, esophagus, and thyroid gland medially. While in this area, palpate the hyoid, situated cephalad from the thyroid cartilage, by probing from the midline laterally and posteriorly with thumb and first finger. Note distinct movement when the patient swallows.

Move caudad from the hyoid and palpate the thyroid cartilage in the anterior midline in the same manner. When diseased, cysts, nodules, swelling, and/or tenderness may be noted. Next palpate the first cricoid ring, locatedjust caudad to the thyroid cartilage. Be gentle to avoid stimulating the gag reflex. Slight movement should be palpable on swallowing. Then palpate the small, deep carotid tubercles, located on each side about an inch lateral from the carotid ring and just anterior to the transverse process of C6. Palpate gently, quickly, and unilaterally (to avoid stimulating a carotid reflex) by placing the fingers of one hand deeply posterior between the cricoid ring and lateral cervical muscles.

The Carotid Pulse.     Palpate the carotid pulse, found next to the carotid tubercle, with the index and middle fingers. Note pulse strength and compare bilaterally. Auscultate the anterolateral neck to assess carotid bruits and venous hums. See Figure 2.8.

The Thyroid Gland.     The thyroid may be palpated from either the back of the patient with bimanual palpation or at each side of the patient using one active hand and the other offering counterpressure. Have the patient swallow and check the normal upward movement. With the patient taking small slips of water, search laterally and cephalad to determine if the upper lobes can be delineated and if their consistency, size, and contour can be appreciated. Increased firmness will be noted during inflammation or an early neoplastic process. A bruit may be heard over the gland in hyperthyroid states.

The Supraclavicular Fossa.     Palpate the supraclavicular fossa, beginning at the sternum and moving laterally. Search for abnormal swellings (eg, traumatic edema), masses (eg, tumors, swollen lymph nodes, cervical rib), or unusual depth of the fossa (eg, clavicular fracture).

Neurovascular Tests.     Perform the neurovascular compressions tests such as rotary compression, hyperextension, costoclavicular maneuver, shoulder depression, Adson's, Allen's, George's, Wright's, and Eden's tests. Then perform other appropriate neurologic and orthopedic tests such as cervical distraction and cervical percussion if advisable.

The Thorax

      Inspection

Inspect the chest for the following points:

(1) size,
(2) general shape and nutrition,
(3) local deformities or tumors,
(4) respiratory movements of the chest walls,
(5) respiratory movements of the diaphragm,
(6) abnormal pulsations,
(7) color and condition of the skin, and
(8) the presence or absence of glandular enlargement.

Check symmetrical bony development, inequality in intercostal spaces retracted by a possible unilateral fibrosed lung, and the normality of the dorsal kyphosis and angles of the sternum. Appreciate every visible and palpable abnormality. Check contours and for consistencies, lumps or swellings. Refer to Figure 2.4.

Evaluate the possibility of a clinical chest such as the paralytic chest, the barrel chest, or the rachitic chest. Observe any flattening or prominence of one side of the chest, local prominence, or effects of a spinal curvature.

      Palpation

Palpate the dynamics involved in respiratory movements with your hands splayed widely above downward, anteriorly and posteriorly. Check respiratorymovements for normal respiration, anomalies of expansion, and dyspnea. Note changes in respiratory rhythm such as asthmatic breathing, restrained or "catchy" breathing, stridulous breathing, shallow and irregular breathing, and sternomastoid breathing. Observe the excursion limits of the diaphragm.

Palpate for tactile fremitus communicated to the hand when it is laid on the chest while the patient repeats some short phrase (eg, 99). Maximum fremitus is obtained over the apex of the right lung in front. It is greater in the upper part of the chest than in the lower, and somewhat greater throughout the right chest than in the corresponding part of the left. A small amount of fremitus can be normally felt over the scapulae behind and still less in the precordial region in front. Crepitation can be palpated when subcutaneous tissues contain fine beads of air caused by air escape from the lung.

      Percussion

Percuss symmetrical points of the thorax and evaluate vesicular resonance, the normal dull areas, tympanic resonance, "cracked pot" resonance, amphoric resonance, and the sense of resistance. With percussion, determine the movability of the lung borders.

      Auscultation

With a stethoscope, evaluate vesicular breathing sounds, bronchial breathing sounds, and seek signs of emphysematous or asthmatic breathing, interrupted or cog-wheel breathing, metamorphosing breathing, exaggerated or diminished vesicular breathing, amphoric breathing, and abnormal bronchovesicular breathing. If rales are present, evaluate bubbling, crackling, or musical causes. Listen for possible pleural friction rub. Auscultate the whispered voice, the spoken voice, and for possible egophony. Listen for succussion sounds, metallic tinkle, and lung-fistula sounds.

      Mensuration

Circumference measurement of the thorax during inspiration and expiration should be taken if not recorded previously.


The Female Breast

      Inspection

Note the size, shape, symmetry, contour, and position of the two breasts. Inspect the relative position of the areolae and nipples along with signs of skin retraction. Check for nipple irregularities and discharge, changes in subcutaneous veins, and skin defects in color and texture. Redness indicates inflammation or may show superficial lymphatic involvement (eg, inflammatory carcinoma). Edema produces a bulging of the skin that will appear like pigskin or the peel of an orange and is often associated with inflammatory carcinoma. Rapidly growing tumors, benign or malignant, often present dilated subcutaneous veins.

The Nipples.   Nipple ulceration points toward Paget's disease of the breast (intraductal carcinoma) unless both nipples are involved (benign dermatologicdisease). Nipple discharge should be inspected for color and type. Nipple bleeding suggests a benign intraductal papilloma; chronic discharge usually points to cystic mastitis. Nipple retraction features a dimpling of any skin of the breast or nipple produced by a tumor shortening Cooper's suspensory ligaments. The cause may be simple fat necrosis (traumatic in origin) or an acute inflammatory process. If the breast does not give definite evidence of acute inflammation, nipple retraction strongly suggests a malignancy.

      Palpation

Gently palpate the quadrants of the breast with the fingertips in a clockwise direction. The patient should be supine with arms abducted 90°. First palpate with light touch to note any soft masses and then with firmer pressure for the deeper tissues. Check for consistency, elasticity, tenderness, and lumps. Tenderness suggests an underlying inflammation; malignant lesions are seldom tender. Palpate the interspaces for a possible small deep-seated mass. Check for thrombophlebitis of the superficial veins of the breast. A palpable mass within breast tissue is a significant sign of an abnormality; however, while nodularity, thickening, and hardness are important signs, they should not be considered as masses.

With the patient sitting on the edge of the examining table with her arms raised and her hands clasped on top of her head, again palpate each breast in a clockwise direction. Palpate the nipples for central lumps or duct thickening. Gently elevate different parts of the breast with your fingertips under the breast and note any abnormal nipple or skin changes. Palpate the far lateral aspects to the axillae while passively moving the extremity through a full range of motion. Then have the patient lean far forward and note any subtle skin changes, dimpling, or nipple deviation.

Next, place the patient in the relaxed position with her hands loose at the sides, and palpate the supraclavicular areas for lumps and tenderness. The deep jugular chain of nodes is a frequent route of metastatic spread of breast cancer. Then have the patient place her bands on her hips and press toward the midline contracting the pectoral muscles. Note any abnormal signs, and palpate the deep axillae tissues for lumps, edema, swellings, or tenderness.

      Transillumination

After inspection and palpation of the breasts, transilluminate the breasts with a flashlight as a final check.


The Heart Area

      Inspection

Inspect the normal cardiac impulse area, and seek evidence of displacement of the impulse, apex retraction, epigastric pulsation, and visible pulsations. The precordium is relatively prominent in 25% of normal people; thus, allowance should be made for this normal deviation from the average chest conformity in estimating prominence due to such conditions as cardiac hypertrophy, pericardial effusion, aneurysm, or pleural effusion.

With each systole of the heart, most chests show an outward movement of cardiac impulse is produced by the impact of a portion of the right ventricle against the chest wall and not by the apex of the heart.

The point of maximum impulse (PMI) in adults is usually in the 5th intercostal space just inside the nipple line when erect, in the 4th space when recumbent. In children under the age of 6 years, the PMI is often one interspace lower and outside the nipple. In people with a low diaphragm, it may descend as low as the 6th interspace. Unless there is an unusual body shape, the PMI in health is not over 9 cm to the left of the midsternal line; it is usually less, according to the size of the subject. Keep in mind that the position of the impulse varies to a certain extent depending on the position of the body. The PMI is occasionally absent in adults in perfect health and under certain pathologic conditions.

Note displacement of the cardiac impulse and signs of apex retraction, epigastric pulsation, or visible pulsations due to uncovering of portions of the heart normally covered by the lungs. Palpation is considerably more effective than inspection in giving us information of the nature of the cardiac movements that produce the apex beat.

      Palpation

Palpate the site of the observed apex beat, which is normally an area about the diameter of a half dollar just below the left nipple. The fingers should conform to the contour of the chest to appreciate the gross movements of the heart and confirm or modify what was learned by inspection. The powerful, slow, widespread impulse of a hypertrophied heart, the diffuse slap often felt in dilatation of the right ventricle, and the sudden rap of mitral stenosis may thus be evaluated. Note regularity and character of the beat. Palpation may localize a cardiac impulse that is not visible; on the other hand, pulsations can be seen that are not felt in some cases. Simultaneously monitor the pulsation of the carotid artery, and judge ejection time.

During palpation of the cardiac impulse with the palm of the hand, you are in a good position to notice the presence or absence of a "thrill" that is usually confined to a small area in the region of the apex pulse but sometimes felt in the 2nd right intercostal space or elsewhere in the precordial area. In right ventricle hypertrophy, a precordial "heave" near the sternum may be felt. Strong pulsations in the suprasternal notch point toward aortic aneurysm or dilatation. Areas of marked tenderness in different parts of the chest may be found in mitral disease, dry pleurisy, necrosis of the rib, and sometimes in tuberculosis.

Next, carefully palpate the 2nd right intercostal space over the ascending aorta, just right of the sternum. In cases of hypertension, closure of the aortic valve can usually be perceived. Thrills from aortic stenosis are best felt in this area. Move over to the 2nd left intercostal space and palpate the pulmonary area, just left of the sternum. In cases of hypertension, closure of the pulmonary valve may be felt. Thrills from pulmonary stenosis are also best sensed in this site. Thrills near the lower left sternal border suggest a ventricular septal defect, while a diastolic thrill at the apex suggests mitral stenosis.

Shocks produced by the closure of valves and by thrills can be distinguished best by holding the palm of the hand rigid with the fingers hyperextended, allowing the vibrations to be transmitted to the bones of the hand. A normal heart after exercise or other stimulus may transmit a distinct "jar" to the hand palpating the PMI that lacks the truly snapping quality found in mitral stenosis. A diastolic shock may be felt at the aortic area in the presence of hypertension, congenital stenosis of the aorta, or aneurysm. An aneurysm or dilated aorta may also transmit pulsations to the chest wall.

Aneurysm, a dilated aorta, or pulsating pleurisy may cause abnormal thoracic pulsations. Pulsations due to a dilated aorta or an aneurysm are most likely seen in the 1st or 2nd right interspace near the sternum, but not infrequently the clavicle and the adjacent parts may be seen to rise slightly with every beat of the heart. In cases of purulent pleurisy in which fluid has worked its way between the ribs so that it is covered only by skin and subcutaneous tissues, a pulsation transmitted from the heart may become visible. Such a pulsation is commonly seen in the upper and front portions of the chest.

In inflammatory roughening of the pleura, a grating or rubbing of the two surfaces on each other may be felt as well as heard during the movements of respiration, especially at the end of inspiration. This friction is usually felt at the bottom of the axilla, on one side or the other, where the diaphragmatic pleura is in close apposition with the costal layer. Likewise in roughening of the pericardial surfaces, it may be possible to feel a grating or rubbing in the precordial region more or less synchronous with the heart's movements. Such friction is most often felt in the region of the 4th left costal cartilage. Sometimes low-pitched snoring rales communicate a sensation to the hand placed on the chest in the region beneath the area where the rales are produced.

      Related Inspection

Note vascular phenomena apparent in the neck and extremities because such phenomena have a direct bearing on the interpretation of conditions within the chest. Look for venous, arterial, and capillary abnormalities. Peripheral pulsation in the healthy is usually seen over the carotid arteries, under the outer ends of the clavicles, in the episternal notch, and frequently over the brachial arteries, especially in the elderly. When the tissues of the neck are wasted, the veins may be quite prominent even when no disease exists within the chest; and in such cases, the veins may distend during each expiration, especially if dyspnea or cough is present. If these overdistended veins are completely emptied bilaterally during deep inspiration, overdistention of the right side of the heart is inferred. When a similar phenomenon occurs unilaterally, something causing pressure on one innominate vein should be determined.

Deviation from the normal appearance of jugular waves may offer a vital clue about cardiac status, Venous changes need not be synchronous with respiration, however. A presystolic pulsation or undulation may be seen either in the external jugular vein or in the bulbus jugularis between the two attachments of the sternocleidomastoideus. Pulsation seen just before each cardiac systole may not be abnormal and must be distinguished from systolic venous pulsation. Systolic venous pulsation in tricuspid regurgitation is more often seen on the right side than the left side of the neck. There may be a visible wave during systole of the auricle and another during the systole of the ventricle, the latter closely following the former. If doubt arises whether a pulsation in the veins of the neck is due to tricuspid regurgitation, empty the vein by stroking it from below upward. If it immediately fills from below, tricuspid regurgitation is likely.

Sometimes carotid pulsations are seen in thin or nervous patients independent of any abnormal condition of the heart. Violent throbbing of the carotids occurs in severe anemias and occasionally in simple hypertrophy of the heart, and visible pulsation may occur in the subclavian, axillary, brachial, and radial arteries, as well as in the large arterial trunks of the lower extremities. Also judge jugular pressure.

Capillary Pulsation.     A microscopic slide placed against the mucous membrane of the lower lip to partially blanch its surface may show with the beat of the heart a delicate flushing of the blanched surface beneath the slide. This pulsation is sometimes seen beneath the fingernails or better brought out by transilluminating the fingertip. The phenomenon of capillary pulsation occurs in aortic regurgitation, anemia, thyrotoxicosis, conditions associated with low tension in the peripheral arteries, and in any area of inflammatory hyperemia. It also occurs in some healthy people.

      Percussion

Percuss the precordial area to determine the extent of deep cardiac dullness that marks the approximate border of the heart and the superficial cardiac flatness, which represents that portion of the heart not covered by the lung.

      Auscultation

Auscultate the heart for the first, second, and third heart sounds. The "mitral" first sound is increased by whatever induces increased vigor of the heart and by valvular diseases (especially mitral stenosis). It is weakened or reduplicated when the heart is weakened. These changes may occur temporarily from physiologic causes. The "pulmonic" second sound is usually more intense than the aortic in children and up to early adult life. Later, the aortic second sound predominates. Pathologic accentuation of the second pulmonic sound usually points to obstruction in the pulmonary circulation (eg, mitral disease, emphysema, etc). Weakening of the pulmonic second is characteristic of serious failure of the right ventricle. The aortic second sound is increased pathologically by any cause that increases the work of the left ventricle (eg, arteriosclerosis, chronic nephritis). It is diminished when the blood stream entering the aorta by the left ventricle is abnormally small (eg, mitral disease, cardiac failure). Changes in tricuspid sounds are rarely recognizable. Changes in the first sound heard in the aortic and pulmonic areas have little practical significance. During auscultation of the heart, listen for signs of gallop rhythm, protodiastolic gallop, presystolic gallop, and midsystolic clicks. Seek the presence of a reduplicated first sound, a physiologic third sound, or the opening snap of mitral stenosis. If a murmur exists, record its time, localization, transmission, intensity, quality, length, and the effects of position, exercise, and respiration. Differentiate functional from organic murmurs. Auscultate the peripheral vessels, especially the carotids, subclavian, femoral, brachial, and radial.


The Abdomen

      Inspection

Judge body type tendency and general abdominal shape and size. Inspect the skin and note any abdominal veins, pulsations, visible peristalsis, or respiratory movements. Note any distention, mass, or scars. Observe the color of the skin, pigmentation, eruptions, skin texture, and hair distribution. Seek evidence of vasomotor instability such as erythema, ischemia, or dermographia. Inspect the lineae alba, nigra, semilunaris, and presence of linea albicantes.

      Palpation

Palpation should thoroughly survey the abdominal viscera. Begin in the lower left quadrant and palpate the colon, transverse colon, and ascending colon, Note if the spleen, gallbladder, kidneys, or pancreas are palpable, Determine the presence of localized or generalized tenderness. Seek signs of possible fluctuation, peritoneal crepitus, or masses. Note signs of restricted mobility with tenderness that may indicate postsurgical adhesions.

Use light and gentle palpation, and elicit muscle resistance. In many cases, no part of the normal intestine, including the appendix, can be felt through the abdominal wall. The same is true of the stomach, spleen, left kidney, pancreas, bladder, and pelvic organs, except in certain very thin patients. The tissues that can usually be perceived are the abdominal aorta, the spinal column near and above the umbilicus, the lower edge of the liver in some people, the tip of the right kidney at the end of long inspiration in thin youngsters, the iliopsoas muscle, and sometimes the beginning of the iliac arteries in lean people.

      Percussion and Succussion

Percuss the abdomen for signs of tympany or ascites and to outline the borders of the liver, spleen, or a possible tumor. Use succussion to determine signs of fluid.

      Auscultation

Auscultate for aneurysm, bruits, hums, gurgling borborygmi, and friction rubs. Percussion and tuning fork auscultation may be necessary for confirmation of various phenomena. Carefully evaluate any signs and symptoms pointing toward an acute abdomen.


The Rectum

Rectal examination is essential in low back pain, bleeding, diarrhea, pelvic disease, bowel symptoms, female complaints, urinary symptoms, and suspected carcinoma. Inspect the perianal skin and palpate for evidence of fistula, hemorrhoids, abscess, prolapse, and pruritus. Palpation of the perianal area should precede digital examination of the rectum. Note sphincter resistance on inserting the gloved finger into the anus.

Carefully palpate along the rectal wall for undue dilation or narrowing. In checking the posterior wall, note

(1) the levator and piriformis muscles in the high lateral wall and
(2) the mobility and sensitivity of the coccyx and lower sacrum. Check the anterior aspect, noting the prostate or cervix.

The Upper Extremity

      Inspection

Observe general characteristics and then inspect for details. Inspect overall bilateral symmetry, rhythm of motion, arm swing during gait, smoothness in reach, and patterns of pain, and confirm general circulatory and neurologic symptoms. Check for abnormal limb rotation or adduction. Note skin discolorations, masses, scars, blebs, swellings and lumps, abrasions, and signs of underlying pathology. Check the relationship of the neck to the shoulder girdle.

With the patient sitting, inspect the anterior aspect of the shoulder girdle starting with the clavicle. Note the normal symmetrical fullness and roundness of the anterior aspect of the deltoid as it drapes from the acromion over the greater tuberosity of the humerus. Stand behind the patient and observe the symmetrical dimensions of the scapulae such as size, position, conformity with the rib cage, and outline.

Note the carrying angle of the elbow. Inspect the arm, elbow, and forearm for scars that may have resulted in contractures. Seek needle-puncture marks. Observe overall contour, lumps, and skin texture. Inspect the hands in their rest attitude and during function such as in writing, undressing, and shaking hands. Note the bony framework, contours, finger webbing, muscle development, color and texture of the skin. Inspect for swellings, nodes, asymmetrical development or deformities, nail abnormalities or discolorations. Check for nodes and swan-neck deformity. Inspect the fingertips and nails for signs of infection.

      Palpation

Screen bilateral skin temperature and for abnormal protuberances, crepitation, abnormal continuity and asymmetry. Soft-tissue palpation should evaluate tissue firmness, muscle tone and size (hypertrophy, atrophy), tenderness, and normal relationships with bone. Seek masses, lumps, exostoses, or other anatomical variations. See Figure 2.11.

Stand behind the sitting patient and begin bilateral anterior palpation at the suprasternal notch and sternoclavicular junction, then move laterally along the anterior superior surface of the clavicle. Palpate the bony anterior and posterior portion of the acromion, then the greater tuberosity of the humerus lying below the lateral edge of the acromion. Three of the four muscles comprising the rotator cuff present palpable insertions at the greater tuberosity of the humerus. To palpate the cuff as a whole, place your active fingers slightly inferior to the anterior border of the acromion while your other hand grasps the patient's lower arm and moves his elbow posteriorly.

Gently palpate the bicipital groove with the fingers of one hand while your other hand grasps the patient's forearm and rotates the humerus in and out. Note crepitation on movement, tenderness, or unusual mass. Next, palpate the deltopectoral groove. The tip of the coracoid process, level with the lesser tuberosity, will be found below, posterior, and lateral to the deepest portion of the lateral clavicular concavity in the deltopectoral triangle under the pectoralis major muscle.

Starting at the shoulder tip, palpate the acromion posteriorly and medially as it tapers into the scapular spine. Next, probe the scapula's superior medial angle, the entire medial border of the scapula, the inferior triangle, and the entire lateral border until it disappears under the heavy shoulder muscles. From the superior-lateral border of the scapula, begin to palpate the axilla. Probe for tenderness, lymph node enlargement, muscle tone and size, masses, and other abnormal findings. Roll the soft tissues gently between your thumb and fingers to check tone, consistency, enlarged nodes, tenderness, or masses.

Check the major muscles throughout their origin, belly, and insertion (eg, the pectoralis major, deltoid, biceps, triceps, serratus anterior, trapezius, rhomboids, and latissimus dorsi). Recheck the sternocleidomastoideus if abnormalities have been found in associated muscles. Probe for anatomical deviations, gaps, tone, spasm, swelling, and lumps. Always compare signs bilaterally.

In the elbow, carefully palpate the medial and lateral epicondyle of the humerus, the medial and lateral supracondylar line of the humerus, the olecranon process and fossa, and the posterior ulnar border. The limb should be hanging in a relaxed position during palpation. Check general bony relationships by placing your thumb on the lateral epicondyle, index finger on the olecranon, and middle finger on the medial epicondyle. With the elbow flexed, palpate the radial head located within the depression medial and posterior to the wrist extensors while you pronate and supinate the forearm with the stabilizing hand. See Figure 2.12.

Palpate the soft tissues of the elbow and forearm in a linear fashion, proximally to distally, beginning with the medial aspect. Then palpate the posterior aspect, lateral aspect, and finally the anterior aspect of the forearm. The patient's elbow should be flexed 90°, and the patient's shoulder should be slightly extended and abducted to make the medial soft tissues available throughout palpation.

Gently palpate the soft, tubular ulnar nerve within the groove between the medial epicondyle and the olecranon, and follow its course until it disappears. Then palpate the wrist flexor-pronator muscles from their common tendon at the medial condyle down the forearm throughout their course into the wrist. Check the deeper medial soft tissues for tenderness, lumps, gaps, etc, both with the patient's fist tight and relaxed. Check for enlarged lymph nodes along the medial supracondylar line. Move to the posterior aspect and palpate the olecranon bursa area for signs of inflammation or rheumatoid nodules. Trace the distal triceps muscle heads to their origin.

Palpate the wrist extensors on the lateral aspect of the forearm, felt as a mobile mass originating from the lateral epicondyle and its supracondylar line. Check the area over the lateral collateral ligament. The biceps belly and tendon is best palpated when the patient tightens his supinated fist and lifts upward against the examiner's resistance. The musculocutaneous nerve lies just lateral to the biceps tendon but is not palpable because of its deep location. Medial to the biceps tendon is the brachial artery (and pulse), and medial to the artery is the median nerve, which is felt as a round tube.

Palpate the bones of the wrist as a whole, and probe around the radial styloid process. Have the patient extend his thumb away from his fingers and palpate the anatomical snuffbox. Note if the radial artery is palpable as it crosses the carpal navicular bone. A palpable nontender ganglion may be found on either the dorsal or volar aspect of the wrist. Palpate each of the six wrist tunnels and their tendons along their course. Check for rupture of the tendon in the third tunnel. Check the easily fractured scaphoid by sliding it out from under the radial styloid by ulnar deviating the wrist. Have the patient flex and extend his thumb while you lower your fingers to check the trapezium and 1st metacarpal articulation.

On the dorsum of the waist, palpate Lister's tubercle of the radius and down around the lunate, capitate, and third metacarpal, with the wrist slightly flexed. Palpate the ulnar styloid process, then radial deviate the wrist and check the cuneiform --a common site of fracture. Palpate the dorsal extensor tendons as the patient extends his wrist and fingers.

Turn the patient's hand over and inspect the plantar surface of the wrist. Palpate the pisiform and over the hook of the hamate. Next, palpate (with the patient's wrist flexed) above the pisiform for the enclosing flexor carpi ulnaris, which may contain calcific deposits. The pulse of the ulnar artery is felt just proximal to the pisiform as it runs along the ulnar bone. Palpate the palmaris longus as it bisects the anterior wrist and the deeper carpal tunnel. Move radially to palpate (with the patient's wrist flexed) the flexor carpi radialis as it crosses the navicular. Note any atrophy of the thenar or hypothenar eminence. Probe the palmar aponeurosis for nodules leading to flexion deformity. Note any audible or palpable snapping of tendons as the patient flexes and extends his fingers. Then, with your thumb and 1st finger, bidigitally palpate each metacarpal and interphalangeal joint.

      Joint Ranges of Motion

Active ranges of joint motion should be tested for the shoulder girdle, elbow, wrist, and fingers. If active motion is normal, there is usually no need to test passive motion unless unusual circumstances exist that make active motion difficult. As in all range of motion tests, passive motion should not be attempted if there is possibility of fracture, dislocation, or severe tissue tears.

Test shoulder girdle elevation and depression by having the patient hunch his shoulders and return to the normal position. Test active external rotation and abduction by having the patient reach up and over his shoulder and attempt to touch the spinal border of the opposite scapula. External rotation and abduction can be tested bilaterally at the same time by having the patient place both hands behind his neck with interlocking fingers; then the elbows, which are initially pointing forward, are moved laterally and posteriorly in an arc. If you wish to check solely glenohumeral joint passive abduction, your stabilizing hand should anchor the scapula while your active hand passively abducts the patient's arm with his forearm held horizontal.

Check internal rotation and adduction by having the patient reach across his chest, keeping his elbow as close to the chest as possible, to touch the opposite shoulder tip. Test full active bilateral abduction by having the patient abduct his arms horizontally to 90° while keeping elbows straight and palms turned upward, then continuing abduction in an arc until his hands meet in the middle over his head. During passive flexion and extension, the stabilizing hand should be placed on the acromion to fix the upper shoulder area and scapula.

Active flexion of the elbow is judged by having the patient touch his ipsilateral shoulder with his supinated hand, and extension is checked by the patient straightening his elbow as far as possible. Test active pronation and supination with the patient's elbow flexed 90° and firmed against the waist. Instruct the patient to turn his closed fist first downward so that the palmar surface is parallel with the floor and then upward so that the dorsal surface is parallel with the floor. If a blockage is obtained in active motion, check passive motion and note the type of block and degree of restriction.

Active flexion, extension, ulnar deviation, and radial deviation of the wrist are tested simply by having the patient flex and extend his wrist, and then deviate the wrist medially and laterally. Supination and pronation tests have been described previously with the forearm.

Test finger active metacarpophalangeal motion by stabilizing the patient's wrist and having him extend and flex with your hand holding the digits straight. Judge active proximal interphalangeal motion by stabilizing the metacarpophalangeal joints and having the patient extend and flex his proximal interphalangeal joints. Check active distal interphalangeal movement by stabilizing the proximal interphalangeal joints and having the patient extend and flex his distal interphalangeal joints. Observe finger abduction and adduction by having the patient place his hand flat and spread his fingers apart and then tight. Judge individual joint motion restriction in all normal directions and test passively if necessary.

Test active overall thumb flexion, extension, abduction and adduction by having the patient touch the tip of his thumb to the base of his little finger, to each fingertip, then extending the thumb as far as possible laterally. If joint restriction is noted, check both joints passively.

      Muscle Strength

Test muscle strength of the shoulder by applying increasing resistance against shoulder flexion, extension, adduction, abduction, external rotation, internal rotation, scapular elevation, scapular retraction, and scapular protraction. Test muscle strength of the elbow by applying resistance to elbow flexion, extension, forearm supination, and forearm pronation. Test muscle strength of the wrist muscles in extension and flexion. Test muscle strength of the hand through finger flexion and extension, finger abduction and adduction, thumb extension and flexion, thumb abduction and adduction. Finish by testing general grip strength with a dynamometer.

While described separately in this chapter, muscle strength is generally tested immediately following joint range of motion tests. This conserves examination time.

The Lower Extremity

      Inspection

Observe the weight-bearing knee, and note carriage, stance, and swing during gait. Inspect for loss of normal contours and signs of possible muscle atrophy, especially above the knee. From the anterior, note symmetry and level of patellas. Check degree of genu varum or valgum bilaterally. Compare quadriceps bilateral symmetry and seek signs of atrophy. From the side, observe any degree of hyperextension and possible genu recurvatum.

Before the ankle and foot are inspected, check the patient's shoes for unusual wear, scuffing, creases, bulges, and deformity. Palpate the foot within the shoes for stress points. Observe the patient's foot posture first in the standing position with shoes on, both A-P and P-A. Note inward and outward roll of foot and ankle. Check shoe size by placing an index finger at the widest part of the shoe. Check shoe length by palpating for the longest toe in the shoe. Then, check shoes for heel balance and slippage. Next, check for shank strength, heel and sole wear, and inside the shoes for sharp fasteners or rough stitching.

Remove the patient's shoes and inspect again the A-P and P-A foot posture, and the degree of pronation or supination. Drop a plumb line from the center of each patella and note deviation from the midline of the ankle. Insert an index finger under the inner longitudinal arch to a point midway under the foot and palpate the plantar fascia for tension. Rotate the foot to its outer border and the knee laterally, then repeat plantar palpation. Check the effects of foot pronation by measuring the amount of knee rotation.

Place a mark with a skin pencil in the middle of each patella, and measure the distance between the marks. Then roll the feet to outer borders and measure the distance between patella marks.

Count the toes, and note gross deformities. The toes should be straight, flat, equal bilaterally, and proportional to each other. Note any swelling, redness, abnormal skin texture, overlapping toes, and the general shape of the dorsum of the foot and longitudinal arch in both the weight-bearing and relaxed positions. Inspect the toes for ingrown nails, claw toes, or hammer toes.

      Circulatory Screening

An elevated pink foot that markedly deepens in color in the standing position suggests arterial insufficiency or vascular disease. Note venous filling time on the dorsum of the foot simultaneously. Collapsed veins should fill within 12 seconds on standing. If pulses are absent in an ankle, seek the most distal palpable pulse and auscultate for an audible bruit (suggesting the site of obstruction).

Apply finger pressure to the medial dorsal area of the weight-bearing foot, and note time for the white spot to disappear. Then rotate weight to the outer border and repeat the test. To evaluate capillary filling time of the toes, compress a selected toe until it blanches white, then release pressure quickly. Normal color should return within 6 to 10 seconds.

      Palpation

The major bony areas to palpate on the medial aspect of the knee are the medial tibial plateau, the tibial tubercle, the medial femoral condyle, the medial epicondyle, and the adductor tubercle. See Figure 2.13. Check such soft tissues as the medial meniscus and collateral ligaments bilaterally. Then palpate the sartorius, gracilis, and semitendinosus muscles. Examine the infrapatellar tendon from the patella to the tibial tubercle. Assess the superficial and deep infrapatellae bursae and the prepatellar bursa. Try to locate for the small coronary ligaments. It is helpful to rotate the tibia internally during palpation; retraction of the meniscus is often felt when the tibia is externally rotated.

Next, palpate the medial collateral ligament located between the medial femoral epicondyle and the tibia. It is usually unpalpable unless torn by valgus stress. The medial femoral condyle is medial to the patella, below the junction of the femur and tibia. Check for possible signs of osteoarthritis in this area. Move slightly upward, check the medial epicondyle, then move further upward and check the adductor tubercle located on the posterior part of the medial femoral epicondyle. Check tautness and tenderness of the tendons of the sartorius, gracilis, and semitendinosus muscles that form a visible ridge on the posteromedial aspect of the knee prior to inserting into the lower portion of the medial tibial plateau.

On the anterior aspect of the knee, check the quadriceps insertions, the infrapatellar tendon, and the bursae of the knee. Palpate upward along the femoral condyles to above the patella, and then palpate the midline trochlear groove in which the patella glides. With the knee extended, check patellar mobility, and attempt to palpate the tissues under the medial and lateral sides of the patella. To test the quality of the articulating surface of the patella in the trochlear groove of the femur, perform the patella "grinding" test. Check for possible patella subluxation, dislocation, and subpatellar edema. Next, palpate the insertion of the quadriceps along the upper and medial borders of the patella, and then check the quadriceps tendon over the patella as it becomes the infrapatellar tendon. Examine for transverse tears just above the patella in the rectus femoris and vastus intermedius.

Palpate each thigh simultaneously to check symmetry and possible unilateral atrophy. If doubtful, measure the circumference of each thigh with a flexible tape.

On the lateral aspect of the knee, palpate the lateral tibial plateau, the lateral tubercle, the lateral femoral condyle, the lateral femoral epicondyle, and the head of the fibula. Then check such soft tissues as the lateral meniscus, the lateral collateral ligament, the anterior superior tibiofibular ligament, the biceps femoris tendon, the iliotibial tract, and the common peroneal nerve. Palpate deeply into the lateral joint space for the lateral meniscus, which is attached to the popliteus muscle rather than the lateral collateral ligament. Before palpation of the lateral aspect is concluded, roll the common peroneal nerve very lightly between your fingertip and the neck of the fibula to check its integrity.

On the posterior aspect of the knee, examine the popliteal fossa, wherein is found the posterior tibial nerve, the popliteal vein and artery, and the two heads of the gastrocnemius muscle. Examine the area of origin of the two heads of the gastrocnemius found above the lateral and medial condyles.

Next, palpate the ankle (Fig. 2.14) and foot. Note any bony excrescences, masses, deep callosities, or tenderness. Check skin moisture, note skin texture and tone, evaluate muscle tone, and seek tight ligaments. The head of the 1st metatarsal bone is easily palpated at the ball of the foot. Palpate the joint of the first metatarsophalangeal and the head of the 1st metatarsal. Check for hallux valgus, bunion, or gouty tophi. Then proceed proximally to the 1st metatarsocuneiform bone. Move to the navicular tubercle, which is felt as the next bony prominence. Next, place your fingers on the head of the talus, which is found midway on a line between the medial malleolus and the navicular tubercle.

Move palpating fingers to the small sustentaculum tali (if palpable), which is less than an inch below the malleolus. Move to the medial malleolus at the distal end of the tibia. The medial collateral ligament may be palpable just distal to the malleolus and will be quite sensitive in sprain. Palpate the often visible long saphenous vein just anterior to the malleolus, and note signs of varicosity. Move your fingers to the small medial tubercle of the talus, and then palpate the medial aspect of the calcaneus.

In palpating the sinus tarsi area anterior to the lateral malleolus, fix the heel with one hand and place the thumb of the active hand in the soft-tissue depression in front of the lateral malleolus. Palpate the underlying aspect of the calcaneus and the cuboid articulation. With the thumb in the same position, invert the foot and deeply palpate the neck of the talus. Invert and plantar flex the foot, and palpate the dome of the talus. Then examine the area over the inferior tibiofibular joint located just above the talus.

Passing between the malleoli from medial to lateral is the prominent and medial tibialis anterior tendon, which is best felt during foot inversion and dorsiflexion; the next lateral extensor hallucis longus tendon, which is best felt during extension of the great toe; the superficial dorsal pedal artery; and the extensor digitorum longus tendon, which is best felt when the toes are extended. The pulse of the dorsal pedal artery can be felt between the extensor hallucis longus and extensor digitorum longus tendons of the dorsum of the foot.

Palpate the joint of the 5th metatarsophalangeal and the prominent head of the 5th metatarsal. Carefully palpate the bursa overlying the lateral side of the head of the 5th metatarsal. Next, proceed proximally to the styloid process, to the cuboid bone, to the peroneal tubercle on the calcaneus distal to the lateral malleolus, to the lateral malleolus, to the lateral aspect of the calcaneus, and then to the sinus tarsi area. Then palpate the easily injured lateral collateral ligaments of the ankle.

Palpate the tendon of Achilles as it inserts on the calcaneus and its course in the lower third of the calf. Signs of tenderness, swelling, tenosynovitis, or crepitation should be noted. To test the integrity of the gastrocnemius and soleus, firmly squeeze the calf of the prone patient. Normally, foot flexion results, which will be diminished or absent if a tendon rupture exists. Palpate the area of the retrocalcaneal bursa located between the anterior surface of Achilles tendon and the top of the heel. Lift the skin away from the tendon with one hand while you palpate anterior to the tendon. Then check the calcaneal bursa situated between the insertion of Achilles tendon and the skin.

The soft-tissue depressions at the sides of the Achilles tendon should be examined. Within the depression are found the tibialis posterior tendon, the flexor digitorum longus tendon, the posterior tibial artery and nerve, and the flexor hallucis longus tendon (which is usually unpalpable). The pulse of the posterior tibial artery is often difficult to locate. If the pulse is found, compare bilaterally. Next, palpate the dome of the calcaneus from above plantarward. Examine the area of the medial tubercle lying on the medial plantar surface of the calcaneus and check for spurs in adults or signs of epiphysitis in children. The peronei tendons, passing behind the lateral malleolus, are best palpated during active eversion and plantar flexion.

Start palpation of the plantar surface at the medial tubercle of the calcaneus and proceed distally along the medial longitudinal arch to the end of the toes. The plantar aponeurosis should feel smooth without areas of acute tenderness. Palpable nodules within the fascia suggest Dupuytren's contracture (tender under deep pressure) or plantar warts (tender to pinching). Callosities, as are contractures, are tender to pressure but not to pinching. Soft corns are often found between the toes, especially between the 4th and 5th toes. Hard corns most often arise in areas of excessive pressure, especially near the 5th interphalangeal joint. Deep palpation within the flexor hallucis brevis tendon may elicit signs of sesamoiditis. Palpate each metatarsal head laterally and the transverse arch immediately proximal. Note abnormal prominence of any bone, which is especially common at the 2nd or 5th metatarsal heads and associated with callosities, Check for Morton's neuroma between the heads of the 3rd and 4th metatarsals.

      Stability Screening

When palpation is concluded for the lower extremity, test knee joint stability for

(1) external rotation-recurvatum,
(2) anterolateral rotary instability,
(3) anterior drawer sign,
(4) posterior drawer sign, and
(5) posterolateral rotary instability. Apply the draw test and lateral/medial instability tests to the ankle.

      Ranges of Motion

To assess active and passive range of motion of the knee, test active flexion by having the patient attempt to slowly squat in a deep knee-bent position. Active extension is tested by having the patient arise from this position to the standing position. Note dominance of one knee over the other and the smoothness of movement, especially of the last 10° of extension. Test flexion and extension passively if necessary with the patient prone. Stabilize the popliteal space with one hand, and grasp the patient's ankle with the other hand. Flex the leg as far as possible bilaterally, noting the distance from the heel to the buttock. In testing active knee rotation, have the patient flex his knee slightly and rotate his foot laterally and medially. Passive rotation is tested with the patient supine. Place your stabilizing hand just above the knee and rotate the tibia internally and externally with your active hand.

Screening tests for active range of motion for the ankle and foot can be made by toe walking to test plantar flexion and toe motion, heel walking to test dorsiflexion, lateral-sole walking to test inversion, and walking on the medial borders of the feet to test eversion.

To test passive ankle dorsiflexion and plantar flexion, firmly stabilize the heel and hindfoot with one hand and grip the forefoot with the other hand. Then push the foot into dorsiflexion and plantar flexion with your active hand. To test passive subtalar inversion and eversion, stabilize the distal end of the tibia with one hand and firmly grip the patient's heel with your active hand. Alternately invert and evert the calcaneus. To test passive forefoot adduction and abduction, stabilize the heel and ankle with one hand and grip the forefoot firmly in the active hand. Then manipulate the forefoot medially and laterally to test passive range of motion of forefoot adduction and abduction. In testing flexion and extension toe motion, first test the great toe. To test motion of the 1st metatarsophalangeal joint, stabilize the foot with one hand while the active hand flexes and extends the joint.

      Muscle Strength

To generally evaluate muscle strength of the knee, apply increasing resistance during knee extension and flexion. Test muscle strength of the ankle and foot during dorsiflexion and plantar flexion against resistance.

Concluding Remarks

It takes only a few seconds to throw a baseball. Yet, to describe the biomechanics involved accurately would take scores of pages. The same has been true for the descriptions in this chapter. The time necessary to complete a comprehensive physical examination is only a small fraction of the time necessary to read a description of the procedures involved. With practice, examination time can be shortened without jeopardizing thoroughness.

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