Chapter 13: The Spine, Pelvis, and Extremities

Patients with problems referable to the spine and extremities present in such a way that their condition can be classified rather rapidly by the following parameters: type of symptom(s), and its acuity, and its location(s). Symptoms are pain, tenderness, swelling, deformity, limited function (restricted motion, weakness), or unusual sensations like clicking and snapping. The symptoms are either localized to a single body part, affect two to four parts either simultaneously or sequentially, or are diffuse and either symmetrical or asymmetrical. Symptoms can be acute, subacute, or chronic; in the latter case they may be slowly progressive. Describing the problem by symptom, site, acuity, aggravating or alleviating factors, and progression can rapidly narrow the possibilities to be considered. The examination can then be focused on the specific body part and signs.

When the problem is a single symptom in a single location, the symptom, the signs, and the condition are inseparable and should not be thought of as separable descriptors. These will be addressed in the symptom, sign, or syndrome section depending, somewhat arbitrarily, on which is the key to diagnosis, the symptom, the sign, or the whole picture.

Traumatic injuries will be discussed at the end of the Syndrome section, organized by site of injury.

The musculoskeletal system has four major functional components: bones and ligaments, synovial and fibrocartilaginous joints, muscles and tendons, and nerves innervating the muscles. Tendons anchor muscle to bone, whereas ligaments anchor bone to bone. The shape and body contour is attributable to its bony structure and overlying muscles.

Bones

The ossified skeletons provide mechanical support for the body and protection for the viscera within the body cavities, vertebral column, and skull. Mature bone forms by mineralization of osteoid laid down by osteoblasts on a cartilaginous matrix in the epiphyses of the long bones, endplates of the vertebrae and cartilaginous structures (endochondral bones of the skull and face). Cortical bone forms a thick cortex surrounding a central hollow, the marrow space. Trabecular bone forms an intricate lattice laid down along the lines of stress within the marrow cavity. Bone reabsorption by osteoclasts and new bone formation by osteoblasts is continuous. Bone must maintain strength sufficient to resist compression and tension applied by mechanical loading forces and muscle traction. Bone strength depends upon normal architecture, collagen, and mineralization; abnormality of any component results in susceptibility to fracture. The shape of mature bone is influenced by muscle pull at their anatomic origins and insertions during skeletal maturation. Muscles that insert on a small portion of bone and exert large forces deform the bone into prominences. Adjacent bones are connected by ligaments, collagenous bands continuous with the collagen of the bone itself. Ligaments stabilize the bones relative to one another and the intervening joints.

Joints

Joints separate articulated bones. Fibrocartilage separates bones at joints where motion is minimal, for example, the intervertebral discs. Synovial (diarthrodial) joints separate bones where motion is extensive. The bone surfaces of diarthrodial joints are covered with hyaline cartilage built to resist repeated axial loading with minimal deformation while providing a smooth, virtually friction-free surface for motion. The avascular cartilage derives its nutrition by diffusion from the synovial fluid. The diarthrodial joints are enclosed within a synovial envelope of collagen lined with a single synovial cell layer that secretes the proteoglycans necessary for joint lubrication. Joint integrity is maintained by ligaments anchoring bone to bone and the forces exerted by muscles whose tendons cross the joint.

Muscles, Tendons, and Bursae

Striated skeletal muscles exert contractile force proximally on one bone at its origin and distally via a variably elongated tendon onto its insertion on another bone. Therefore, muscular contraction serves to change the relative position of the bones. Most muscles originate diffusely directly from the periosteum, whereas some attach by tendons at both their origin and insertion, for example, the long head of the biceps. Tendons are elongated, relatively avascular collagen structures that are continuous at their origin with the interstitial collagen of the muscle and at their insertion with that of the bone. Tendons may lie free in the tissue but are often surrounded by synovial sheaths or bursae where they cross mobile joints or pass around bony prominences. Bursae are synovial-lined sacs serving to reduce friction between tendons or muscles and underlying bone. Muscles are highly vascular since they require maximal oxygen delivery to efficiently convert stored glycogen and fatty acids into effective mechanical power. Muscle is enclosed in an inelastic collagenous fascia. Muscle is susceptible to tearing from the force of its own contraction. Ischemic necrosis may occur when contracting with a compromised blood supply. Body contours result from muscles and subcutaneous fat overlying the skeleton. Asymmetry or abnormalities of body contour suggest changes in the underlying muscles, or less commonly, fat distribution.

See the descriptions of each anatomic location given under the sections on Physical Examination and texts on anatomy for artist’s renditions.

The Axial Skeleton: Spine and Pelvis

Cervical spine

There are seven cervical vertebrae (Fig. 13-1A); three of which are specialized: C1 is the atlas (bearing a globe, like the Greek god after whom it is named); C2 is the axis about which the atlas rotates; and C7 is the vertebra prominens. Nodding of the head occurs chiefly at the atlantooccipital joint. Flexion and extension involve the occiput—C1 and C3 to C7. All vertebrae permit lateral bending. Half of rotation occurs at the atlantoaxial joint, with the remainder distributed through the cervical spine. For measurements of cervical motion, see Figure 13-1B.

Thoracolumbar spine and pelvis

Below the neck, there are 12 thoracic and 5 lumbar vertebrae, a fused mass of five sacral vertebrae articulated with the pelvic bones at the sacroiliac (SI) joint and four variously separated coccygeal vertebrae. Viewed laterally, the vertebral column presents four curves (Fig. 13-2A). Least pronounced is the cervical curve, which is concave backward, beginning at C2 and ending at T2. The thoracic curve is convex backward, beginning at T2 and ending at T12. The lumbar curve, more pronounced in the female, is concave backward, from T12 to the lumbosacral joint. The pelvic curve, convex backward and downward, extends from the lumbosacral joint to the tip of the coccyx. The spinal motions are flexion–extension, lateral bending, and rotation. For methods of measurement, see Figure 13-2B. The geometry of the vertebrae, discs, and especially the facet joints at each level, and the presence of the ribs in the T-spine, determines the extent of movement. The thoracic spine allows lateral bending most freely, whereas flexion, extension, and rotation are quite restricted. In the lumbar spine there is considerable freedom of flexion and extension, moderate capacity for lateral bending, and very limited rotation.

Appendicular Skeleton

The hand

The hand includes the carpal, metacarpal, and phalangeal bones, their joints, and the covering soft tissues. Abnormalities in size and disproportions in a part are usually caused by bone abnormalities. The posture of the hand results from the relative tone of the finger and wrist flexors, extensors, and intrinsic hand muscles and the presence or absence of joint disorders.

The wrist

The wrist includes the radiocarpal joint, the eight carpal bones in two parallel rows, and the overlying tendons and tendon sheaths (Fig. 13-3). The radiocarpal joint is the articulation of a concave with a convex surface. The proximal concave surface is formed by the distal radius and the triangular articular disk that caps the distal ulna. The distal convex surface consists of the curving sides of three proximal row carpal bones, the navicular, lunate, and triquetrum. The pisiform does not participate because it lies on the volar aspect of the triquetrum. The navicular is most commonly fractured because the radius has wider contact with it than with the lunate, and the forces transmitted from the ulna to the triquetrum are cushioned by the articular disk. The major synovial cavity lies between radius and the navicular. A minor cavity separates the distal ulna and the articular disk, extending proximally between the radius and ulna.

The topography must be known to properly examine the wrist (Fig. 13-4). Volar Aspect of the Wrist: The pisiform bone can be palpated as a bony prominence on the ulnar side, just distal to the palmar crease and proximal to the base of the hypothenar eminence. Four tendons can be palpated and often seen. With the digits slightly flexed and muscles tensed, three tendons are apparent in most persons. From the ulnar to the radial side, they are the flexor carpi ulnaris, palmaris longus, and flexor carpi radialis. The palmaris longus is absent in approximately 10% of persons. With the fist clenched hard, the tendon of the flexor digitorum sublimis also appears between the flexor carpi ulnaris and the palmaris longus. Dorsal Aspect of the Wrist: The most conspicuous prominence is the ulnar styloid process. Extension of the thumb accentuates the borders of the anatomist’s snuffbox, a recess formed between the extensor pollicis longus and brevis.

The forearm

The forearm extends from the elbow to the wrist. Inspection and palpation are used for examination. The radius and ulna articulate with the humerus proximally. They are connected by an interosseous membrane throughout most of their length. The radius and ulna are practically subcutaneous, so their entire length can be palpated. The dorsal muscle mass is formed by the wrist and finger extensor muscles which insert on the lateral epicondyle of the humerus. The volar mass is the finger and wrist flexors inserting on the medial epicondyle.

The elbow

There are two articulations in the elbow. The hinged humeroulnar joint is formed by the semilunar notch of the ulnar olecranon process embracing and moving around the transverse drum of the spool-shaped trochlea of the distal humerus (Fig. 13-5A). When the elbow is in full extension, the olecranon process fits into the olecranon fossa of the humerus just above the trochlea. The trochlea forms the medial two-thirds of the lower humeral articulation. The lateral third is the rounded capitulum on which a cup-shaped depression in the radial head pivots and glides to form the humeroradial joint. The radial head is a squat cylinder whose sides rotate in the annular ligament during pronation and supination of the forearm.

Viewed from the back (Fig. 13-6), the flexed elbow presents three bony prominences of an inverted equilateral triangle: the two basal points are the medial and lateral epicondyles of the humerus; the tip of the olecranon process forms the apex. During full extension, the three points form a straight transverse line.

The shoulder

The shoulder girdle includes bones (humerus, scapula, clavicle, and sternum), joints (glenohumeral, acromioclavicular, sternoclavicular, and scapulothoracic), their ligamentous connections, and the overlying muscles, tendons, and bursae. The shoulder joint is a ball-and-socket articulation with the hemispheric humeral head fitting into the shallow cavity formed by the scapular glenoid and its surrounding fibrous labrum (Fig. 13-7). The articulating surfaces are enclosed by a short tube of joint capsule. The scapular coracoid process projects anterior and medial to the joint and the acromion forms a rigid fender above the joint. They are connected by the coracoacromial ligament. The clavicle is connected to the acromion by the superior acromioclavicular ligament and to the underlying coracoid process by the coracoclavicular ligament. From its origin within the joint capsule, the tendon of the long head of the biceps emerges anteriorly between the greater and lesser tubercles of the humeral head. The joint capsule is lined by a synovial membrane with a prolongation forming a tubular sheath for the biceps tendon which follows the tendon distally to the surgical neck of the humerus.

The joint capsule is loose, exerting little tension except in extreme positions. Shoulder stability is maintained by muscle tension. Great freedom of motion results from the shallow glenoid cavity, large articular surface of the humeral head, and absence of restraining ligaments; this also makes it vulnerable to dislocation. The scapula is held to the thoracic wall entirely by its muscular attachments, its wing gliding freely over the thoracic muscles. Scapular movements add greatly to upper limb mobility; scapular motion must be distinguished from movements at the glenohumeral joint. The shoulder girdle is connected to the axial skeleton via the acromioclavicular joint, clavicle, and sternoclavicular joint.

The principal bony landmarks of the shoulder, the tip of the coracoid, the greater tubercle of the humeral head, and the acromion, form a right triangle at the greater tubercle. The acromion is easily seen and felt beyond the end of the clavicle. The coracoid is palpated near the anterior border of the deltoid muscle on a horizontal line with the greater tubercle.

The hip joint and thigh

In the diagnostic examination, the hip joint and thigh are considered together. The femoral axis slants medially toward the knee. The greater trochanter of the femur presents a lateral bony mass, palpable through the thigh muscles (Fig. 13-8A). On the medial side and a little distal is the lesser trochanter, smaller in size and inaccessible to palpation. Arising between the trochanters, the femoral neck slants proximally and medially, forming an angle with the femoral axis of 120 to 160 degrees. An increase in the angle produces lateral deviation of the femoral shaft, coxa valga, a decrease in the angle deviates the shaft medially, coxa vara. The neck is surmounted by the globular femoral head, which fits into the cupped acetabulum of the pelvis, forming a ball-and-socket joint. This joint permits flexion–extension, abduction–adduction, and internal–external rotation (Fig. 13-8C). An important topographic relationship is defined by the Nélaton line; extending from the anterosuperior iliac spine to the ischial tuberosity. With the thigh flexed, the line passes through the tip of the greater trochanter; an upward deviation of 1 cm is considered normal (Fig. 13-8B).

The knee

The knee region includes the tibiofemoral and tibiofibular joints, the patella, the adjacent segments of the femur, tibia, and fibula, their ligaments, menisci, and muscles. Viewed from below (Fig. 13-9), the articular surface of the femur is shaped like a horseshoe with its open end posterior. The two anteroposterior legs of the shoe are formed by nearly parallel lateral and medial femoral condyles, separated by the intercondylar fossa. The surface of the anterior bow is indented by a shallow median groove curving upward onto the anterior femur, the patellar articular surface. Superior to the articular surfaces of the condyles is the medial and lateral epicondyles. Viewed from above, the articular surface of the tibia presents two lateral almost flat, oval facets, the medial and lateral tibial condyles, separated by an intercondylar fossa with anterior and posterior segments. The lateral borders of the intercondylar fossa are the intercondylar eminences. On the central anterior tibia, slightly below the joint, is the tibial tuberosity.

The knee joint has three articulations: a medial and a lateral condylar articulation and an anterior joint where the patella glides over the femur (Fig. 13-9). The femoral condyles may be likened to two thick disks with their edges resting on the almost flat tibial condyles. The small radius of curvature of the femoral condyles presents little apposing surface with the tibia in any position. The lateral and medial menisci are flattened crescents of fibrocartilage that rim the peripheral borders of the tibial condyles. Their radial cross-sections are wedge-shaped, with the thickest part outward. This arrangement deepens the articular surfaces of the tibial condyles and fills the space between the curved femoral condyles and the flatter tibial surface. The ends of their crescents are attached to the intercondylar fossa.

The principal internal ligaments are the anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL), named for the positions of their tibial attachments and their crossing arrangement (Fig. 13-9). The ACL begins in front of the anterior tibial intercondyloid eminence and passes upward, backward, and lateralward to the back of the lateral femoral condyle. The PCL attaches to the posterior intercondyloid fossa, passes upward, forward, and medially, to the front of the medial femoral condyle. The lateral (fibular) collateral ligament is a strong fibrous cord ascending vertically from the lateral aspect of the fibular head to the back of the lateral femoral condyle. Its opposite is the thinner and broader medial (tibial) collateral ligament ascending from the medial tibial condyle to the medial femoral condyle.

The flat triangular patella is a sesamoid bone embedded in the quadriceps tendon. The tendon distal to the patella is the patellar ligament, attached distally to the tibial tuberosity. During knee extension the patella rides loosely in front of the distal femur. In flexion, the patella opposes the lateral part of the medial femoral condyle (Fig. 13-10), while with active extension it is often pulled against the lateral femoral condyle.

The head of the fibula articulates with the lateral tibial condyle by an arthrodial joint inferior to the knee joint and entirely separated from it. The fibula is held to the tibia by the joint capsule and anterior and posterior ligaments.

The joint capsule of the knee is a complex of fibrous sheets reinforced by bands from the muscle tendons crossing the joint. It is a single synovial sac that envelops the articular surfaces of both pairs of condyles forming the largest joint cavity in the body. A large suprapatellar pouch ascends anteriorly, first between the patella and the anterior aspect of the femur, then between the quadriceps tendon and a fat pad in front of the femur. Understanding the extent of this sac is diagnostically important.

The principal bursae of the knee are of diagnostic importance: (1) a bursa lying between the skin and the patella, the prepatellar bursa; (2) a smaller bursa between the skin and the patellar ligament, the superficial infrapatellar bursa; (3) a bursa between the skin and the tibial tuberosity; and (4) the anserine bursa medial and inferior to the knee joint between the tibia and the tendons of the semitendinosus, gracilis, and sartorius muscles. The suprapatellar pouch of the knee joint between the quadriceps tendon and femur is not a true bursa, though it functions as such. It may be erroneously called the suprapatellar bursa.

Full motion at the knee is flexion to over 140 degrees and extension to 180 degrees or slightly beyond.

The ankle

The ankle joint is a hinged articulation between the tibia proximally and the talus of the foot distally. The superior articular surface of the talus is rounded superiorly and tipped slightly medially and is continuous with the flattened, nearly vertical medial and lateral faces (Fig. 13-11). The upper curvature articulates with the flat surface of the lower tibia. The sides of the proximal portion of the joint are the medial malleolus of the tibia and the lateral malleolus of the fibula. These serve as the sides of a mortise, articulating with the flat lateral surfaces of the talus and stabilizing the joint laterally and medially. During ankle flexion and extension, the tibial surface glides over the curved surface of the talus changing the angle between leg and foot and rotating the leg medially on the foot with increasing dorsiflexion helping to transfer weight toward the medial foot and great toe during stance and push-off phases of gait. The lower ends of the tibia and fibula are bound together by the anterior and posterior tibiofibular ligaments. The medial malleolus is attached to the talus and calcaneus by a triangular band, the deltoid ligament. The lateral malleolus is attached below to the talus and calcaneus by the calcaneofibular ligament and the anterior and posterior talofibular ligaments. The joint capsule surrounds the articulation and is lined with synovial membrane.

The motions of the ankle joint are dorsiflexion (extension) and plantar flexion (flexion) (Fig. 13-12). The only bony landmarks are the lateral and medial malleoli; the lateral is lower than the medial.

The foot

The foot is a complex structure designed to withstand the enormous forces transmitted bidirectionally between the body and the ground during walking, running, and jumping. It is both flexible and strong, and able to adapt to virtually any ground surface. It is divided into the hindfoot (talus and calcaneus), midfoot (navicular, cuboid and medial, intermediate, and lateral cuneiforms), and the forefoot (metatarsals, phalanges, and sesamoids). The hindfoot and midfoot are separated by the transverse tarsal joint separating the talus and calcaneus from the navicular and cuboid, respectively. The transverse tarsal joint is responsible for inversion and eversion. The midfoot is separated from the forefoot at the tarsometatarsal joint. The foot has two prominent arches: the longitudinal arch forms the instep medially from the tubercles of the calcaneus to the heads of the metatarsals; and the mediolateral metatarsal arch from the first to the fifth metatarsal heads. The calcaneus is palpable on all but its superior and distal surfaces. The bones of the midfoot and forefoot are best palpated dorsally where they are not covered by muscle. There is a bony prominence on the midlateral margin just above the sole formed by the tuberosity of the fifth metatarsal.

The foot can be visualized anatomically as a tripod constructed of a series of triangles, each with an apex and a base. The tripod has its apex at the tibiotalar joint and a triangular base made up of the calcaneus and the first and fifth metatarsal heads. This tripod allows stable weight bearing on uneven ground. One of the triangles is the longitudinal arch with its apex at the transverse tarsal joint and its base the calcaneus and first metatarsal head. Another is the metatarsal arch, with its base the first and fifth metatarsal heads and its apex the third metatarsal head. The tip of the great toe with the first and fifth metatarsal heads forms the stable triangular base for the pushoff phase of gait. Last, each toe forms a triangle with the apex at the proximal interphalangeal (PIP) joint and the base at the pad of the toe and the metatarsal head. These functionally interlocking structures give the foot extraordinary strength and dynamic stability. Any disruption of this complex architecture results in significant loss of function.

The examination must integrate the observations of bones, joints, and muscles. Most clinicians examine anatomic regions in a sequence dictated by convenience for the doctor and patient, rather than examining each component sequentially. This also requires constant cross-referencing to the nervous and peripheral vascular systems.

Examination of the Spine

The cervical spine examination

STOP: Following trauma or suspected cervical injury, the cervical spine must ALWAYS be immediately IMMOBILIZED in a rigid collar PRIOR TO ANY MOVEMENT or examination of the patient.

In the absence of acute trauma, examine the patient in the seated position viewing the neck from the front, sides, and back for deformities and unusual posture. Have the patient point to the site of pain. Test active motions of the neck with the instructions: “chin to chest,” “chin to right and left shoulder,” “ear to right and left shoulder,” and “head back.” With the flat of the hand, palpate the paravertebral muscles for muscle spasm, tender points or trigger points. Palpate and percuss the spinous processes for tenderness.

The thoracolumbar spine and pelvis examination

STOP: Following trauma or suspected spinal injury, the spine must ALWAYS be immediately immobilized on a back board PRIOR TO ANY MOVEMENT or examination of the patient.

The patient should be gowned such that the spine can be easily observed while maintaining patient comfort. With the Patient Standing: Observe from the back and side for deformity, muscle wasting, local swelling, abnormal curvature, or lateral deviations of the spine. If the spinal processes are not visible, palpate and mark each to disclose a scoliosis. When lateral curvature is present, have the patient bend forward observing the spine and the chest wall on either side of the spine. Note whether the spine straightens and any asymmetry of the chest wall. In structural scoliosis, one side will be higher than the other (Fig. 13-13); with muscle spasm or ligament and joint disease, the chest will be symmetrical. Have the patient tense the glutei to reveal wasting. Percuss each spinous process to elicit tenderness. Have the patient walk observing the gait. Have the patient hop on each foot to identify muscle weakness and pain. Direct the patient to flex, extend, and laterally bend the spine without assistance. Test rotation by grasping the hips while the patient turns first one shoulder, then the other. Palpate for tenderness, muscles spasm or tender, or trigger points. With the Patient Supine: Have the head pillowed and the knees slightly flexed for comfort. Do the straight-leg-raising test, (Fig. 13-14A) by grasping the ankle, with the knee held in extension, and lifting the lower limb to its limit. Note the location of pain elicited, especially contralateral radiation indicating nerve root compression (Lasèque sign). With the straight leg elevated at a little-less-than-complete flexion, dorsiflex the foot looking for aggravation of pain. An alternative test is to gradually extend the flexed knee, with the finger pressing on the tibial nerve in the popliteal fossa; this produces pain if there is irritation of the lower lumbar nerve roots. With the Patient Prone: Ask the patient to turn from the supine to the prone position and note the amount of guarding, an indication of pain severity. For comfort, place a pillow between the table and the patient’s pelvis. See if the muscle spasm and spinal deformity observed while erect persists in the prone position. Reexamine for areas of tenderness and deformity. A step deformity between L5 and S1 indicates spondylolisthesis. With the heel of the hand, press along the spinous processes. Pain from light pressure suggests approximating spines with an intervening bursa; pain from deep pressure arises in intervertebral facets or disks. With the Patient Sitting: Examine for muscle wasting and check the knee and ankle reflexes.

Schober test for lumbar flexion

With patient standing erect, heels together, place a mark on the spine at the lumbosacral junction (the L5 spinous process or the point where a horizontal line between the posterior superior iliac spines intersects the spine) and a second mark 10 cm above the first. Have the patient bend forward maximally, trying to touch the fingers to the toes. Normally, the distance between the marks increases by ≥5 cm. If the distance increases <4 cm, mobility is restricted.

Additional examinations for herniated disk

Test neurosensory function by assessing knee and ankle reflexes, flexion and extension strength at the knee and ankle, great toe extension strength, and sensation to touch. Crossed-Straight-Leg-Raising Test: Have the patient lie supine and lift the unaffected limb with the knee held straight. In the presence of herniated disk, this maneuver will exacerbate the pain in the affected limb and may cause sciatic pain in the hitherto unaffected limb. This is considered by some writers to be pathognomonic of herniated disk. Reverse Straight-Leg-Raising Test: With the patient lying prone and the knee flexed maximally on the thigh, the normal person complains of quadriceps tightness in the anterior thigh. With true disk disease, as the root tightens over the involved disk and abdominal compression increases the subarachnoid pressure, the pain is felt in the back or in a sciatic distribution on the affected side.

Testing the SI joint

Examine the patient while sitting facing away from you. Locate the posterior superior iliac spines by the dimples in the overlying skin or by placing your thumbs on the iliac crests with your hands around the patient’s trunk (Fig. 13-15) and following the crests medially to the iliac spines. The portion of the SI joint most accessible to palpation is one fingerbreadth medial to the spines. As the patient bends forward slowly, press your thumbs deeply along the joint looking for tenderness. In the Gaenslen test of the SI joint (Fig. 13-14C), the supine patient holds the knee of the affected side with both hands, flexing the knee and the hip to fix the lumbar spine against the table; then hyperextend the other thigh by pushing it downward over the side of the table. An affected SI joint will be painful with this maneuver. Active prone hyperextension of the spine (Fig. 13-14D) may aggravate SI pain when the patient attempts to lift the spine against the resistance of the examiner’s hand held in the lumbar region.

Low back pain—Magnuson pointing test for malingering

Low back pain is a favorite complaint of malingerers. Identify the painful spot by palpation and mark it with a skin pencil. After completing the rest of the examination, palpate once again for the painful spot. The patient with organic disease identifies the same point each time; the malingerer identifies a somewhat different spot.

Examination of the Appendicular Skeleton

Examine all joints systematically from head to foot or in reverse sequence, comparing right and left. To minimize pain and guarding, place the patient so the joint to be examined is supported. Inspect the bony landmarks, the size and contour of the joint (visualizing the location of the joint capsule), the overlying skin color and any deformity (swelling, angulation, rotation, subluxation, contracture, or ankylosis). Palpate gently, for skin temperature and tenderness in the skin, muscles, bursae, ligaments, tendons, fat pads, and joint capsule. The normal synovium is not palpable, whereas a thickened synovium feels “doughy” or “boggy.” Test the joint for effusion by placing the finger(s) of each hand on opposite sides of the joint, then compress with one hand; an effusion will displace the receiving fingers. Test active range of motion by directing the patient to move the joint through its full range. To test passive range of motion, anchor the joint proximally with one hand whereas the other moves the distal member gently to its full limits. Observe how the motion terminates: muscle spasm, gelling that improves with repeated movement, effusion in the joint, locking from loose bodies in the joint or fibrosis cause “soft arrests,” whereas bony ankylosis causes a “hard arrest.” Palpate over the joint for crepitus with motion. Test for ligament integrity by anchoring the bone proximal to the joint while gently displacing the distal bone in the plane to be tested. The muscles must be relaxed when testing ligament stability. Always compare right and left since normal ligament tightness is quite variable, from tight to loose (“double jointed”).

The upper limb

This anatomic region includes the structures of the neck, shoulder girdles, upper arms, forearms, wrists, and hands. Its principle function is the placement and manipulation of the hands. The examination usually begins with the hands and works proximally, the sequence used here.

The hand

Hand structures are relatively superficial and easily examined. Inspection: The fingertips in extension form an arc with the apex at the middle finger. With flexion the finger tips align at the base of the thenar eminence with the nails in the same plane; if there is shortening or crossing of the fingertips then prior injury with shortening and/or rotation of the affected phalanges or metacarpal is present. Have the patient gently make a fist and observe the knuckles, the distal metacarpal heads. There should be a smooth arc between the index and little fingers. Depression of a knuckle indicates shortening of the metacarpal. Observe the bulk of the intrinsic hand muscles on the dorsum of the hand and the web space between the thumb and index finger. Prominence of the tendons and bones occurs with loss of muscle mass, usually resulting from an ulnar nerve lesion. Inspect the palmar aspect of the hand for normal skin creases, the bulk of the thenar and hypothenar muscle masses, callosities or thickening of the palmar fascia. Inspect the nails and finger tips for deformities, ulcers, and signs of previous trauma. Palpation: Examine each joint for bony prominences, synovial thickening, or effusion. Palpate the thenar, hypothenar and first web space muscles both relaxed and with contraction. If bone injury is suspected, palpate the entire length of the bone. Squeeze the palm from front to back and laterally across the knuckles to detect tenderness.

Functional tests of fingers

Complete functional examination of the hands is beyond the scope of this text, requiring an in-depth understanding of the anatomy of the bones, muscles, tendons, ligaments, and nerves of the hand and forearm. Here, we present a screening examination. The fingers are named thumb, index, long or middle, ring, and little, or they are numbered one through five. The phalangeal joints are termed distal interphalangeal (DIP), proximal interphalangeal (PIP), and metacarpophalangeal (MCP). The aspects of the fingers are dorsal (extensor surface) and volar (flexor or palmar surface). Figure 13-16 illustrates the functional assessment of the joints. Muscle testing is described on Testing Muscle Strength. Test active flexion and extension against resistance at the DIP and PIP joints. The superficial flexors attach on the middle phalanx assisting flexion of the MCP and PIP. Flexion at the DIP is performed solely by the deep flexors. Next, test abduction and adduction of the fingers; these movements are powered by the interosseus and lumbrical muscles innervated by the ulnar nerve. Test the thumb flexion and extension power at the MCP and IP, as well as abduction and adduction performed by the thenar muscles innervated by the median nerve.

The wrist

Inspect and palpate the wrists for asymmetry, swelling, tenderness, deformities, and crepitus. Testing Wrist Motion: The primary motions of the wrist are extension–flexion (dorsiflexion and palmar flexion) and radial–ulnar deviation; Figure 13-4 depict the methods of measurement.

The forearm

Inspect the muscle masses for symmetry; often the dominant arm is better muscled. Assess for weakness and/or wasting. Both the radial and ulnar arterial pulses are palpable proximal to the wrist. The motions of the forearm are pronation and supination (Fig. 13-17). Test for active and passive range of motion and power against resistance. Pain with resisted motion is especially important and the sites of pain should be palpated.

The elbow

Inspect and palpate the region for deformity, tenderness, and swelling. Swellings are more common on the extensor surface. Subcutaneous nodules are often found in the olecranon bursa and distally in the ulnar region. Testing Elbow Motion: The movements of the humeroulnar joint are extension-flexion. Pronation–supination principally involves the humeroradial and the distal radioulnar joints. Measurements of these motions are indicated in Figure 13-5B. Test passive and active motions and strength by resisting active motion.

The shoulder

Examine the disrobed patient from front and back while sitting with the arms relaxed (Fig. 13-18). Inspect the shoulder anteriorly and the scapula posteriorly for deformities and muscle wasting; nearly everyone carries one shoulder higher than the other. Palpate the scapular spine, following it to the acromion and the acromioclavicular joint. Palpate the sternoclavicular joint for deformity or tenderness. Next, palpate the subacromial space and the deltoid muscle and its subdeltoid bursa. Palpate the tendons of the rotator cuff for defects or tenderness. Palpate their insertions on the greater (supraspinatus, infraspinatus, and teres minor tendons) and lesser (subscapularis tendon) tuberosities of the humerus. Feel the bicipital groove between greater and lesser tuberosities for tenderness in the bicipital tendon sheath. Stand behind and to the side of the patient to palpate the supraspinatus tendon and the subacromial bursa. For the right shoulder, place your left hand over the shoulder so your index finger palpates the tendon just behind its attachment on the greater tubercle of the humeral head, and your middle finger palpates the subacromial bursa. With your right hand on the patient’s flexed elbow, move the arm backward and forward a few times to detect crepitus or tenderness at either point. Finally, place your fingers in the axilla with the pulps facing laterally and palpate the humeral head and the lateral aspect of the glenoid synovial sac.

Measurements of shoulder motion

Imagine the shoulder joint as the center of a sphere, marked as a globe with a north and south poles and meridians (Fig. 13-19). Then an anterior-posterior (parasagittal) plane through the shoulder joint describes an anterior meridian on the sphere’s surface that is 0 degree of abduction–adduction. Meridians lateral to it mark degrees of abduction and those medial to it are degrees of adduction. When the arm hangs at the patient’s side, it is in 0 degree of elevation and abduction. The arm can be lifted from the South Pole to the North Pole or from 0 to 180 degrees of elevation. While elevating, the arm must follow in a meridian that designates abduction or adduction. If the arm is raised directly forward to the horizontal, the position is 90 degrees of elevation with 0 degree of abduction; this is the cardinal motion of FLEXION. When the arm is raised laterally to the horizontal, the position is 90 degrees of elevation with 90 degrees of abduction; this is the cardinal motion of ABDUCTION. When the arm is raised directly posteriorly, the position is elevation with 180 degrees of abduction; this is the cardinal motion of EXTENSION. If, however, the arm is raised to the horizontal in a meridian 20 degrees medial to 0 degree, the position is 90 degrees of elevation with 20 degrees of adduction.

Testing shoulder mobility

Shoulder mobility includes scapulothoracic and glenohumeral joint motions. Test the unaffected shoulder first and compare the affected side with it. The cardinal movements of the shoulder are abduction (elevation at 90 degrees abduction), adduction (at 90 degrees elevation), flexion (elevation at 0-degree abduction), extension (posterior elevation at 180 degrees abduction) and internal and external rotation. Range of motion should be assessed both actively and passively. Active motion is accomplished by the patient and assesses joint mobility and muscle and tendon integrity and reveals limitations of motion as a result of pain. The examiner provides the power during passive motion while the patient relaxes, eliminating muscle and tendon limitations, to reveal the full range of motion available to each joint. Elevation with abduction involves both scapulothoracic and glenohumeral movement. Have the patient slowly raise the arm laterally from the side to straight overhead; the scapula should begin to move when elevation of the arm attains 60 degrees. To test glenohumeral motion alone, grasp the scapular wing and hold it fast to the thorax with one hand while the patient’s arm is resting at his side (Fig. 13-18B). Alternatively, place one hand on top of the acromion to stabilize the scapula. Have the patient raise the arm laterally (90 degrees of abduction) and let the patient complete the motion as far as possible, with the scapula fixed. For adduction (at 90 degrees elevation), from the side rest the fingers of one hand on top of the patient’s shoulder with your thumb behind, fixing the patient’s scapula. Have the patient move the arm across the front of the chest as far as possible trying to place the wrist over the opposite shoulder. Flexion (elevation at 0-degree abduction) is tested by having the patient elevate the arm forward from rest to straight overhead in the anterior–posterior plane. For extension (posterior elevation at 180 degrees abduction), have the patient push the arm straight backward in the same plane to the limit of motion. Test internal and external rotation with the arm at 90 degrees of abduction and 90 degrees of elevation, starting with the elbow flexed at 90 degrees and the palm facing the floor. For internal rotation, ask the patient to lower the hand, palm down, as far as possible without moving the elbow. For external rotation, start from the neutral position and have the patient raise the hand, palm forward, as far as possible without moving the elbow. Repeat internal and external rotation with the elbow flexed 90 degrees and held at the side (0 degree of elevation and abduction). When there is a deficit in active motion, test passive range of motion by repeating the maneuver with the patient relaxed and the examiner supporting the arm and gently putting it through the motion. Test for abduction strength and pain by resisting abduction at 30 degrees (supraspinatus) and 90 degrees (deltoid).

Auscultation of bone conduction through the shoulder

The olecranon–manubrium percussion sign is useful in evaluating patients with possible shoulder dislocations, clavicular fractures, or humeral fractures. Place the bell of the stethoscope over the manubrium with the patient’s elbows flexed at 90 degrees and percuss the olecranons. Normally, with no disruption of bony conduction, percussion of right and left will produce equal crisp sounds. When dislocation or fracture disrupts bony conduction, the affected side will have decreased intensity and duller pitch.

The lower limb

This region includes the pelvis, buttocks, hip joints, thighs, knees, legs, ankles, feet, and toes. Its principal functions are maintenance of an upright stance against gravity and locomotion.

Leg length

Leg length is measured in straight lines from the anterior superior iliac spines to the medial malleoli (Fig. 13-20E). Be sure the tape is in a straight line running medial to the patellae. Both feet should lie exactly equidistant from the midline. If one leg cannot be placed in normal position, its opposite should be measured in a similar position. A difference of >1.5 cm suggests hip deformity in the shorter leg.

Thigh and leg girth

Girth is usually a function of muscle mass; wasting not detected by inspection can be identified. The circumference of the thighs is measured with a tape measure at symmetrical levels from the anterior superior iliac spines (Fig. 13-20D). The leg girth is measured at symmetrical distances from the tibial tuberosities.

The hip

The patient should be disrobed from the waist down, covering the genitalia but not the buttocks. Have the patient point to the site of pain. An affected hip joint commonly causes pain in the inguinal region or in the buttocks posterior to the greater trochanter. Pain from the hip joint may be felt only in the knee; this has led to many diagnostic errors.

Begin the examination with the patient standing. Have the patient walk looking for abnormalities of gait: swinging the leg from the lumbar spine suggests ankylosis; a waddling gait is typical of bilateral hip dislocation; the gluteal gait (Trendelenburg gait), with the trunk listing to the affected side with each step, suggests gluteus medius weakness, or, rarely, unilateral hip dislocation. With the patient standing still, look for a list to one side, asymmetry of the buttocks or other muscle masses, and scars or sinuses.

Lateral tilting of the pelvis

To determine if the pelvis is level, sit in front of the standing patient, with your thumbs on the anterior superior iliac spines; the interspinous line should be horizontal. Lateral tilting results either from adduction of one thigh or from shortening of the limb. Next, measure the distance between the greater trochanters and the anterior superior iliac spines: with your middle fingers, find the tips of the greater trochanters and palpate the distances to the spines. Small differences can be detected (Fig. 13-8B). If the pelvis is not horizontal, place books or blocks under the foot of the shorter limb until the pelvis becomes horizontal; this provides an accurate measurement of shortening.

Next, have the patient lie on the examining table. All the following tests except that for extension are made in the supine position.

Test for rotation in extension

This motion should be tested first because it is gentlest; if it is painful, all other maneuvers should be carried out cautiously. With the patient supine, place a hand on each side of the lower thigh and rock it from side to side, watching the patella or the foot for the range of rotation (Fig. 13-20A). Alternatively, the foot may be rocked from side to side.

Test for rotation in flexion

Flex the knee and hip to 90 degrees, then move the foot maximally both medially (external rotation) and laterally (internal rotation) (Fig. 13-8C).

Test for abduction

Have the patient lie supine with the legs together. Place a hand on the iliac crest and grasp the ankle with your other hand; gradually abduct the patient’s thigh until you feel the pelvis move, and note the angle attained (Fig. 13-8C).

Test for adduction

With each hand, grasp an ankle, holding one leg down in extension while you move the other thigh across it (see Fig. 13-8C). Note the angle attained from the neutral position. Normally, the thigh should cross the other at midthigh.

Test for hip flexion contracture

Flexion contracture of the hip is compensated for by a lumbar lordosis, allowing an upright stance that masks the contracture. Place your hand under the lumbar spine flexing the unaffected thigh until the spine presses your hand against the table to indicate that the lumbar lordosis has been straightened. Now, extend the other thigh. It should be able to lie flat on the examination table. Lack of full extension reveals a flexion contracture on the affected side, a positive Hugh Owen Thomas sign (Fig. 13-20C).

The anvil test

Raise the leg from the table with the knee in extension and strike the calcaneus with your fist, using a moderate blow in the direction of the hip joint (Fig. 13-20B). This may elicit pain in early disease of the joint.

Palpation of the hip joint

Facing the patient, examine the left hip with your right hand, and the right hip with your left hand. Hook your fingers about the greater trochanter with your thumb placed on the anterior superior iliac spine (Fig. 13-8B). With your thumb, follow the inguinal ligament medially until you feel the femoral artery, then move your thumb just below the inguinal ligament and lateral to the artery; this should bring your thumb over the small portion of the femoral head that is extra acetabular. Apply increasingly firm pressure to elicit pain from arthritis. Rock the femur gently to feel crepitus. If the head does not move, fracture of the neck is probable. If the head cannot be felt, dislocation is suggested.

Patrick (FABER) test

Passively flex the knee to a right angle and place the foot on the opposite patella. Push the flexed knee toward the table as far as the hip joint permits (Fig. 13-14B). This is also known by its acronym FABER (Flexion, Abduction, and External Rotation). Painless and full external rotation (negative Patrick sign) excludes symptomatic disease of the hip joint and SI joints.

Test for extension

With the patient prone, steady the pelvis with one hand while you raise the limb posteriorly (Fig. 13-8C). Normal extension is about 15 degrees.

The knee

The normal movements of the knee are flexion and extension. For measurements, see Figure 13-10B.

Screening knee examination

Inspection: Have the legs and thighs uncovered; observe the patient standing and supine. Inspect the knee region for deformities, swelling, redness, and muscle wasting. Note the position of the patella. Palpation: With the patient supine, test swellings for fluctuance, joint effusion, crepitation with motion, and points of localized tenderness in the ligaments, bones, and along the joint line. Palpate for doughy synovial thickening with obscuration of bony landmarks. Test the range of flexion and extension, anterior and posterior mobility of the tibia on the femur, and the medial and collateral ligaments for laxity or pain. With a history of pain or locking, test for internal disorders as described on The injured knee.

Examination for knee effusion

Inspection may reveal bulging obliterating the natural hollows on both sides of the patellar tendon and in the suprapatellar pouch; it may assume a horseshoe shape around the patella (Fig. 13-21A). Palpate with the patient supine and the knees extended. Gently press the thumb and fingers of the right hand against the anterior femoral condyles at the medial and lateral sides of the distal patella slightly proximal to the joint line. Slide the left hand down the distal thigh with constant pressure until the patella rests in the space between the thumb and the first finger; you will be compressing the suprapatellar pouch. If effusion is present, you will palpate and often see a bulge of fluid appear under the palpating thumb and/or fingers. Small amounts of fluid can be detected visually by compressing the swelling in one of the obliterated hollows beside the patella then watching for the hollow to slowly refill spontaneously or with compression of the suprapatellar pouch. Test for patellar ballottement (patellar tap or floating patella) by compressing the suprapatellar pouch, as described above, while the fingers of the other hand push the patella sharply against the femur (Fig. 13-21B). If fluid is present in sufficient quantity to elevate the patella from the femur, the brisk pressure on the patella will force it down against the femoral condyles with a palpable tap, the patellar ballottement sign.

Examination of the knee ligaments

This is part of the routine knee examination. Determine the degree of tightness or laxity of the anterior and posterior cruciates and both collateral ligaments. Always compare right to left since considerable individual variation exists for joint stability.

Collateral ligaments

With the patient supine, flex the knee to 10 degrees. Palpate the insertions proximally and distally and each ligament at the joint line. The rope-like lateral ligament is easily identified at the joint line posterolaterally. The broader medial ligament is more difficult to identify. Grasp the calf with one hand while the other hand supports and stabilizes the femur from behind with the thumb and fingertips on opposite joint margins overlying the collateral ligaments (Fig. 13-22). Stress the lateral then the medial collateral ligaments by exerting a varus then a valgus force on the calf while palpating over joint margin. Feel for separation of the tibia from the femur and look for medial or lateral displacement of the tibia.

Cruciate ligaments

Test the anterior cruciate with the Lachman test (Fig. 13-23A). Have the patient lie supine and flex the affected knee to an angle of 30 degrees. Sit on the patient’s foot to fix it. Grasp the upper part of the leg with your fingers in the popliteal fossa and your thumbs on the anterior joint line. Pull the head of the tibia toward you so it glides on the femoral condyles. Forward movement of more than 1 cm is a positive Lachman test, indicating rupture of the ACL. To test the posterior cruciate, start as in the Lachman test and observe for sagging of the tibia posteriorly. Then push the head of the tibia posteriorly. Displacement should be <5 mm. Always compare the two knees because considerable individual variability in ligament tightness is normal; asymmetry indicates previous injury.

The injured knee

Obtain a detailed account of previous trauma, including the exact mechanism of injury. This is essential to understanding which structures might have been injured. Ask which motions cause discomfort or locking, and ascertain whether unlocking is sudden or gradual (as in muscle spasm). Have the patient point to sites of pain and demonstrate the position of fixation if locking has occurred. Inspection: Examine the patient supine on the table. Note evidence of joint effusion and muscle wasting. Palpation: Feel the knee carefully for point tenderness, especially over the quadriceps tendon, patellar tendon, collateral ligaments, anserine bursa, and along the joint line. Palpate the surface of the patella and under its edges, then push the patella aside and palpate the underlying femoral condyles. Feel for a click with pain while putting the knee through a full range of motion. A painless click is relatively unimportant as it may be caused normally by tendons moving over a bony prominence. Have the patient put the knee through a full range of active motion and compare with the passive range of motion. Remember that joint effusion limits flexion and full extension. Immediately after injury, muscle spasm and swelling may make full examination impossible, in which case, immobilize the knee for a day or two and then reexamine it [Solomon DH, Simel DL, Bates DW, Katz JN, Schaffer JL. The rational clinical examination. Does this patient have a torn meniscus or ligament of the knee? Value of the physical examination. JAMA. 2001;286:1610–1620].

Testing for meniscus injury

Several tests can be performed to identify meniscus injury.

McMurray test

With the patient supine on the table, grasp the patient’s knee with one hand so that your fingers press the medial and lateral aspects of the joint (Fig. 13-24A). Grasp the patient’s heel with your other hand so that the plantar surface of the foot rests along your wrist and forearm. First, flex the knee until the heel nearly touches the buttock. To test the posterior half of the medial meniscus, rotate the foot laterally, and then slowly extend the knee fully. If a click is felt or heard during the extending motion, and the patient recognizes it as the sensation preceding pain or locking, the medial meniscus is torn. For the lateral meniscus, repeat the examination with the foot rotated medially.

Apley grinding test

Have the patient lie prone on a low couch, approximately 2 feet (60 cm) high, with the patient’s affected limb toward you (Fig. 13-24B). Grasp the foot with both your hands, flex the knee to 90 degrees, and rotate the foot laterally. This should cause little discomfort. Now, rest your knee on the patient’s hamstrings to fix the femur, and pull the leg to further flexion while the foot is held in lateral rotation; pain indicates a lesion of the MCL. Next, compress the tibial condyles onto the femoral condyles by placing your body weight onto the plantar surface of the foot, still in lateral rotation. Pain from this maneuver indicates tear of the medial meniscus.

Childress duck-waddle test

This test is strenuous and is reserved for athletes (Fig. 13-24C). Have the patient squat and waddle on the toes, swinging from side to side. With rupture of the posterior horn of the meniscus complete flexion cannot be attained; the maneuver elicits pain or clicking in the posteromedial portion of the joint.

The ankle

Inspect and palpate the ankle for edema, effusion, or tenderness. Test, dorsiflexion and plantarflexion, by grasping the heel firmly with your left hand to immobilize the subtalar joints while your right hand grasps the midfoot and moves the ankle through the full range of flexion and extension. Test anterior stability (drawer test) by stabilizing the distal tibia with one hand while grasping the heel and pulling it directly forward with the other. Test inversion and eversion stability by stabilizing the tibia as above while alternately firmly inverting and everting the heel. Increased mobility with each test indicates injury to the ankle ligaments stabilizing that motion.

The foot

Inspect the shoes for uneven wear. Normal wear is on the lateral edge of heel. Wear on the medial side of the heel and tilting of the vertical heel seam indicates abnormal foot mechanics. With the patient barefoot and standing inspect the heels from behind, the sides and the front. Always compare right to left. Look for the normal slight outward angulation of the heel which should rotate medially when standing on the toes. Note any deformities (e.g., hammertoes or bunion), the height of the pedal arches, and alignment (a plumb line hanging from the mid-patella should point between the first and second metatarsals). Have the patient point to the site of pain and palpate there for tenderness or crepitus. With the patient supine, inspect the sole for calluses and palpate the fat pads under the calcaneus and metatarsal heads. Test motion by supporting the heel with one hand while moving the foot in dorsiflexion, plantarflexion, eversion, and inversion with the other hand (Fig. 13-12A).

Examination for flatfoot

Have the patient stand with the feet parallel and separated by approximately 10 cm. Note the height of the medial longitudinal arch. If it is flattened, see if it resumes a normal height when weight is removed. Test strength of the anterior leg muscles by having the patient stand on the heels. Test for shortening of the Achilles and peroneal tendons by dorsiflexion and inversion, respectively, in the supine position. Test eversion, which is limited in rigid flatfoot.

Muscle examination

See Chapter 14, The Neurologic Examination.

Brief examination for skeletal injuries

STOP: If pain or other symptoms or signs lead you to suspect injury to the spine, IMMEDIATELY IMMOBILIZE the patient and obtain radiographic confirmation of stability before moving the neck or spine or proceeding with the examination. Trauma of sufficient force to cause injury to major skeletal structures is frequently accompanied by internal visceral injuries, which ALWAYS take precedence over the skeletal injuries.

The following procedure is recommended for the rapid examination of injured but conscious persons to uncover skeletal lesions in the absence of specific complaints.

Head

Have the patient open and close his mouth and bite down with your fingertips on the masseter muscles; if no pain is elicited, the facial bones are not affected. Palpate the zygomatic arch and nose for tenderness. Palpate the scalp for bruises and lumps. With your hands, press from opposite sides of the patient’s head for the pain of a skull fracture.

Neck

Palpate the spines of the cervical vertebrae with your fingers before moving the neck. Have the patient roll his head gently from side to side while your fingers palpate the neck muscles for tenderness or spasm. Ask the patient to lift his head while you place your hand under it. Ask the patient to push down with his head to estimate his strength and discomfort.

Stop

If PAIN is elicited with any of these maneuvers, IMMEDIATELY IMMOBILIZE the neck and cease further movement or examination until the neck is cleared by adequate radiologic examination.

Chest

Ask the patient to take a deep breath; if this is painful, place your hands on opposite sides of the patient’s chest and squeeze to locate the point of tenderness of a rib fracture. Palpate the length of each clavicle.

Spine

With the patient supine, slip your hand under the patient’s back, lift the patient’s chest slightly, and run your fingers over the spinous processes for tenderness and angulation. Determine if there is limitation of spinal motion.

STOP: If PAIN is elicited with any of these maneuvers, IMMEDIATELY IMMOBILIZE the spine and cease further movement or examination until the spine is cleared by adequate radiologic examination.

Arms and hands

Have the patient move his fingers, hands, and arms in succession and through a full range of motion. Palpate each finger for phalangeal and metacarpal injuries. Shake hands, both right and left, and ask the patient to twist his arm, with elbow both straight and flexed. Painless performance of these motions with normal strength excludes injuries of hand, wrist, forearm, elbow, arm, shoulder, clavicle, and scapula.

Pelvis

Place downward pressure with a hand on each anterior ilium, then on the symphysis pubis. Place your clenched fist between the patient’s knees and ask the patient to squeeze it; lack of pain excludes fractures of pelvis and femora.

Legs and feet

Ask the patient to move first one leg, then the other, through a full range of motion. Palpate each toe. Have the patient stretch his legs flat on the table. Press his feet together and have him rotate them laterally against your resistance. Normal strength without pain on these maneuvers excludes major injuries of legs and pelvis.

Pain

Pain arising in the bones, ligaments, and joints is very well localized by the patient. Ask them to point with a single finger to where they feel the pain. Remember that pain from deep structures will radiate to superficial sites having the same segmental innervation. For instance, femoral neck fracture may be felt as pain on the medial side of the knee. Increased pressure within a closed medullary cavity is felt as a severe less well localized boring aching pain. Acute injuries are described as sharp or stabbing pain. Pain elicited by movement and relieved significantly with repose indicates mechanical aggravation of one of the moving or supporting structures. By isolating the movements, the affected structures can be identified. Throbbing or pulsating pain suggests increased pressure in a closed or tightly encapsulated compartment which is aggravated by arterial pulsation. With the exception of the intramedullary space, the compartment can be localized by squeezing or putting deep pressure on the tissues in the area of the pain.

Joint pain—arthralgia

Joint pain with or without objective signs of inflammation may precede arthritis by weeks or months. The onset, location, severity, and temporal pattern of pain are important. Inquire for morning stiffness and whether activity makes the pain better or worse and how quickly it recurs with rest. Morning stiffness lasting more than 60 minutes suggests an inflammatory etiology.

Bone pain

Mechanical injury, inflammation, infarction, increased intraosseous pressure, and stretching of the periosteum are causes of bone pain. Somatic afferent nerves carry the pain fibers and the pain is well localized, especially when the periosteum or endosteum is involved. Pain is often the only symptom of bone disease, although it may be accompanied by localized tenderness and swelling. Characteristically, bone pain is constant, well localized, worse at night and often intensified by movement or weight bearing. Bone pain may be referred to the nearest joint, but careful examination can usually distinguish between articular and bone pain. Squeezing the overlying muscles should exclude tender muscles as the source of pain. Bone pain should prompt imaging. CLINICAL OCCURRENCE: Congenital: Hemoglobin S and C (bone infarction), aseptic necrosis (Legg–Calvé–Perthes disease) of the femoral head; Endocrine: Hyperparathyroidism (osteitis fibrosa cystica); Idiopathic: Paget disease, hypertrophic osteoarthropathy (HOA); Inflammatory/Immune: Eosinophilic granuloma; Infectious: Osteomyelitis, syphilis, tuberculosis; Metabolic/Toxic: Osteoporosis, osteomalacia, drugs (GCSF), erythropoietin; Mechanical/Traumatic: Fractures, tendon avulsions and ruptures, ligament avulsions, epiphyseal plate injuries; Neoplastic: Osteosarcoma, multiple myeloma, giant cell tumor, large cell lymphoma, Ewing tumor, metastases to bone, fibrosarcoma, chondrosarcoma; Vascular: Avascular necrosis (with glucocorticoids, hemoglobin S and C diseases).

Muscle pain—myalgia

Muscle pain is carried on somatic sensory neurons and is generally well localized. Pain can result from external trauma, repetitive or sustained contraction, inflammation, ischemia, and metabolic disturbances. Chronic myofascial pain is of unknown etiology, but probably represents alterations in the peripheral or central pain circuits. Pain is frequently referred to and from muscles and regional structures. History is the key to diagnosis: note the onset, duration, and character of the pain, its relationship to activity, rest, and symptomatic therapy. Myalgias accompanying systemic inflammatory illnesses are often more severe at night or with prolonged inactivity. Neuromuscular examination is performed looking for wasting, hypertrophy, spasm, tenderness, trigger points, tender points, weakness, or fasciculations. CLINICAL OCCURRENCE: These are examples, only. Congenital: McArdle disease (paroxysmal myoglobinuria); Endocrine: Hyper-/hypoparathyroidism, hypothyroidism; Inflammatory/Immune: Rheumatic fever (RF), dermatomyositis, polymyositis, systemic lupus erythematosus (SLE), vasculitis, polymyalgia rheumatica (PMR); Infectious: Any acute infection, for example, influenza, (less common but important: malaria, rubella, dengue, rat-bite fever, trichinosis, leptospirosis, typhus, rickettsiosis, Bartonella), epidemic pleurodynia, pyomyositis; Metabolic/Toxic: Fever, acute hyponatremia, hypocalcemia, hypophosphatemia, hypomagnesemia, dehydration, diuresis, osteomalacia, drugs (statins and others); Mechanical/Traumatic: Trauma, strain, hematoma, march myoglobinuria, hypertonia, spinal stenosis; Neoplastic: Paraneoplastic myopathy and dermatomyositis; Neurologic: Fibromyalgia, neurogenic claudication; Psychosocial: Abuse; Vascular: Compartment syndromes, ischemia, atheroemboli, vasculitis.

Back pain

The pain may be acute and/or chronic; the quality may be sharp or aching. It is useful to think of back pain in terms of the anatomic structures that cause pain in or radiating to the back. It is essential to remember that pain from internal organs can be referred to the back. Acute pain is usually sharp and severe and results from mechanical forces applied to the back. Chronic pain, usually of an aching quality, can be the consequence of any acute injury or a repetitive use disorder. [Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001;344:363–370; Deyo RA, Rainville J, Dent DL. The rational clinical examination. What can the history and physical examination tell us about low back pain? JAMA. 1992;268:760–765]. CLINICAL OCCURRENCE: Acute: Bones and Ligaments: Fractures, dislocations, torn or avulsed ligaments; Cartilage: Herniated intervertebral disk, diskitis; Joints: Reactive arthritis; Muscles: Strain, myositis, hematoma; Nerves: radiculopathy (disk compression, diabetes), epidural mass or abscess, subarachnoid hemorrhage, polio, tetanus; Acute Referred Pain: Dissecting aortic aneurysm, angina, retrocecal appendicitis, pancreatitis, cholecystitis, biliary colic, pneumothorax, pleurisy, nephrolithiasis, pyelonephritis. Chronic: Bones and Ligaments: Osteoporosis, osteomalacia, osteomyelitis, diffuse idiopathic skeletal hyperostosis (DISH), spondylolysis and spondylolysthesis, spondyloarthritides, tuberculosis, syphilis, Paget disease, primary or secondary bone neoplasm, spina bifida; Cartilage: Herniated intervertebral disk; Joints: Osteoarthritis (OA); Muscles: Chronic muscle strain, fibromyalgia, myositis; Nerves: Syringomyelia, Chiari malformation, arachnoiditis; Chronic Referred Pain: Esophageal carcinoma, peptic ulcer, chronic pancreatitis, pancreatic carcinoma, renal cell carcinoma, retroperitoneal lymphoma, hepatomegaly from any cause, spinal cord tumor, aortic aneurysm.

Upper arm, forearm, and hand pain

When pain is well localized to one part of an extremity, the diagnosis is relatively simple. However, often the pain is more or less diffuse throughout the upper limb, so an anatomic classification of causes is useful. Limb pain does not always arise in musculoskeletal sources, for example, pain may be referred to the upper arm from myocardial ischemia. CLINICAL OCCURRENCE: Well-Localized Pain: Arthritis, bursitis, bone fracture, tendon rupture, tenosynovitis, cellulitis, muscle strain, neoplasm, ischemia and claudication; Diffuse Pain: Herniated cervical intervertebral disk, PMR, spondylitis, spinal tuberculosis, neoplasm of bone, Pancoast tumor, syringomyelia, radiculitis, carpal tunnel syndrome, ulnar tunnel syndrome, complex regional pain syndrome (reflex sympathetic dystrophy).

Pain in ulnar side of hand—ulnar tunnel syndrome

The ulnar nerve passes posterior to the medial humeral epicondyle in the ulnar groove, and then deep to the superficial flexors and above the deep flexors of the forearm, where it is stretched and compressed during vigorous muscular activity. Injury to the ulnar nerve at the elbow causes pain or numbness in the little finger, the ulnar half of the ring finger, and the ulnar side of the palm. Wasting of the hypothenar eminence and interosseus muscles may result from prolonged compression. The ulnar nerve may be stretched or injured by a cubitus valgus deformity or an old elbow fracture. Other risk factors for ulnar entrapment include alcoholism and diabetes. Press on the ulnar nerve in its groove behind the median epicondyle; tingling in the ulnar distribution of the hand suggests ulnar tunnel syndrome.

Shoulder pain

Pain around the shoulder is common but may be poorly localized. Diagnosis requires identifying the provocative and palliative movements, the quality of the pain; the anatomic region of the pain; its severity; and timing. It is helpful to consider the common conditions arranged by anatomic location [Steinfeld R, Valente RM, Stuart MJ. A common sense approach to shoulder problems. Mayo Clin Proc. 1999;74:785–794]. Attention should focus on identifying the structures involved and shoulder stability. Several physical examination maneuvers are helpful in shoulder examination but none are definitive for identifying instability [Luime JJ, Verhagen AP, Miedema HS, et al. Does this patient have instability of the shoulder or a labrum lesion? JAMA. 2004;292:1989–1999]. CLINICAL OCCURRENCE: Shoulder Joints: Arthritis of sternoclavicular, acromioclavicular, and glenohumeral joints; subluxations of humeral head, acromioclavicular joint, sternoclavicular joint; Bursae: Subacromial and subdeltoid bursitis; Tendons: Supraspinatus tendonitis, tear of supraspinatus tendon (partial or complete), other rotator cuff tears, rupture of long tendon of the biceps, bicipital tenosynovitis; Muscles: Strain, fibromyalgia (tender points), myositis, hematoma, muscle rupture (complete or incomplete), PMR; Bones: Fractures of humeral neck, scapular neck, clavicle; snapping scapula; Nerves: Nerve compression by the scalenus anticus muscle (scalenus anticus syndrome), first rib and clavicle (costoclavicular syndrome); complex regional pain syndrome (shoulder–hand syndrome); Vascular: Aneurysm or thrombosis of the subclavian artery.

Pain referred to the shoulder

Pain is referred to the shoulder from many sites in the chest, especially those innervated by branches of the vagus nerve or cervical sympathetic chain. When the diaphragm is involved (phrenic nerve) patients present with aching or sharp pain usually felt over the top of the shoulder or in the trapezius at the base of the neck (see Pleuritis, and Fig. 8-43). Angina is most often referred to the inner arms, jaw, and shoulder. Pain from nerve injury is often burning in quality and follows a dermatome. The following anatomic sites and conditions must be considered. CLINICAL OCCURRENCE: Cardiovascular: Acute coronary syndrome and angina pectoris (to either or both shoulders), aortic aneurysm or dissection; Pleura: Pleuritis of the central part of diaphragm, pneumonia, tuberculosis, pneumothorax, or carcinoma of the superior sulcus (Pancoast syndrome); Spleen: (left shoulder only) Infarction, rupture; Diaphragm: Subphrenic abscess, leaking peptic ulcer; Stomach and Duodenum: Gastritis, peptic ulcer, gastric carcinoma; Liver and Gallbladder: Cholelithiasis, cholecystitis, hepatitis, hepatic cirrhosis or carcinoma, hepatic abscess; Pancreas: Chronic pancreatitis, carcinoma, calculus, or pseudocyst; Nerves: Herpes zoster, brachial plexitis, neoplasm of cervicothoracic vertebrae, myelitis, spinal cord tumor.

Hip, thigh, knee, or leg pain

Pain in the lower extremity requires distinguishing between the primary lesion and pain resulting from redistribution of weight bearing to favor the original disorder. For example, limping on a chronically painful foot causes muscle strain in the back, pelvic girdle, and both lower limbs. Painful structures are identified by localization of palpable tenderness and accentuation of the pain with specific movements. Pain arising in somatic tissues (muscle, bone, tendon, and ligament) is usually well localized by the patient. Pain also is frequently referred to regional structures innervated by the same spinal segment. As an example, lesions involving the femoral neck frequently produce pain in the medial aspect of the knee. An anatomic organization for diagnostic purposes is useful. Patients will often describe pain in the general region of a joint as arising from the joint so a broad approach should be maintained to “hip,” “knee,” and “ankle” pain. CLINICAL OCCURRENCE: Muscle: Medication (statins), strains and tears, hematoma, PMR, fibromyalgia, ischemia and infarction, infection, tumors; Soft Tissues: Herniation of fat through muscle fascia, bursitis; Tendons: Tenosynovitis, strain and rupture; Joints: Arthritis (inflammatory, septic, crystal-induced, OA), dislocations, sprains; Bones: Fractures, neoplasms, osteomyelitis, osteoporosis, osteomalacia, aseptic necrosis, spondylolisthesis; Arteries: Thrombosis, embolism (thrombus, atheroma, fat, septic vegetations), vasculitis, aneurysm; Veins: Thrombosis, thrombophlebitis, venulitis, venous insufficiency; Nerves: Herniated intervertebral disk, epidural mass, contusion, vasculitis (mononeuritis multiplex), tabes dorsalis, neoplasms (especially neurofibromas), postherpetic neuralgia, peripheral neuropathies (e.g., diabetes and others).

General Signs

Painless nodules near joints or tendons

Several diseases produce painless nodules in joint capsules, tendons, ligaments, or the surrounding connective tissue. Rheumatoid nodules in rheumatoid arthritis (RA) or acute RF are subcutaneous usually over bony prominences in the periosteum or the deeper layers of the skin. Gouty tophi, although usually in bursae, are also formed in the Achilles tendon and the pinna of the ear. The diagnostic xanthomas of hypercholesterolemia occur in tendons of the hands and in the Achilles tendon and patellar tendon. Juxtaarticular nodes (Jeanselme nodules) occur near joints in syphilis, yaws, and other treponemal diseases. Periarticular calcium deposits occur in the CREST syndrome and tumoral calcinosis.

Synovial cyst—mucoid cyst

These are either bursae or tendon sheaths distended by fluid or protrusion cysts herniated by hydrostatic pressure from joint capsules. They are usually nontender and fluctuant. The protrusion cysts may collapse under pressure. Synovial cysts occur in the course of RA, usually on the dorsal aspects of the PIP joints. In OA, they commonly occur over the DIP joints of the hands and feet. When cysts arise from the extensor sheaths of the wrists, they cause oval swellings on the dorsa of the hands often called ganglions. The protrusion cyst of the knee is known as a Baker or popliteal cyst.

Noisy joints

Normal joint surfaces produce a smooth, gliding motion without palpable or audible friction or noise. Inflammation, cartilage injury, and loose bodies are often associated with demonstrable friction, clicks or crepitation on movement. Moving joints may emit several types of sounds. The knees or hips especially may produce creaking. Crepitus is a grating sound whose vibrations may also be palpated. It is produced by the roughened surfaces of cartilage rubbing together and indicates significant damage to the surface of the joint. Some persons have apparently normal joints that crackle or pop under certain conditions.

Muscle tenderness

Pain reproduced by gently squeezing the muscles identifies pain arising in muscles and distinguishes it from referred pain. Tonic muscle contraction is identified as palpable persistent muscle firmness. Both muscle and joint pain are intensified by movement. Neuritic pain is associated with tenderness over the nerve trunk with radiation in the distribution of its branches. Chronic neuritic pain may stimulate secondary tonic muscle contractions.

Increased joint mobility

Passive joint motion is restrained by the ligaments attaching the bones on either side of the joint. Active motion is also restrained by muscular contraction. Excessive motion implies disorders of the ligaments. Abnormalities can be congenital or acquired. Acquired laxity results from acute or chronic ligament injury leading to loss of support. It is limited to the affected joint and involves only the motion usually restrained by the affected ligament. There is asymmetry between the affected and the unaffected side. Diffuse joint laxity results from congenital disorders of connective tissue in the Ehlers–Danlos syndromes. Increased laxity of the skin, easy bruising, and poor scar formation are among the more common manifestations of these syndromes. Benign hypermobility syndrome is more common and can be associated with loose joints, daytime pain and nighttime awakening with discomfort, especially after exercise. It is more common in females and is an important cause of musculoskeletal pain in children and young adults.

Bony swelling

Swelling is detected by inspection and palpation, but the signs are rarely diagnostic. The location of the swelling in a long bone may be distinctive. Hamilton Bailey formulated the following diagnostic aids: (1) swelling in all diameters of the bulbous end of a long bone is most likely caused by giant cell tumor; (2) swelling on one aspect of a bone, near the epiphyseal line, is most likely an epiphyseal exostosis; (3) swelling in all diameters, beginning at the metaphysis and extending toward the center of gravity, may be Brodie abscess, osteoid osteoma, or osteosarcoma; (4) swelling in all diameters, at the center of gravity, may be Ewing tumor, eosinophilic granuloma, or bone cyst; and (5) consider that any localized bone tumor may be metastatic from a distant primary, so complete examination is indicated. X-ray findings may be distinctive, but biopsy is often indicated.

Bony nodule—occupational nodule

Repeated trauma to a limited region of soft tissue and underlying bone during work or sport may cause bosses of the bones with overlying calluses. Examples are surfer’s nodules on the dorsa of the feet (from pressure on the surfboard as the surfer sits cross-legged) and painter’s bosses on the subcutaneous surface of the tibia at the junction of the upper and middle thirds (from standing on a ladder and resting the tibias against the next higher rung).

Thoracolumbar Spine and Pelvis Signs

Dorsal protrusion from the spine—spina bifida cystica

Failure in fusion of the neural arch of a vertebra is spina bifida. When the meninges form a sac protruding through the defective arch, it is a meningocele (Fig. 13-25A). When the sac contains spinal cord or cauda equina, it is termed a myelomeningocele. In spina bifida occulta, there is no protrusion of the meninges; the only external manifestation may be a dimple in the skin, a patch of hair, or a lipomatous nevus. The sac is covered by healthy skin; the local swelling is filled with spinal fluid, so it is fluctuant and translucent. With myelomeningocele, the overlying skin is frequently defective and transillumination may show cord or nerve fibers. Transmission of pressure from the open fontanelle to the meningocele shows the communication to be wide. Sometimes, a sinus leads from a spina bifida occulta to the skin of the sacral region, a congenital sacrococcygeal sinus, often mistaken for a pilonidal sinus.

Scoliosis

Scoliosis is most often idiopathic, occurring most commonly in adolescent girls. Compensatory scoliosis occurs with torticollis, thoracoplasty, congenital dislocation of the hip, and shortened lower limb. Structural scoliosis occurs in congenital deformities and paralysis of back or abdominal muscles. Lateral curvature of the thoracic spine is usually accompanied by some rotation of the vertebral bodies, but only the lateral deviations of the spinous processes are visible. Minor functional scoliosis forms a single lateral curve, usually with convexity to the right. With structural changes, the lateral curve in the thorax produces an opposite compensatory curve inferiorly, so the line of spinous processes forms an S-shaped curve. The spinous processes always rotate toward the concave side. On the convex side, rotation of the vertebral bodies causes flattening of the ribs anteriorly and bulging of the chest posteriorly, elevation of the shoulder, and lowering of the hip. Viewed from the patient’s back, the posterior bulge is augmented with anteflexion of the spine (Fig. 13-12). Lateral deviation with a single curve is usually postural, as proved by its disappearance in extreme spinal flexion. An S-shaped or other complex curve may be compensatory or structural (Fig. 13-25B).

Kyphosis

The forward concavity of the thoracic curve is accentuated, producing a hunchback (Fig. 13-25B). A smooth curve is the result of faulty posture, rigid kyphosis of adolescence (Scheuermann disease), ankylosing spondylitis, Paget disease, osteoporosis (Dowager hump), acromegaly, and senile kyphosis. Of these, only the curve of faulty posture disappears with spinal extension. An abrupt angular curve, a gibbus deformity, is caused by the collapse of one or more contiguous vertebrae (Fig. 13-25B), resulting from osteoporosis, osteomyelitis, tuberculosis, neoplasm (e.g., multiple myeloma), or trauma. In either curved or angular kyphosis, the spinal flexion may force the thorax permanently into the inspiratory position, with increased anteroposterior diameter and horizontal ribs. The distortion is identical with the barrel chest of pulmonary emphysema, but the auscultatory signs of emphysema are absent.

Kyphoscoliosis

The thoracic deformity of scoliosis is accentuated and compounded when kyphosis is also present. The thoracic cavity may be so reduced as to compromise cardiopulmonary function.

Backward spinal curvature—lordosis

The normal posterior concavity of the lumbar curve is accentuated (Fig. 13-25B). Weakness of the anterior abdominal muscles is a common cause. This may occur to counterbalance a protuberant abdomen in pregnancy and obesity. It compensates for other spinal deformities in spondylolisthesis, thoracic kyphosis, flexion contracture of the hip joint, congenital hip dislocation, coxa vara, and shortening of the Achilles tendons. Copper deficiency myopathy is associated with sway-back. Accentuation of the lumbar curve throws the thoracic spine backward and the thoracic cage becomes flattened from the pull of the abdomen, causing an expiratory position of the ribs.

Low back pain with spinal indentation—spondylolisthesis

Most commonly L5 slips forward on S1 (Fig. 13-26A) because of an inherited defect of the lamina or fracture or degeneration of the articular processes of the neural arch. If symptoms occur, there is low back pain, often referred to the coccyx or the lateral aspect of the leg (L5 dermatome). Inspection frequently discloses a transverse loin crease. Palpation of the lumbar spine reveals a deep recession of the spinous process of L5. There is restricted flexion of the lower spine.

Appendicular Skeleton, Joint, Ligament, Tendon, and Soft-Tissue Signs

Finger signs

Some abnormalities of the fingers are included with consideration of the entire hand; the more localized disorders are discussed here.

Fingernail signs

See Chapter 6.

Clubbing

Clubbing has intrigued physicians since Hippocrates because of its association with serious systemic disorders. Recent evidence suggests that vascular endothelial growth factor (VEGF) reaching the systemic circulation either from the lung or via extra pulmonary shunts may be the cause of clubbing [Martinez-Lavin M. Exploring the cause of the most ancient clinical sign of medicine: finger clubbing. Semin Arthritis Rheum. 2007;36:380–385]. Clubbing is reversible when the cause is removed. The three key observations are floating of the nail base, loss of the unguophalangeal angle, and increased longitudinal convexity of the nail plate. Clubbing is painless and usually bilateral. With long-standing clubbing, the soft tissue and terminal phalanx become thickened, the convexity of the nail plate is extreme, and the fingers are bulbous. In the literal sense, the term clubbing should be reserved for this late stage, but it is now applied to the general process in all stages, from the first sign of floating nail. Convexity alone is seen in other conditions or as a normal variant. The floating nails and alteration of the unguophalangeal angle distinguish clubbing from all other conditions.

Demonstrating clubbing

Obliteration of the Unguophalangeal Angle (Lovibond Angle): Inspect the profile of the terminal digit. Normally, the nail makes an angle of 20 degrees or more with the projected line of the digit. With clubbing, this angle is diminished, may be obliterated, or extend below the projected line of the digit (Fig. 13-27). Floating Nail: Palpate the proximal nail with the tip of your finger. You can feel and see the springy softness as the root of the nail is depressed (Fig. 13-27). This may be simulated as follows: with your right index finger press the mantle of your left middle finger; the plate rests snugly against the bone without movement. Now depress the free edge of the nail with your left thumb and test the mantle again with your right index finger; the plate root now sinks with pressure and springs back when released. Convexity of the Nail: A month or so after the floating nail and nail angle changes occur, a transverse ridge appears in the plate from beneath the mantle. The ridge marks the change from the normal distal curve to a new curve of smaller radius in the proximal nail.

The floating nail and flattened angle occur rapidly, for example, within 10 days after a tonsillectomy complicated by lung abscess. With chronic illness of more than 6 months, the entire nail has abnormal convexity. The sequence of changes can occasionally be observed in a patient with subacute bacterial endocarditis. When first seen with a 3-month history of illness, a transition ridge is visible (Fig. 13-27). After treatment of the infection a second ridge appears, this one marking the transition between distal abnormal curvature and proximal normal profile. CLINICAL OCCURRENCE: Congenital: Cyanotic congenital heart disease, familial, cystic fibrosis; Endocrine: Hypothyroidism; Idiopathic: COPD, bronchiectasis; Inflammatory/Immune: Inflammatory bowel disease, biliary cirrhosis, alcoholic cirrhosis; Infectious: Infective endocarditis, lung abscess, pulmonary tuberculosis; Neoplastic: Lung cancer, metastatic cancer to lung, mesothelioma; Vascular: HOA, pulmonary arteriovenous malformations (including dialysis shunts).

Ulnar collateral ligament sprain

There is a history of a fall onto the palm, often while grasping an object with the thumb. The patient complains of pain in the MCP joint of the thumb and an inability to exert significant pressure on the pad of the thumb tip without pain or giving way. Examination shows tenderness and laxity of the ulnar collateral ligament.

Painless interphalangeal joint nodules—Heberden and Bouchard nodes

These are marginal osteophytes on the DIP and PIP joints. Heberden nodes of the DIP joints are hard nodules, 2 to 3 mm in diameter, one on either side of the dorsal midline (Fig. 13-30K). They are usually painless, motion is slightly limited, and deformity is progressive, but function is preserved. They are more pronounced on the dominant hand. Involvement begins in several joints most commonly in peri- or postmenopausal women. The condition in women is usually hereditary and the process is a result of OA. A single Heberden node may result from trauma. Nodules on the PIP joints are Bouchard nodes. They occur together with Heberden nodes, but somewhat less frequently than the latter.

Dactylitis—sausage digits

Enthesitis of one or more fingers produces diffuse “sausage-like” swelling with or without joint effusion. Dactylitis is seen in reactive and psoriatic arthritis and hand–foot syndrome of sickle cell or sickle–thalassemia disease.

Monarticular swelling—interphalangeal joint sprain

A painful fusiform joint swelling may persist for several months. In most cases, there is a history of trauma.

Localized swelling—synovial or mucous cyst

A synovial cyst results from myxomatous degeneration of a joint capsule. A small, tense nodule appears over an interphalangeal joint; frequently it is mistaken for a sesamoid bone. It may be so tense that it feels bony hard; usually, it is not fluctuant. Pressure may elicit slight tenderness. Often there is slight transverse mobility.

Flexion deformity of distal finger joint—mallet finger

This is caused by rupture or avulsion of the extensor tendon that inserts on the distal phalanx. The DIP is flexed and cannot be voluntarily extended (Fig. 13-28A).

Extension PIP deformity—swan neck deformity

Fixed extension of the PIP joint is caused when the flexor tendons are injured or sublux to the dorsum of the joint, holding the joint in extension. This deformity is common in RA and SLE. In the latter, it is usually reducible, a Jaccoud deformity.

Flexion PIP deformity—Boutonnière deformity

Rupture of the central band of the extensor tendon that inserts on the middle phalanx leads to volar subluxation of the intact lateral band to the distal phalanx which holds the PIP in flexion. The finger is flexed at the PIP and lacks voluntary extension (Fig. 13-28B). Extension followed by flexion of the PIP joint may produce a palpable or audible diagnostic click, as the lateral slips of the distal extensor tendons diverge and slip laterally over the head of the proximal phalanx, hence, buttonhole rupture.

Flexion thumb deformity—saluting hand

Extension at the thumb MCP and interphalangeal joint is performed by the extensor pollicis longus tendon; rupture leads to loss of function. This is approximately the position of the hand in an American military salute (Fig. 13-28C). The thumb is limply flexed and cannot be voluntarily extended. The tendon is often worn through by moving over the fragments of a Colles fracture.

Flexor tendon contracture

Adhesions between a tendon and its sheath are caused by tenosynovitis. Fibrotic shortening of the tendon without synovial adhesions occurs in Volkmann ischemic contracture (Forearm pain and weakness—flexor compartment syndrome and Volkmann ischemic contracture). Distinction between the two mechanisms can be made with the wrist flexed. Grasp the tip of the flexed finger and pull it into extension. With the slack provided by wrist flexion, the shortened tendon permits partial extension; adhesions to the sheath or palmar fascia entirely prevent extension (Fig. 13-28E).

Tight skin—sclerodactyly

See Scleroderma. All digits are usually involved, Raynaud phenomenon is nearly always present, and calcinosis of the skin may occur. Abnormalities of nail bed capillaries are common and should be sought.

Finger pad nodules

Osler nodes

Septic emboli from infective endocarditis lodge in the cutaneous vessels producing microscopic abscesses. These pea-sized, tender bluish or pink nodules, sometimes with a blanched center, occur on the pads of the fingers, palms of the hands, and soles of the feet in some patients with infective endocarditis.

Janeway spots

Janeway spots are only a few millimeters in diameter. They appear over a few hours or days as crops of erythematous or hemorrhagic, macular or nodular lesions. They occur in the palms, soles, or distal finger pads. Although painless and nontender, they may ulcerate. Most writers consider them hallmarks of bacterial endocarditis or mycotic aneurysm. Bacteria have been isolated from the lesions.

Circulatory disorders of the fingers

See Chapter 8.

Palm signs

Yellow palms—carotenemia

See Carotenemia.

Thenar wasting

The thenar eminence is formed by the bellies of opponens pollicis, abductor pollicis brevis, and flexor pollicis brevis innervated by the median nerve. Wasting suggests a lesion of the median nerve, most commonly carpal tunnel syndrome or severe OA at the base of the thumb. It may accompany wasting of all intrinsic hand muscles with axonal neuropathies (Fig. 13-29B).

Hypothenar wasting

The hypothenar eminence is formed by the bellies of palmaris brevis, abductor digiti quinti, flexor digiti quinti, and opponens digiti quinti innervated by the ulnar nerve. Wasting suggests damage to the ulnar nerve (Fig. 13-29C). If both thenar and hypothenar wastings are present, consider cervical myelopathy.

Thickening of palmar fascia—Dupuytren contracture

See Localized thickening of palmar fascia—Dupuytren contracture.

Granular palms—hyperkeratosis

Palpation with the fingertips discloses rough granular excrescences in the horny layer. The most common cause is chronic arsenic poisoning. A rare cause is hyperkeratosis (tylosis) palmaris et plantaris, an autosomal dominant disease.

Normal and abnormal hand posture

Position of anatomic rest

The relaxed posture of the hand is with the wrist slightly extended and the fingers and thumb flexed, the index finger less bent than the others (Fig. 13-30C). Injury or inflammation with the hand or the muscles and tendons powering it produces this posture to reduce painful tension on the involved structures.

Ulnar deviation or drift of fingers

The fingers deviate at the MCP joints toward the ulna. There may also be subluxations of the MCP joint (Fig. 13-30B). It results from hyperplasia of the MCP joint capsules which stretches the capsules and ligaments with subluxation of the extensor tendons to the ulnar sides of the joints.

Diabetic hand—diabetic cheiropathy

In long-standing diabetes, the soft tissues of the hand become thick and contracted, bending the fingers into a slightly flexed position. Have the patient attempt to place the palms together; a space will remain between the opposing palms and fingers in a “prayer sign.”

Carpal spasm

The thumb is flexed on the palm, the wrist and MCP joints are flexed, while the interphalangeal joints are hyperextended and the fingers are adducted in the shape of a cone. All the hand muscles are rigid. The spasm is involuntary and usually painless. This posture occurs in tetany; it is involuntary and cannot be relaxed by the patient (Fig. 13-30F). It is also seen in hand dystonia associated with repetitive hand activities.

Clawhand

This occurs from the predominant pull of the extensor communis digitorum and the flexor digitorum against weak or paralyzed interosseus and lumbrical muscles. The claw is caused by hyperextension of the MCP joints and flexion of the interphalangeal joints (Fig. 13-30D). Paralysis may result from brachial plexus, ulnar and median nerve injuries, syringomyelia, the muscular atrophies, or acute poliomyelitis.

Ape hand

The thumb is held in extension by its inability to flex (Fig. 13-30E). This may occur in syringomyelia, progressive muscular atrophy, or amyotrophic lateral sclerosis.

Benediction hand—preacher’s hand

The ring and little fingers cannot be extended whereas the other digits move normally and may be extended to produce the posture (Fig. 13-30G). This occurs in ulnar nerve palsy, syringomyelia, and extensor tendon rupture in RA. It is named from the ecclesiastical gesture of pronouncing benediction. Do not confuse it with Dupuytren contracture.

Wrist-drop

When the pronated hand is held horizontally, it drops from the wrist because of weak wrist extensors (Fig. 13-30H) which are unable to overcome gravity. The cause is radial nerve injury of any etiology.

Athetoid hand

A grotesque pattern is seen in athetosis in which involuntary muscle contractions produce simultaneous flexion of some digits and hyperextension of others, resembling the writhing of a snake (Fig. 13-30J).

Large hands

Acromegaly and gigantism

See Acromegaly and gigantism. Soft-tissue overgrowth increases the finger girth and thickens the palm, called a paw or spade hand. Arthritis is frequently present.

Large hands—HOA

See Muscle signs. All dimensions of the hands are increased, as in acromegaly, but the condition is invariably accompanied by finger clubbing.

Enlargement of one hand—hemihypertrophy and local gigantism

An entire side of the body may be enlarged in a congenital deformity known as hemihypertrophy. Local gigantism is often the result of a congenital arteriovenous fistula of the upper limb. In either case, the hand is normally proportioned.

Long, slender hands—arachnodactyly, Marfan syndrome

All the long bones of the hands are slender and elongated, often with hyperextensible joints. The wrist sign is useful to distinguish elongated fingers from long, normal fingers. The patient encircles his own wrist, with his thumb and little finger proximal to the styloid process of the ulna. In normal persons, the encircling digits scarcely touch, but in arachnodactyly they may overlap by 1 to 2 cm because of the long digits and narrow wrist. The thumb sign (Steinberg sign) may also be positive: when the fingers are clenched over the thumb, the end of the thumb protrudes beyond the ulnar margin of the hand (Plate 29) [Falk RH. The “thumb sign” in Marfan’s syndrome. N Engl J Med. 1995;333:430]. Neither sign is specific for Marfan syndrome.

Interosseous wasting

The hands show prominence of the extensor tendons and metacarpals on the dorsum. There is loss of muscle mass, most easily detected in the first dorsal interosseous between the thumb and index finger. Adduction–abduction of the fingers is weak. Wasting suggests injury to the ulnar nerve (ulnar nerve entrapment at the elbow, diabetic neuropathy) or severe disuse (RA).

Dorsal hand swelling

Painless swelling

Edema arising from the deep spaces of the hand accumulates in the loose subcutaneous tissue dorsally, rather than the palmar surface, because of the restricting palmar fascia. Causes include infection, obstruction of the superior vena cava, anasarca, and relapsing symmetrical seronegative synovitis with pitting edema (RS3PE). Unilateral edema may also occur from occlusion of the venous or lymphatic drainage in the upper arm.

Painful dorsal swelling

Infection and extensor tenosynovitis cause edema, erythema, and localized tenderness. Fluctuation may not be present even with an abscess. A rare cause is thyroid acropachy associated with Graves disease and treatment of hyperthyroidism.

Wrist signs

Hypertrophic osteoarthropathy

See Muscle signs.

Swollen wrist

Physical examination can identify which structure is swollen. Periarticular edema in the subcutaneous tissues around the joint, but outside the synovium, pits with pressure. With thickening of the joint capsule and synovium the tissues feel boggy. When the synovial envelope is bulging and fluctuant, fluid is present. Effusion, pus, and blood can be distinguished by aspiration.

Painful swelling or limited motion of the wrist—arthritis

With active inflammation, there is swelling accompanied by variable degrees of pain and tenderness. The overlying skin may be warm and reddened. In RA there is swelling and limited motion, but no redness or excessive warmth. In contrast, with gout, pseudogout, and septic arthritis the joint is swollen, red, hot, and tender. Primary OA does not affect the wrist.

Localized swelling and tenderness—tenosynovitis

See Painful swelling in the anatomic snuffbox—tenosynovitis.

Localized painless dorsal wrist swelling—ganglion

This is a protrusion cyst of the joint capsule usually seen on the dorsum of the naviculolunate joint (Fig. 13-40D). It is painless, round, sessile, tense, translucent and more prominent in flexion.

Numbness, tingling, and pain—carpal tunnel syndrome

See Carpal tunnel syndrome.

Dorsal angulation of the wrist—Madelung deformity

The pronated hand presents a profile in which the wrist is deformed by a sharp protrusion upward (dorsally) of the lower ulna (Fig. 13-44C). This is caused by a nontraumatic dorsal subluxation of the distal end of the ulna, usually in young women.

Forearm and elbow signs

Deformity of the elbow—cubitus valgus and varus

The normal elbow carrying angle is approximately 170 degrees as measured on the lateral side of the arm and forearm, an angle less than 165 degrees is a valgus deformity, and one greater than 175 degrees is a varus deformity (Fig. 13-31A). A difference of >10 degrees between right and left is also abnormal.

Elbow swelling—effusion

The synovial sac of the elbow joint is very loose and easily distended with fluid, giving a characteristic outline. There is fluctuant bulging posteriorly, on both sides of the olecranon process and triceps tendon (Fig. 13-31B). It is most easily palpable laterally between the lateral epicondyle, radial head, and olecranon. The elbow is held in semiflexion to accommodate maximal fluid volume. The joint may be distended by synovial fluid, pus, or blood.

Elbow arthritis

Any type of arthritis may involve the elbow joint. Suppurative arthritis produces painful swelling, with pus in the joint. RF and RA cause painful swelling; the chronic stage of RA often results in limited extension. A loose body in the joint is suggested by a history of locking. An enlarged, painless joint, suggesting OA but unilateral, may be neurogenic arthropathy (Charcot joint); when encountered in the elbow, syringomyelia is the most likely cause.

Olecranon bursitis

Trauma, inflammation, infection, or gout produces an accumulation of fluid in the olecranon bursa, a subcutaneous space overlying the olecranon process (Fig. 13-31C). The swelling is fluctuant. The location of the bulge readily distinguishes it from fluid in the joint.

Elbow pain—lateral and medial epicondylitis

See Elbow pain—lateral and medial epicondylitis, tennis elbow.

Upper arm signs

This region includes the shaft of the humerus and its covering muscles, principally the biceps brachii and the triceps brachii.

Pain in the upper arm—bicipital tenosynovitis

See Pain in the upper arm—bicipital tenosynovitis.

Pain in the shoulder—coracoiditis

See Pain in the shoulder—coracoiditis.

Bicipital humps—rupture of the biceps

The smooth profile of the biceps is interrupted by one or two humps. One hump results with rupture of the tendon or muscle sheath (Fig. 13-44F). Rupture of the belly causes two humps. Rupture occurs during lifting and is usually painful. Absence of this history suggests degeneration of the bicipital long-head tendon in the shoulder joint, often associated with chronic impingement or shoulder synovitis. Rupture of the long-head tendon is most common, resulting in mild weakness. Rupture of the muscle may not greatly impair strength.

Shoulder signs

See Figure 13-41

Full painless abduction effectively excludes serious injury to the shoulder. Pains with elevation or limited active range of motion suggest pathology in the shoulder. Pain between 60 and 120 degrees of elevation, with the remainder of the arc painless, suggests partial rupture of the supraspinatus tendon, supraspinatus tendinitis, or subacromial bursitis. Minimal elevation and support of the arm with the opposite hand point to fracture, dislocation, or complete rupture of the supraspinatus; in the latter case, passive motions are normal. Pain throughout elevation indicates arthritis. Descriptions of these conditions follow.

Painful arc and impingement sign—rotator cuff injury

See Painful arc and impingement sign—rotator cuff injury.

Minimal arm elevation—complete rupture of the supraspinatus tendon, torn rotator cuff

See Minimal arm elevation—complete rupture of the supraspinatus tendon, torn rotator cuff.

Adhesive capsulitis—frozen shoulder

See Adhesive capsulitis—frozen shoulder.

Painful trigger points in shoulder muscles

Pain is usually present on arising or after inactivity, whereas exercise diminishes or abolishes the pain. Small nodules may be palpated on the surface of the trapezius or other muscle. Pressure on the nodule reproduces the pain, often with radiation to the neck and upper arm.

Shoulder-pad sign—amyloidosis

Bilateral anterolateral swelling of the shoulder joints is a conspicuous, although uncommon, sign of amyloid disease. The periarticular swellings feel hard and rubbery.

Winged scapula—paralysis of the long thoracic nerve

Paralysis of the serratus anterior permits the scapula to be separated posteriorly from the thoracic wall, a winged scapula. Have the patient stand and push the hands against a wall while you observe the scapulae (Fig. 13-32A). Injury to the long thoracic nerve is caused by stretching, during heavy lifting or surgical trauma.

Hip, buttock, and thigh signs

Femoral triangle mass—psoas abscess

A painless abscess is usually an extension of spinal tuberculosis. Painful abscess suggests purulent infection from an intraabdominal source. A conical mass appears beneath the inguinal ligament (Fig. 13-33B). DDX: There is a similar swelling in the iliac fossa distinguishing it from effusion in the psoas bursa. Abscess must be distinguished from fluctuant lymphadenopathy.

Femoral triangle mass—psoas bursitis

A painless effusion in the psoas bursa, occasionally associated with OA of the hip, produces tense, nonfluctuant, immobile conical swelling beneath the inguinal ligament (Fig. 13-33B). The absence of a mass in the iliac fossa excludes psoas abscess.

Lymphadenopathy

See Lymphadenopathy.

Femoral hernia

See Femoral hernia and Figure 9-35.

Knee signs

Neurogenic arthropathy—Charcot joint

Figure 13-21C and Charcot Joint.

Genu varum—bowleg

The legs deviate toward the midline so that the knees are farther apart than normal when the medial malleoli are together (Fig. 13-10C). The feet are turned inward when walking. The most common cause is medial knee compartment OA. Other causes are rickets affecting the upper tibial and lower femoral epiphyses, Paget disease, and occupational stress.

Genu valgum—knock-knee

The legs deviate away from the midline, often bilaterally (Fig. 13-10C). The most common cause is osteoarthritic narrowing of the lateral knee compartment.

Knee swelling—fluid in the joint

An excess of synovial fluid in the knee joint is an effusion. Blood in the joint space is hemarthrosis. Pus indicates suppurative arthritis. Fluid signs are independent of fluid type, so specific diagnosis can only be made by aspiration. Effusion is commonly caused by trauma, RA, reactive arthritis, OA, gout, other crystalline arthritides (calcium pyrophosphate, basic calcium phosphate), or intermittent hydrarthrosis. Traumatic hemarthrosis suggests intracapsular fracture or ligament disruption. Nontraumatic hemarthrosis occurs with hemophilia and neoplasms.

Anterior knee swelling—prepatellar bursitis

A fluctuant subcutaneous swelling occurs anterior to the lower patella and patellar ligament, the distribution of the prepatellar bursa (Fig. 13-21D). It is often found associated with occupational trauma to the tissue overlying the patella. This differs from fluid in the joint cavity that produces swelling beside the patella.

Anterior knee swelling—infrapatellar bursitis

Swelling appears in a bursa on both sides of the patellar ligament near the tibial tuberosity (Fig. 13-21E). Fluctuation can be demonstrated from one side of the ligament to the other. This often results from occupations requiring kneeling, such as roofing and laying floors.

Anterior knee swelling—infrapatellar fat pad

The infrapatellar fat pad becomes inflamed, causing tenderness and swelling on both sides of the patellar ligament. The tenderness and lack of fluctuance distinguish it from bursitis and synovitis.

Popliteal swelling—semimembranosus bursitis

Fluid accumulates in the bursa between the head of the gastrocnemius and the tendon of the semimembranosus, forming the upper medial border of the diamond-shaped popliteal fossa (Fig. 13-34). Extension of the knee causes painful tensing of the bursa, while flexion relaxes it. Fluctuation is difficult to demonstrate.

Popliteal swelling—Baker cyst

The cyst is a pressure diverticulum of the synovial sac protruding through the posterior joint capsule of the knee. Sometimes, dull pain is present. The cyst is best seen by inspection of the fossa when the patient is standing. In contrast to the semimembranosus bursitis, the swelling is in the midline at or below the tibiofemoral junction (Fig. 13-34). The cyst protrudes when the knee is extended and, unless it is very large, is not visible with flexion. When the cyst freely communicates with the joint, gradual, steady pressure on the sac forces some fluid back into the joint cavity, temporarily reducing the swelling. The swelling may be translucent. Baker cysts often complicate RA and OA. Large cysts can compress the popliteal vessels. If the artery is compressed, forced extension of the knee or strong dorsiflexion of the foot may obliterate the pedal pulse.

Popliteal mass—popliteal aneurysm

This feels like a cyst and only a conscious effort to detect pulsation will identify it.

Medial knee swelling—cyst of the medial meniscus

This is a developmental anomaly of the medial meniscus felt as a fluctuant joint line swelling. Dull pain may be present on standing. The oval, transversely elongated cyst may protrude either anterior or posterior to the MCL. Knee flexion makes it more prominent.

Lateral knee swelling—cyst of the lateral meniscus

This congenital cyst occurs at the tibiofemoral junction, posterior to the fibular collateral ligament. Flexion accentuates the transverse fluctuant swelling. It may be painful and, occasionally, protrudes into the popliteal fossa.

Knee pain and recurrent locking

A history of intermittent joint pain with recurrent effusions or locking suggests a loose body in the joint or a torn meniscus. Crepitus may be present; rarely, the examiner may be able to palpate a mass. Loose bodies are usually a chip of bone; resulting from previous injury.

Subacute and chronic knee pain—osteonecrosis and stress fractures

In the absence of direct trauma or signs of disease within the joint, tibial plateau stress fractures and osteonecrosis of the femoral condyles or tibial plateau should be considered.

Subacute and chronic knee pain—remote injury

Pain occurring acutely with or shortly after trauma is discussed on The injured knee. For most practitioners the more common scenario is chronic progressive, though often intermittent, knee pain frequently made worse by exercise. The pain may be accompanied by swelling. The location of the pain and aggravating factors are helpful in distinguishing the likely cause. Crepitation, locking, and instability all suggest previous injury. With no specific history of injury consider abnormalities of the feet, gait, and/or leg length; each produces unbalanced forces about the knee. Overuse, often in the form of sudden increases in activity from a relatively inactive baseline, should also be considered. The location of the pain and the findings on examination will be similar though much less severe than with an acute injury to the same structure.

Leg signs

Thickened Achilles tendon

Thickening is a response to overuse or ill-fitting footwear that puts direct pressure on the tendon causing an injury-repair cycle. Thickening is most easily detected by inspection and palpation when the foot is dorsiflexed. Several diseases may produce inflammation (e.g., seronegative spondyloarthropathies) or deposits in the tendon (e.g., xanthomas).

Ankle signs

Swelling of the ankle joint—joint effusion

The foot is held in slight dorsiflexion and inversion. The distended joint produces bulging beneath the extensor tendons, near the talotibial junction and in front of the lateral and medial malleolar ligaments.

Pain or click during ankle dorsiflexion with eversion—recurrent slipping of peroneal tendons

The tendons of the peroneus longus and brevis curve behind and under the lateral malleolus, held in a groove by the ligamentous band; the superior peroneal retinaculum. Relaxation of the retinaculum may permit slipping of the tendons during dorsiflexion with eversion. Pain or click occurs with the slipping. Physical examination at rest is normal but active motion may produce palpable tendon subluxation.

Pain on inversion of the foot—chronic stenosing tenosynovitis of the peroneal tendon sheath

This causes pain only on inversion of the foot. Tenderness and swelling occur in the sheath behind and below the lateral malleolus.

Foot signs

Nodules in the foot—fibroma

Fibromas are benign growths of fibrous tissue that can occur anywhere on the foot (or elsewhere), usually following minor soft tissue trauma. They frequently are painful, especially on the sole or where they are impinged upon by footwear. They are felt as firm, discrete, rubbery and occasionally tender nodules usually fixed to the underlying soft tissues, not to bone.

Talipes (clubfoot)

Most common are talipes varus (inversion), talipes valgus (eversion), talipes equinus (plantar flexion), talipes calcaneus (dorsiflexion), and talipes or pes cavus (hollowing the instep) (Fig. 13-35). Combined deformities are talipes equinovarus (clubfoot), talipes equinovalgus, talipes calcaneovarus, and talipes calcaneovalgus. The diagnosis is usually made by inspection.

Pes planus (flatfoot)

One or more of the pedal arches is lowered (Fig. 13-35). A functional classification describes relaxed flatfoot, in whom the arch is lowered only while bearing weight; rigid flatfoot, caused by bony or fibrous ankylosis; spasmodic flatfoot, from contraction of the peronei; and transverse flatfoot, from flattening of the transverse arch.

Heel pain—retrocalcaneal bursitis

The bursa between the Achilles tendon and the calcaneus may be inflamed, causing pain, swelling, and tenderness near the tendon insertion (Fig. 13-36B). The lesion is caused by pressure from footwear, especially high-heeled shoes or stiff-backed boots.

Plantar heel pain—plantar fasciitis

The plantar fascia is a thick band of fibrous tissue arising from the medial tuberosity of the calcaneus and spreading like a fan across the sole to insert on the proximal phalanges of the toes. Unusual or prolonged weight-bearing activity leads to microtrauma, which is concentrated at the calcaneal insertion. Pain is present in the plantar aspect of the heel and is usually worst with the first steps in the morning. Pain improves with activity, only to recur after rest. Tenderness is elicited at the insertion of the plantar fascia on the distal calcaneus somewhat medially [Buchbinder R. Plantar fasciitis. N Engl J Med. 2004;350:2159–2166].

Plantar heel pain—inflammation of the calcaneal fat pad

Fibrous bands extend from the calcaneal periosteum to the skin; their interstices are filled with fat. Infection or inflammation is compartmentalized by the fibrous bands leading to increased tissue pressure and intense pain. The region is too tender to permit weight bearing. Usually edema accumulates around the ankle; fluctuation occasionally is present.

Localized swelling on the dorsum—ganglion

This is a cyst arising from a tarsal joint capsule or an extensor tendon.

Pain in the instep—infection in the deep fascial spaces

The central plantar space has four compartments between the sole and the pedal arch (Fig. 13-36D). Infection of the spaces occurs from direct puncture or backward extension from an interdigital space. There is tenderness in the instep (midfoot), dorsal edema, and the curve of the instep becomes obliterated.

Contracture of the plantar fascia

Unilateral or bilateral asymptomatic thickening of the plantar fascia is associated with Dupuytren contracture of the palms and Peyronie syndrome.

Lateral deviation of the great toe—hallux valgus

Lateral deviation and rotation of the great toe produces abnormal prominence of the first metatarsophalangeal (MTP) joint (Fig. 13-36E). The second toe may overlap the first, or it may be a hammertoe. The great toe retains good motion. Pain is caused by accompanying hammertoe, an inflamed bursa over the prominent MTP joint (bunion), or metatarsalgia from transverse flatfoot (splay foot). The most common causes are improper shoes and primary OA.

Stiff great toe—hallux rigidus

A prominent osteophyte is usually present on the dorsal aspect of the MTP joint. Pain may occur with walking and climbing. Extension of the MTP is severely limited and flexion is present mainly in the interphalangeal joint.

Hammertoes

The second through fourth toes can be involved. The MTP is fixed in dorsiflexion and the PIP is fixed in plantarflexion, whereas the DIP is freely movable (Fig. 13-36F). A corn or inflamed bursa frequently occurs over the PIP joint. Hammertoes are usually bilateral with several toes on each foot involved. It often accompanies hallux valgus.

Painful swelling of a toe—fractured phalanx

No matter how trivial the trauma seems, consider the possibility that the bone has been fractured.

Painful swelling of the metatarsal phalangeal joint—gout

This is the classic lesion (podagra) of early gout, described on Gout.

Toenail signs

See Chapter 6, The Skin and Nails, Soft corn.

Muscle signs

Muscular wasting

Loss of muscle substance occurs from disuse or damage to muscle tissue or motor nerves. Fasciculation of the muscles indicates denervation; the history will disclose injury or disuse.

Muscle contracture

Prolonged disuse, immobilization, ischemia leading to muscle necrosis, or inflammatory processes result in fibrosis of muscle with inelastic shortening. The shortened muscle does not permit full range of joint movement. The joints, however, are normal as distinct from joint contracture. The muscle is firm to hard and atrophic.

Muscle hypertrophy

Increased muscle volume results from enlargement of normal muscles or infiltration of the muscle by cellular or extracellular material. Resistance exercise increases muscle bulk and power. Hypertrophy may also occur with anabolic steroid use, hypothyroidism, congenital myotonia, Duchenne muscular dystrophy, and focal myositis.

Muscle masses

To prove that a mass is intramuscular the mass must be freely movable transversely to the long axis with the muscle relaxed. Tensing the muscle must limit the transverse mobility. A mass may result from rupture of a muscle, herniation of a muscle through its sheath, intramuscular hemorrhage, neoplasm, abscess, or localized myositis ossificans.

Trigger points—myofascial pain

Painful firm nodules or bands occur in muscles under frequent tonic contraction. The patient complains of pain, often with projection of pain in a nondermatomal pattern around the area and distally into the arm from trigger points in the upper back and neck, or into the leg from trigger points in the pelvic girdle. The pain often has a burning quality. Motor strength and sensation are normal. Trigger points are characteristic of myofascial pain syndromes. They occur most commonly in large muscles of the back and proximal extremities. Injection of local anesthetic, heat, massage, and stretching, combined with avoidance or changes in precipitating postural activities, is effective therapy. Left untreated, changes may occur in central and peripheral pain pathways leading to chronic persistent pain syndromes.

Tender points—fibromyalgia

Persistent reproducible pain is elicited by palpation of specific muscles. The patient does not complain specifically of pain in these sites, unlike trigger points. Eighteen symmetrically located sites in the neck, back, and extremities have been standardized for the diagnosis of fibromyalgia (Fibromyalgia).

General Syndromes

Complex regional pain syndrome

See Chapter 4.

Bursitis

Some periarticular bursae communicate with the joint space. Effusions occur as a result of repetitive use trauma, direct blunt or penetrating trauma, crystal deposition, or infection. The history and examination combined with knowledge of the local anatomy are essential for diagnosis.

Hypertrophic osteoarthropathy

This is a periostitis of unknown cause with: (1) clubbing of the fingers, (2) new subperiosteal bone in the long bones, (3) swelling and pains in the joints, and (4) autonomic disturbances of the hands and feet, such as flushing, sweating, and blanching. The earliest sign is finger clubbing (see Clubbing). With progression, bone pain occurs while swelling and pain in the joints may become severe and tenderness is elicited by palpation over the distal forearms and legs. In advanced cases, sweating and flushing of the hands and feet may alternate with the Raynaud phenomenon. The condition may be congenital, with signs appearing in childhood, or acquired. Primary hereditary HOA (Marie-Bamberger syndrome) is an autosomal dominant syndrome, which is expressed much more commonly in males. It has clubbing, greasy thickening of the skin, especially noticeable on the face, and hyperhidrosis of the hands and feet. Acquired HOA is caused by systemic disease. CLINICAL OCCURRENCE: Congenital: Familial, cyanotic congenital heart disease, cystic fibrosis; Endocrine: Graves disease, pregnancy; Idiopathic: Emphysema, cirrhosis; Inflammatory/Immune: Ulcerative colitis, Crohn disease, chronic interstitial pneumonitis, sarcoidosis, dysproteinemia; Infectious: Lung or liver abscess, bronchiectasis, tuberculosis, bacterial endocarditis, dysentery; Metabolic/Toxic: Malabsorption, chronic hypoxemia; Neoplastic: Lung, pleural, and gastrointestinal cancer, metastatic disease to lung; Vascular: Aortic aneurysm.

• Necrotizing soft-tissue infection. Rapid expansion of infection in subcutaneous tissue planes produces local vascular thrombosis leading to ischemia of fat, connective tissue, skin and underlying muscle. Infection and necrosis spread proximally and distally along tissue planes and invade deeper structures along neurovascular bundles that penetrate these planes. When the muscle fascia is involved the term necrotizing fasciitis is applied. Pain and fever accompanied by signs of inflammation (erythema, warmth, tenderness) result from infection with group A streptococci or polymicrobial (mixed aerobic/anaerobic) soft-tissue infections. Systemic hypotension, tachycardia, and delirium develop rapidly, and outcome is fatal without complete surgical debridement. Predisposing factors include diabetes mellitus, immunosuppression, and minor puncture wounds. Urgent surgical debridement is mandatory to save limb and life [Hoadley DJ, Mark EJ. Weekly clincopathological exercises: Case 28–2002: a 35-year-old long-term traveler to the Caribbean with a rapidly progressive soft-tissue infection. N Engl J Med. 2002;347:831–837].

Acromegaly and gigantism

The hands enlarge from overgrowth of bone and soft tissues, stimulated by an excess of growth hormone, usually from an adenoma of the anterior pituitary gland. When the condition occurs before the epiphyses close, the enlarged skeleton is well proportioned and the condition is termed gigantism. When growth occurs after epiphyseal closure, the skeletal pattern is called acromegaly, in which the hands, feet, face, head, and soft tissues are thickened. Patients often have diffuse muscle or joint stiffness and may complain of headaches and back pain. Examination shows thickening of the soft tissues, particularly apparent in the face, hands, and feet. Widening without lengthening of the bones leads to prominence of the jaw, wide spacing of the teeth, prominent supraorbital ridge, and enlarged hands and feet. OA is common. In advanced disease with suprasellar extension of the tumor, signs of hypopituitarism and bitemporal hemianopsia may be present.

Marfan syndrome

This is a congenital disease resulting from mutations of the fibrillin-1 gene. It is frequently inherited as an autosomal dominant, but sporadic cases occur. It affects the development of bone, ligaments, tendons, arterial walls, and supporting structures in the heart and eyes. Although the complete syndrome is striking, many persons show only a few stigmas. The long, slender phalanges, spider fingers have given the name arachnodactyly to the disease (Plate 29); some patients lack this sign. The skull is long and narrow, and the palate is high and arched. The long bones are thin and elongated, so the finger-to-finger span with the outspread arms exceeds the body height. Thoracic deformities may be either pectus excavatum (funnel breast) or pectus carinatum (pigeon breast). The spine may exhibit fused vertebrae or spina bifida. Joint laxity permits hyperextension (double-jointedness), dislocations, kyphoscoliosis, pes planus, or pes cavus. The ears may be long and pointed, satyr ear. Weakness of the supporting structures of the eye produces elongation of the globe (myopia), retinal detachment, lens dislocation, and blue sclerae. Degeneration of the vascular elastic media leads to aneurysmal dilatation of the aorta or pulmonary artery. Aortic dissection and rupture are common causes of early death. Deformities of the cardiac valve cusps are sites for bacterial endocarditis. The foramen ovale may remain patent.

Syndromes Primarily Affecting Joints

Arthritis—inflammatory and noninflammatory joint disease

The diagnosis of arthritis requires the examiner to confirm signs of acute or chronic joint inflammation: redness, warmth, tenderness, synovial thickening, effusion, bony enlargement, or erosive changes on X-ray. Careful attention during the physical examination is necessary to distinguish involvement of the joint (synovium and articular cartilage: arthritis) from inflammation of the periarticular tendon and ligament insertions into bone (the enthesis: enthesitis), the tendons and their sheaths (tendonitis and tenosynovitis) or the underlying bone (osteitis). When tendon inflammation is suspected, listen with the stethoscope for a rub over the painful site.

The most diagnostically useful descriptive classification of joint diseases is based upon the history and physical findings. First, the number of joints actively involved is assessed as monarticular (1 joint), oligoarticular (2–4 joints), or polyarticular (>4 joints). For patients with oligo- or polyarthritis, note the pattern of joint involvement: (1) large more proximal joints or distal small joints, (2) axial joints and/or peripheral joints, and (3) whether involvement is symmetric or asymmetric. Widespread and symmetrical joint involvement increases the likelihood of a systemic inflammatory disease primarily involving the joints (e.g., RA and SLE).

A second group of arthritis syndromes are classified as spondyloarthritis. These disorders have in common prominent enthesiopathy, involvement of the SI joints and spine, variable large joint disease (oligoarthritis), and associations with inflammatory and infectious diseases in other organs (gastrointestinal tract, genitourinary tract, skin, and eye).

No classification system is perfect and the examiner must always be alert to evolution of the pattern over days, weeks, or years. Remember that polyarthritic diseases may initially present with single joint involvement. Correct rheumatologic diagnosis requires patience and an open mind.

Monarticular arthritis

Arthritis involving a single joint is likely caused by local mechanical, inflammatory, or infectious factors

Less commonly, it is the initial manifestation of a systemic process that will involve other joints. Sequential involvement of single joints with intervening remissions suggests an underlying systemic disorder (congenital or acquired) with superimposed local precipitating events, for example, trauma in hemophilia. CLINICAL OCCURRENCE: Congenital: Hemophilia; Endocrine: Hyperparathyroidism, hypothyroidism; Idiopathic: OA; Inflammatory/Immune: Postinfectious reactive arthritis, psoriasis, RA (initial presentation), SLE, amyloidosis; Infectious: Acute septic arthritis (Staphylococcus aureus, gonococcemia, others), Lyme disease, syphilis, mycobacteria, osteomyelitis, viral (e.g., HIV, parvovirus, others); Metabolic/Toxic: Crystal-induced diseases (e.g., gout, calcium pyrophosphate deposition, calcium hydroxyapatite, calcium oxalate), scurvy; Mechanical/Traumatic: Blunt trauma, hemarthrosis, fracture, repetitive use/overuse; Neoplastic: Sarcoma (bone, synovium, or cartilage), metastases to bone, benign tumors (e.g., osteochondroma, osteoid osteoma, pigmented villonodular synovitis), leukemia; Neurologic: Neuropathy producing a Charcot joint; Vascular: Osteonecrosis.

Septic arthritis

Direct extension of bacterial infection (most commonly with S. aureus) from skin, soft tissue, or periarticular bone or hematogenous spread (e.g., bacterial endocarditis, gonorrhea bacteremia) produces infection within the joint. Release of lysosomal enzymes can rapidly destroy the joint. Usually one joint is involved, often the knee, but in gonococcal arthritis, three-fourths of the patients have an initial transient (2–4 days) migratory oligoarthritis and/or tenosynovitis. Symptoms often begin suddenly with chills and fever. The joint swells rapidly, the overlying skin is red and warm, and the joint is painful and tender to touch. The swelling becomes fluctuant, indicating fluid in the synovial cavity. In immunosuppressed patients signs of infection are frequently absent. Joint aspiration discloses purulent fluid that must be cultured to identify the causative organism [Margaretten ME, Kohlwes J, Moore D, Bent S. Does this adult patient have septic arthritis? JAMA. 2007;297:1478–1488]. CLINICAL OCCURRENCE: In addition to S. aureus and gonorrhea, less-common organisms to consider are streptococci, meningococci, Haemophilus influenzae (especially in unimmunized infants and children), and, rarely, brucellosis, typhoid fever, glanders, blastomycosis, granuloma inguinale, tuberculosis, fungi, and others.

Gout

Uric acid accumulates in tissue and extracellular fluid as a result of genetic (primary gout) or acquired (secondary gout) causes of uric acid overproduction or decreased excretion. When the fluid becomes supersaturated, crystals form in the tissue. When crystals are shed into the joint fluid and phagocytosed by polymorphonuclear neutrophils, acute inflammation results [Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med. 2005;143:499–516]. The initial attack presents the chief diagnostic problem because a history of recurrent stereotypic episodes is very suggestive of gout. Frequently, the patient is awakened from sleep by severe burning pain, tingling, numbness, or warmth in a joint. The joint rapidly swells and becomes excruciatingly tender, intolerant to the pressure of the bedclothes. Typically, the overlying skin becomes red or violaceous. There may be malaise, headache, fever, and tachycardia. Untreated, the attack lasts for 1 to 2 weeks. In more than half the cases, the MTP joint of the great toe is affected initially (podagra) (Plate 30). Other sites are the midfoot (instep), ankle, knee, elbow, or wrist. Acute gout in the midfoot resembles cellulitis. The attacks may be triggered by trauma, surgery, acidosis, infection, exposure to cold, changes in atmospheric pressure, overindulgence in alcoholic beverages, or any acute illness. Large tissue deposits of uric acid (tophi) occurring around joints over bony prominences are not usually inflamed.

Calcium pyrophosphate dihydrate deposition disease (CPPDD)–pseudogout, chondrocalcinosis

Calcium pyrophosphate dihydrate, shed from articular cartilage, crystalizes within the joint into small, rhomboidal, weakly positive birefringent crystals that trigger inflammation. Articular fibrocartilage may calcify and be detected by X-ray (chondrocalcinosis) in the knee, pelvis (hip joints and symphysis pubis) or wrist. This disorder is quite similar to true gout in both its acute and chronic forms. The attack begins abruptly with painful swelling and heat, usually in a single joint, occasionally in two or more joints. The knee, ankle, and wrist are most commonly affected. Untreated, the pain and tenderness are intense for 2 to 4 days, then gradually subside during the next 1 to 2 weeks. It is associated with increasing age and OA. It may be a clue to hyperparathyroidism or hemochromatosis (approximately 5% of CPPDD).

Charcot joint

Absence of pain or proprioceptive sensation in a joint leads to loss of joint integrity. Repeated injuries cause successively three stages of articular damage: swelling, joint degeneration, and formation of new bone. In the initial stage, erythema and swelling are the only findings. The course is progressive with hypermobility, traumatic osteophyte formation, and subluxation leading to painless deformities and crepitus on movement. In any stage, the diagnostic clue is the absence of the expected pain with movement and loss of pain sensation and proprioception in the involved limb. A single joint may be affected, or, commonly, all the joints in an anatomic region (e.g., the midfoot joints) are involved. Physical examination should try to determine if the neuropathy is part of a local or systemic neuropathic process. Classic clinical conditions, causing Charcot joints, include tabes dorsalis (knee most commonly involved; hip, ankle, lower spine, less frequently involved) (Fig. 13-21C), diabetes mellitus (tarsal and metatarsal joints most commonly, ankle occasionally, knee rarely), syringomyelia (usually joints of the upper limbs), and leprosy [Hartemann-Heurtier A, Van GH, Grimaldi A. The Charcot foot. Lancet. 2002;360:1776–1779].

Trauma

Mechanical trauma as a result of falls, sports, or other activities causes bleeding (hemarthrosis) or effusion with pain as a consequence of damage to the joint capsule, intra- or periarticular ligaments, cartilage, or bone. The knee and ankle are commonly affected, but any joint can be injured. The exact mechanism of injury, time course of pain (immediate versus delayed), and physical examination will assist in suggesting the type and degree of injury. Guidelines for the proper use of radiologic examination for injuries to the ankle and knee have been developed.

Tuberculosis

There is chronic swelling of a single joint with only moderate pain. Joint effusion may be present with thickening of the synovium. Most commonly affected are the hips, knees, and spine. Previous intraarticular or oral corticosteroids and immunosuppressive drugs are major risk factors. Cultures of aspirated joint fluid or synovial biopsy yield Mycobacterium tuberculosis.

Recurrent painless knee effusion

The patient experiences episodes of painless swelling and joint effusion in one or both knees, with no constitutional symptoms over a number of years, with an average duration of 3 to 5 days. The cause is unknown, though, occasionally, the condition presages the onset of RA.

Oligoarthritis and polyarthritis

Arthritis involving several joints, either simultaneously or sequentially, is termed oligoarthritis (2–4 joints) and polyarthritis (>4 joints).

The pattern of involvement can be useful in helping to identify the exact diagnosis. Generally, oligoarthritis involves larger joints and is asymmetric whereas the classic polyarthritis syndromes (RA, SLE) involve symmetric joints, including the small joints of the hands and feet. These are only guidelines and must not be interpreted as hard-and-fast rules. CLINICAL OCCURRENCE: Congenital: Hemophilia, familial Mediterranean fever, hemochromatosis, sickle cell disease, alkaptonuria/ochronosis; Endocrine: Hyperparathyroidism, hypothyroidism, acromegaly; Idiopathic: Inflammatory and noninflammatory OA; Inflammatory/Immune: Reactive arthritis, psoriasis, RA, systemic erythematosus, RF, ankylosing spondylitis, systemic sclerosis (scleroderma), polymyositis/dermatomyositis, antisynthetase syndrome, Still disease, Behçet syndrome, relapsing polychondritis, amyloidosis, sarcoidosis, erythema multiforme, erythema nodosum, drug reactions, serum sickness; Infectious: Septic arthritis, Lyme disease, viral (e.g., HIV, parvovirus, rubella, mumps, others), Whipple disease, mycoses (coccidioidomycosis, histoplasmosis, blastomycosis, cryptococcosis), actinomycosis, secondary syphilis, brucellosis, typhoid fever; Metabolic/Toxic: Crystal-induced diseases (e.g., gout, calcium pyrophosphate deposition, calcium hydroxyapatite, calcium oxalate), ochronosis, scurvy; Neoplastic: Sarcoma (bone, synovium, or cartilage), metastases to bone, benign tumors (e.g., osteochondroma, osteoid osteoma, pigmented villonodular synovitis); Vascular: Osteonecrosis, systemic vasculitis, HOA.

RA—deforming symmetrical distal polyarthritis

RA is characterized by proliferation of inflamed synovial tissue (pannus) that enters the joint cavity in tongue-like projections. The pannus erodes cartilage, periarticular bone, and soft tissues, including tendons and ligaments. Untreated, the result is destruction of the joint surfaces and supporting structures producing subluxation, deformity, and loss of joint function. The onset may be insidious with morning stiffness and pain followed by swelling and tenderness of the joints, proceeding over weeks to months into a small and large joint polyarthritis. Less commonly, the onset is sudden with pain and swelling occurring simultaneously in several joints accompanied by fever and prostration. Smaller joints of the hands (MCP, PIP), feet (MTP), wrists, and ankles are typically involved early and symmetrically; onset in a single larger joint, usually a knee, is not rare. Interphalangeal joints become fusiform from joint effusion (fluctuant) or thickening of the joint capsule (nonfluctuant). DIP joints are invariably spared. Tenderness is confined to the region of the capsule. Joint motion is initially limited by pain or effusion, later by fibrosis or muscle shortening. Muscle weakness and wasting may be rapid and disproportionate to the degree of disuse. Although remissions may occur, the disease is usually progressive over a period of years. Joint contracture and subluxations are frequent, with subluxation of the MCP joints producing characteristic ulnar deviation of the fingers. Tenosynovitis is manifest as swelling of the tendon sheaths. In 20% to 35% of cases, subcutaneous rheumatoid nodules develop over bony prominences and tendon sheaths. They are painless, firm, and freely movable over bones, similar to those in RF. A serious late complication is instability of the cervical spine from subluxation of C1 on C2 that may present as neck pain or upper motor neuron signs. Diagnosis is based upon clinical and laboratory criteria. Frequently, the patient must be observed for many months before the diagnosis is secure. DDX: RA frequently involves the temporomandibular joint unlike RF. In RF, arthritis is migratory, whereas it is persistent in RA. Reactive arthritis is usually oligoarticular and mainly affects large joints, especially ankles and knees. An initial monarthritis may suggest an infectious or crystalline arthritis; however, aspiration of joint fluid excludes these possibilities.

Variants of RA

Felty syndrome is the triad of RA, splenomegaly, and leukopenia. Palindromic rheumatism presents as multiple afebrile attacks of mono or oligoarthritis lasting for only 2 or 3 days, leaving no residua. Secondary Sjögren syndrome is diagnosed when keratoconjunctivitis sicca and xerostomia accompany RA. Vasculitis may accompany RA and involve the skin (necrosis and nodules), nervous system, and lung. Juvenile idiopathic arthritis is a group of disorders which may overlap with the adult disease [Hashkes PJ, Laxer RM. Medical treatment of juvenile idiopathic arthritis. JAMA. 2005;294:1671–1684]. See pediatric texts for descriptions and details.

SLE—nondeforming symmetrical distal polyarthritis

The cause is unknown, but the disease involves inflammation of multiple tissues and organs accompanied by antibodies to specific nuclear antigens usually degraded in the nucleosome. These autoantibodies are the hallmark of SLE, but their role in its pathogenesis is unclear. SLE is a chronic inflammatory multisystem disease, more common in women than men. No one symptom or sign is pathognomonic of SLE; rather, the diagnosis is established by clinical criteria. The most common symptoms and signs are fatigue, malaise, or fever (90% of cases), arthritis or arthralgias (90%), and skin rashes (50–60%). The arthralgias, myalgias, and joint inflammation resemble mild RA, but deformities usually do not develop. The malar (“butterfly”) rash is a macular to maculopapular, sometimes scaly, erythematous process forming the “wings” of the butterfly on each malar prominence, with the “trunk” on the bridge of the nose. It may be more intense after exposure to sunlight. In addition, there may be skin atrophy, telangiectasia, and mucosal ulcers. Serositis is common, presenting as pleurisy (with effusion and/or pleural rubs), abdominal pain, or pericarditis. Nonbacterial endocarditis with valvular insufficiency (usually mitral), central nervous system disease (with personality change, psychosis, or seizures), and glomerulonephritis can occur at any time and may be the presenting syndrome. Other signs are recurrent urticaria, mononeuritis multiplex and lymphadenopathy. Fetal wastage and thromboembolic disease are associated with antiphospholipid antibodies [D’Cruz DP, Khamashta MA, Hughes GRV. Systemic lupus erythematosus. Lancet. 2007;369:587–596; Caro I, Zembowicz A. Case 5–2003: a 16-year-old girl with a rash and chest pain. N Engl J Med. 2003;348:630–637].

Rheumatic Fever—migratory polyarthritis

This disease is a delayed inflammatory reaction following infection with specific Lancefield groups of group A beta-hemolytic streptococci. Tissues affected include the heart, joints, skin, and central nervous system. The disease is protean in its clinical manifestations. The classic presentation begins from 1 to 4 weeks after streptococcal pharyngitis, with gradual onset of malaise, fatigue, anorexia, and fever. A single large joint becomes painful, tender, and swollen, and the overlying skin is red and hot. An effusion forms that is turbid and sterile. Although the fever and other signs of illness persist, the joint inflammation spontaneously subsides in a few days, only to reappear in another joint, and later in another joint—a migratory polyarthritis. Joint involvement may be so mild that pain is unaccompanied by physical signs of inflammation. Months of observation may be required to distinguish it from RA; involvement of the temporomandibular joint often occurs in RA, practically never in RF. RF leaves no residual joint deformity. At onset, the inflammation of a single joint with effusion requires distinction from suppurative arthritis. Carditis is manifest as tachycardia, muffled heart sounds, heart enlargement, valvular insufficiency murmurs, pericardial friction rub, or gallop rhythm on examination. The electrocardiogram may show PR prolongation. Two distinct types of skin lesions may be associated with RF, although neither is pathognomonic. Erythema marginatum or circinatum is characterized by coalescing circular erythematous areas over the trunk and extremities, migratory and transitory, changing within the hour. With chronic disease, subcutaneous rheumatic nodules may appear as firm, nontender masses over the joint prominences and tendon sheaths of the limbs, scalp, and spine. They are loosely attached to the underlying tissue; when numerous, their distribution tends to be symmetrical. Sydenham chorea may appear several months after onset. There are no diagnostic laboratory tests, but the full clinical picture is fairly distinctive. Diagnosis is based upon the Jones criteria of major and minor manifestations.

Tophaceous gout

See Gout. Tophi are masses of monosodium urate crystals deposited in the tissues often over bony prominences and around joints where they erode bone. Acting as foreign bodies, they stimulate low-grade inflammation that may extrude the tophi through the skin. The asymmetrical nodular swellings and cartilage degeneration may impair joint function. Clinical signs of inflammation are variable, from mild to moderately severe. The olecranon, bunion and prepatellar bursae, and hands are most frequently affected.

OA, degenerative joint disease (DJD)—noninflammatory polyarthritis of large and small joints

This is a disease of articular cartilage with degradation of the proteoglycan matrix leading to fissuring, thinning, and loss of articular cartilage, and secondary thickening of subchondral bone. In late stages, the bone ends rub directly on each other so their surfaces become worn and polished. The joint capsules are little affected, so adhesions are not formed, and although joint motion is restricted, ankylosis does not result. The bony margins proliferate to form spurs, lipping, and exostoses. Genetic and acquired factors (trauma, surgery, obesity, excessive use) contribute to the pathogenesis. Symptoms are usually first noticed in the weight-bearing joints after age 40 and signs of inflammation are relatively slight. Symptoms correlate poorly with the objective extent of joint disease. The most common symptom is pain with use that disappears with rest. The patient may note grating during motion. Initially, the range of motion is normal, with a gradual decrease occurring as the disease progresses. Enlargement of the DIP and PIP joints of the fingers (Heberden and Bouchard nodes, respectively), is frequently encountered. Painless knee effusion is frequent as is asymmetric loss of knee cartilage leading to valgus or varus deformity.

Gonococcal arthritis—migratory oligoarthritis

Neisseria gonorrhoeae infects the urethra or uterine cervix and then disseminates hematogenously to synovial membranes and skin, causing local inflammation. Infectious arthritis, tenosynovitis, and skin lesions are the most common extragenital complications of gonorrhea. One to four weeks after the onset of urethritis, inflammation may suddenly occur in the knees, wrists, and ankles, although other joints may be affected. The most common pattern is a migratory oligoarthritis and tenosynovitis. Small amounts of thin fluid may accumulate in joint cavities. In other cases, suppurative arthritis develops, with inflammation of a single joint and production of purulent exudate. Tenosynovitis in the hands, wrists, or ankle is more common in gonorrhea than in arthritis from any other cause. The diagnosis may not be easy because the gonococcus is difficult to culture from the joints. Pustular skin lesions on an erythematous base are seen with gonococcal bacteremia and help to distinguish gonococcal arthritis from other conditions. Genital, rectal, and throat specimens for culture or polymerase chain reaction testing of urine for gonococcus and chlamydia should be obtained. Reiter syndrome (nonspecific urethritis, arthritis, and conjunctivitis) following nongonococcal urethritis may cause confusion, because conjunctival infection is present in up to 10% of patients with gonorrhea.

Hemochromatosis

The second and third MCP joints and the radiocarpal joint of the wrist are most commonly affected. Chondrocalcinosis is present. Symmetric noninflammatory arthritis of the MCP joints should initiate a search for an iron-storage disorder.

Relapsing symmetrical seronegative synovitis with pitting edema

This condition of unknown cause presents with recurrent episodes of symmetrical synovitis of the hands and wrists with pitting edema and erythema of the dorsum of the hands. Pain is relatively mild and the condition usually remits after several days to a couple of weeks. When RS3PE occurs as a paraneoplastic condition, it may be more chronic.

Spondyloarthritis

Inflammation at the insertion of ligaments and tendons into bone (the enthesis, enthesitis) leads to joint and tendon sheath effusions and ossification of periarticular structures.

Genes (HLA-B27) and acquired illness (inflammatory bowel disease, infectious colitis, nongonococcal urethritis, and psoriasis) predispose to these disorders. Asymmetric oligoarthritides of the large joints with prominent involvement of the spine and SI joints and negative tests for rheumatoid factor are described as the seronegative spondyloarthritides. Patients present with back pain and stiffness, and occasionally with fever, malaise, and weight loss. Look for extraarticular disease, such as genitourinary or gut symptoms, eye involvement (uveitis), and skin disease. [Khan MA. Update on spondyloarthropathies. Ann Intern Med. 2002;136:896–907]. CLINICAL OCCURRENCE: Ochronosis, disk disease, DISH, ankylosing spondylitis, enteropathic arthritis (inflammatory bowel disease), psoriasis, reactive arthritis after diarrheal and genitourinary infections.

Ankylosing spondylitis

Inflammation of the ligamentous attachments to the vertebrae (enthesitis), the SI joints and the junction of the annulus fibrosis and the vertebral end plates leads to new bone formation and bridging resulting in ankylosis. This chronic, progressive arthritis begins with SI involvement and progresses proximally often leading to severe ankylosis. Nonspecific symptoms often begin in adolescence and occur intermittently for 5 or 10 years. Pain and morning stiffness are felt in the lumbar region, buttocks, and SI region. Fatigue, fever, and weight loss may occur. Decreased lumbar spinal motion is an early sign with the normal lumbar lordosis straightened, diminished anterior flexion, and spinal rotation and lateral bending impaired. Slowly, the process ascends the lumbar and thoracic spine, the cervical region may be involved late. Episodes of acute or subacute arthritis may involve hip, shoulder, sternoclavicular, or manubriosternal joints. Tenderness is found over the involved joints. Iridocyclitis occurs in one-fifth of the cases. Aortic regurgitation is a late complication in 3% of patients. Idiopathic ankylosing spondylitis needs to be distinguished from psoriatic arthritis and enteropathic associated spondyloarthritis (Crohn disease and ulcerative colitis), Whipple disease, and DISH.

Reactive arthritis

Following infection of the urethra (chlamydia) or gut (Shigella, Salmonella, Yersinia, and Campylobacter) an oligoarthritis, predominately of the lower extremities, develops. It may be accompanied by enthesitis of the hands, ankles, and feet, conjunctivitis, urethritis, and rash on the glans penis (circinate balanitis) and feet (keratoderma blenorrhagica). Sacroiliitis and spine involvement may occur. Eighty-five percent of patients are HLA-B27-positive.

Enteropathic arthritis

Inflammatory asymmetric arthritis predominately of the ankles and knees may occur in association with inflammatory bowel disease (ulcerative colitis and Crohn disease). Enthesitis is common, especially at the Achilles tendon insertion, and symmetrical SI and spinal involvement occurs. The arthritis may precede clinical manifestations of the inflammatory bowel disease.

Psoriatic arthritis

The joint disease is usually an asymmetrical oligo- or polyarthritis of small and large joints. It is occasionally a symmetrical polyarthritis resembling RA. Destructive arthritis of the DIP joints is seen in psoriatic arthritis but not in RA. Spondylitis and sacroiliitis occur in up to 25% of patients with psoriatic arthritis, especially those with HLA-B27. Enthesitis may predominate in some patients. The arthritis may precede, accompany, or follow onset of the skin rash. Physical examination should include a careful skin examination, especially of the scalp (the rash may be hidden by hair or dismissed as seborrhea) and fingernails (looking for pits and onycholysis).

Conditions Primarily Affecting Bone

Osteoporosis

Bone resorption exceeds bone formation, leading to decreased bone mass and decreased mechanical strength. Trabecular bone is affected more than cortical bone. Increased resorption of bone results from immobilization, inflammation, multiple myeloma, and hyperparathyroidism. Decreased bone formation results from gonadal hormone deficiency, glucocorticoid steroid excess, and advanced age. Trabecular bone deficiency is especially important in the vertebrae and pelvic bones, whereas cortical bone loss is predominant in long bones. Osteoporosis is asymptomatic until insufficiency fractures occur, usually in the thoracic or lumbar spine and pelvis. Thoracic kyphosis results from anterior wedging of thoracic vertebrae. Bone mineral density is assessed by dual X-ray absorptiometry (DEXA) scan. The bones are much more susceptible to fracture with minor trauma; hip and wrist fractures from falls should initiate evaluation for osteoporosis in both men and women [Green AD, Colón-Emeric CS, Bastian L, Drake MT, Lyles KW. Does this woman have osteoporosis? JAMA. 2004;292:2890–2900]. CLINICAL OCCURRENCE: Congenital: Vitamin D-resistant rickets, Marfan syndrome, hemochromatosis, Ehlers–Danlos syndrome, hemophilia, thalassemia, positive family history; Endocrine: Postmenopausal estrogen deficiency, premature menopause, hypogonadism, hyperthyroidism, hyperparathyroidism, Cushing syndrome, glucocorticoid use, diabetes mellitus, pregnancy, adrenal insufficiency, acromegaly, hyperprolactinemia; Idiopathic: Advanced age; Inflammatory/Immune: Sarcoidosis, amyloidosis, RA, ankylosing spondylitis; Metabolic/Toxic: Vitamin D deficiency, malnutrition, chronic renal insufficiency, heparin, cirrhosis, postgastrectomy, parenteral nutrition, cigarette smoking, low body weight; Mechanical/Traumatic: Immobilization, disuse, and nonweightbearing; Neoplastic: Multiple myeloma, paraneoplastic (parathyroid hormone (PTH)-related protein secretion), lymphoma, prolactinoma; Neurologic: Paralysis, stroke, multiple sclerosis; Psychosocial: Anorexia nervosa; Vascular: Hyperemia of bone.

Osteomalacia

Vitamin D deficiency, hypocalcemia, or hypophosphatemia after the epiphyses are closed prevents calcification of newly formed bony matrix. Early there are no symptoms or signs, whereas later, bone pain and tenderness occur. Low back pain and striking muscle weakness are common. Low serum calcium levels may produce spontaneous carpopedal spasm with the Chvostek and Trousseau signs. Insufficiency (stress) fractures are common and pseudofractures may be seen by X-ray. CLINICAL OCCURRENCE: Congenital: Vitamin D-resistant rickets; Endocrine: Hyperparathyroidism, rapid deposition of calcium and phosphorus in the tissues after ablation of the parathyroid glands in osteitis fibrosa cystica, hypoparathyroidism; Inflammatory/Immune: Celiac disease; Metabolic/Toxic: Vitamin D deficiency, hypocalcemia, hypophosphatemia, malabsorption, pancreatic insufficiency, malnutrition, chronic renal insufficiency, renal tubular acidosis, Fanconi syndrome, ureterosigmoidostomy, essential hypercalciuria, drugs (anticonvulsants, e.g., phenytoin, glucocorticoids, etidronate), fluoride and aluminum intoxication.

Rickets

Vitamin D deficiency in childhood before epiphyseal closure results in inadequate calcification of cartilage and new bone. See Chapter 8, Figure 8-30. Softening of bone produces widening of the cranial sutures and fontanelles (craniotabes), Parrot bosses, rachitic rosary, Harrison grooves, thoracic kyphosis or lordosis, genu valgum or varum, and a contracted pelvis. With the sole exception of the rosary, all deformities are permanent stigmas of childhood disease.

Paget disease

Increased resorption of bone combines with rapid growth of new bone with disordered architecture and decreased mechanical strength. The cause is unknown. Bone pain may occur but is seldom severe. With the exception of the hands and feet, any bones may be involved. The skin over affected bones may be warm. The classic osseous deformities are increased girth of the calvarium, thoracic kyphosis, genu varum, and shortening of the spine by flattening of the vertebrae, giving the appearance of disproportionately long arms (Fig. 13-37). Spontaneous or stress fractures can occur and rarely osteogenic sarcoma develops. Increased blood flow through the spongy bone may produce an arteriovenous fistula leading to high-output cardiac failure.

Primary hyperparathyroidism—osteitis fibrosa cystica

Increased production of PTH causes bone resorption to exceed new bone formation, leading to hypercalcemia, hypercalciuria, hyperphosphaturia, and hypophosphatemia. The disease may be asymptomatic, although diffuse musculoskeletal aching and fatigue is seen in many patients. Late findings are bone tenderness, muscle weakness, and waddling gait. Subperiosteal cysts in the skull and long bones can cause visible and palpable swellings. Peptic ulcer and urolithiasis should prompt a search for hyperparathyroidism.

Hyperparathyroidism, secondary, and tertiary

Hyperphosphatemia and hypocalcemia combined with disordered vitamin D metabolism in chronic renal failure (renal osteodystrophy), or osteomalacia from other causes, leads to increased production of PTH, hyperplasia of the parathyroid glands, and progressive bone disease. Combinations of dietary, hormonal, and renal replacement therapies can help control the disorder. When PTH production is not suppressible with appropriate treatment, it is termed tertiary hyperparathyroidism.

Multiple myeloma

This malignant clonal proliferation of immunoglobulin-producing plasma cells (terminally differentiated B cells) in the bone marrow causes destruction of bone by activation of osteoclasts leading to hypercalcemia. Normal immunoglobulin production is suppressed, there is production of monoclonal plasma proteins (heavy chains, light chains, and intact immunoglobulin), and anemia and thrombocytopenia develop. Renal insufficiency results from tubular toxicity of light chains (Bence Jones proteins), hyperuricemia, and hypercalcemia. This is the most common malignant tumor primarily affecting bone. Fatigue or generalized aching discomfort may be the only early symptoms. The most common specific symptom is bone pain. With spinal compression fractures, localized pain in the back with radicular distribution occurs. The presenting complaints may be referable to anemia, renal failure, or a pathologic fracture. Multiple myeloma should be considered in patients more than 45 years of age with back pain and anemia.

Bone metastases

Metastatic disease presents as a localized swelling or pain in a bone, a pathologic fracture, or is found incidentally on radiographs taken for another reason. The most frequent primary carcinomas are breast, lung, and prostate.

Fractures

Mechanical disruptions of the mineralized bone and its collagenous matrix are caused by application of forces exceeding the tensile and/or compressive strength of the bone. This can occur from a single forceful event or from repetitive less forceful loading. Fracture of the mineralized bone leaving the collagenous matrix intact results from trauma in children (greenstick fracture) and repetitive activities in adults (stress fracture). If the bone is inherently weak because of local destructive disease, it may fracture at usual loads (pathologic fracture). When fracture fragments penetrate the skin, it is an open fracture. When fracture is suspected, immobilize the part and assess neurovascular function distal to the injury. Inspection often reveals deformity. Unavoidable movement reveals abnormal mobility, and bone crepitus, distinctive signs of fracture one should not deliberately try to elicit. Muscle contraction attempting to splint the fracture often aggravates pain. Localized bone tenderness indicates the site of the fracture. Shortening of a long bone may be the crucial sign of an impacted fracture.

Spontaneous or pathologic fracture

This is a fracture that occurs with trauma insufficient to break a normal bone. Judging the amount of trauma is difficult, hence spontaneous fractures are easily mistaken for traumatic fractures; a high index of suspicion is warranted. X-ray signs of generalized or local bone disease should be sought if pathologic fracture is suspected. Sometimes spontaneous fractures are less painful than those of healthy bone. Osteomalacia, osteoporosis, Paget disease, hyperparathyroidism, multiple myeloma, osteogenesis imperfecta, and primary and metastatic neoplasms in bone are common underlying conditions.

Osteomyelitis, acute

Blood borne bacteria from superficial infections are carried to the terminal capillary loops of the metaphyseal cortex, causing a necrosing infection that erodes to the periosteum. The initial infection is in the metaphysis, near but not involving the epiphysis. S. aureus is the most common organism. Osteomyelitis is most common in children. The onset is usually sudden, with fever and pain. Older children may be able to point to the painful site, although the pain may be referred to the nearest joint where sympathetic effusion may be noted. Localized swelling and redness of the overlying skin with increased warmth may be seen. Light bone percussion frequently discloses tenderness; localize the site with finger pressure on the bone moving toward the suspected site until the point of maximum tenderness is located. The proximal femoral metaphysis is within the hip joint in children, so they present with a septic hip. Sometimes deep cellulitis cannot be distinguished clinically from osteomyelitis.

Osteomyelitis, chronic

After the acute phase, the purulent discharge from the necrosing bone breaks through the periosteum and drains through sinuses in the skin. The circulation of the cortex becomes impaired, producing islands of dead bone, sequestra. A sequestrum may be absorbed, discharged through the sinus, or surrounded by new bone, the involucrum. Continuing necrosis of bone and retention of sequestra is the cause of persistent infection.

Osteogenesis imperfecta

An inherited disorder of type I collagen results in decreased mechanical strength of all bones and pathologic fractures during the first decade of life. Autosomal dominant inheritance occurs in 60% of cases, but several different types have been recognized. The bones are harder and more brittle than normal, so spontaneous or pathologic fractures are common. The fractures are sometimes painless. Blue sclerae may be observed. Short stature is usual and skull deformity is often present. Hypermobility of joints is common.

Fibrous dysplasia of bone

The cause of this disease is unknown. The architecture of one or more bones is distorted by fibrosis; the cranium and long bones are especially involved. There is asymptomatic bowing of the affected long bones. The skin often contains melanotic spots with jagged borders. In young girls, precocious puberty may occur.

Hereditary multiple exostoses—osteochondromatosis

The autosomal dominant disease is characterized by exostoses arising from the bony cortex, deforming the metaphyseal region of some long bones. Involvement is usually bilateral but not symmetrical. The ulna may be shortened, producing ulnar deviation of the hand. Valgus deformities of the ankle are common. The only symptom may be mechanical interference with normal joint function.

Neck, Spine, and Pelvis Syndromes

Neck, shoulder, and arm pain—cervical spondylosis and radiculopathy

Spondylosis results from degeneration of the intervertebral disks. Contusion of a cervical root in the neural foramen produces severe pain in the nerve distribution. Commonly, the cause is narrowing of intervertebral foramina or compression of nerve roots by osteophytes. Uncommonly, the lesion is caused by protrusion of an intervertebral disk or by C1–C2 instability from RA. Usually, minor trauma precedes the onset of pain. Painful spasm of the neck muscles causes temporary torticollis, with the head tilted away from the painful side. Sharp, shooting pains spread slowly down the shoulder, the lateral aspect of the upper arm, and the radial aspect of the forearm, to the wrist. The neck muscles are rigid on the affected side. The biceps tendon reflex is frequently diminished or absent with a radiculopathy of C5 or C6. The triceps reflex is decreased with a radiculopathy of C7. There may be tingling and numbness in the thumb, index, and middle fingers, but muscle wasting is rare. Extend and laterally rotate the neck; when pain is elicited, Spurling sign is present. Active and passive motions of the neck are restricted and may be painless, but often produce subjective and objective crepitus. Coughing with the head held in extension may reproduce the pain [Carette S, Fehlings MG. Cervical radiculopathy. N Engl J Med. 2005;353:392–399]. DDX: Other causes, such as incomplete rupture of the supraspinatus, Pancoast tumor, and peripheral neuropathy must be excluded. Symptoms remit gradually over days to weeks.

Neck and shoulder pain—Pancoast tumor, superior sulcus syndrome

Lung cancer at the thoracic apex invades locally to involve the pleura, thoracic muscles, and neurovascular bundles, including the brachial plexus and cervical sympathetic chain. Pain is felt in local structures and is referred in the distribution of the involved nerves. Severe pain is present in the posterior part of the shoulder and axilla, often shooting down the arm, with paresthesia of the arm and hand. Paresis or wasting of arm muscles may occur. In addition to neck and shoulder pain, the complete syndrome includes Horner syndrome (unilateral miosis, ptosis, and absence of sweating on the ipsilateral face and neck). It may be confused with rupture of the supraspinatus tendon, cervical spondylosis, and peripheral neuritis.

Back pain and stiffness—infectious spondylitis

Spinal infection most commonly starts in the disks (diskitis) and anterior endplates of the vertebrae leading to vertebral erosion and collapse. Infection may extend anteriorly into the psoas or posteriorly into the epidural space leading to spinal cord compression. Pain and tenderness of the spinous vertebral processes are usually present over the site of infection, often with spasm of the sacrospinalis. The pain may be referred along a spinal nerve to be mistaken for appendicitis, pleurisy, or sciatica, if the back is not examined. Collapse of the vertebral body causes a gibbus and paraplegia may result. Psoas abscess, classic in tuberculosis, may form along the sheath of the psoas and point beneath the inguinal ligament. Pain in the spine may be localized by the heel-drop test: have the patient rise onto tiptoes, and then drop onto the heels; pain will be elicited at the site of infection. Infections with pyogenic organisms (S. aureus) are most common. Tuberculosis, Salmonella, brucellosis, fungi, and actinomycosis are less common.

Tuberculous spondylitis (Pott disease)

Tuberculosis of the spine is an indolent osteomyelitis of the anterior vertebral endplates with extension to the paravertebral soft tissues. Patients present with fever, night sweats, and pain. With cervical infection, the neck is held stiffly and spontaneous rotation of the head is absent. When seated, the patient may support the head with the hands (Rust sign). An abscess of the cervical vertebra may track to the retropharyngeal space. Patients with epidural extension can develop spinal cord compression. Vertebral collapse in the thoracic or lumbar spine can produce gibbus deformity and risk of instability. Rarely, cold abscess present as an inguinal mass from prevertebral extension.

• Back pain—epidural spinal cord compression. Masses in the closed epidural space may erode bone, compress spinal nerves, and compress the spinal cord. Most epidural masses extend from the adjacent vertebrae or from retroperitoneal malignancy to press on the anterior or anterolateral cord. Progressive axial, radicular, or referred back pain, unrelieved by recumbency, should prompt an immediate search for spinal cord compression. Pain is the most common presenting symptom followed by leg weakness, constipation, incontinence, and sensory disturbances. The latter indicate advancing cord compression, from which there is less chance for complete recovery. Paraplegia may occur in a matter of hours after the onset of neurologic signs. The pain may occur at any level and is increased by straight-leg raising, Valsalva maneuver, neck flexion, and movement. MRI of the entire vertebral column and cord is the most sensitive and specific test. CLINICAL OCCURRENCE: Breast, prostate, and lung cancer are the most frequent causes. Other cancers in adults include multiple myeloma, malignant lymphoma, renal carcinoma, sarcoma, and melanoma. In children, consider lymphoma, sarcoma, and neuroblastoma. Epidural abscess complicates infectious spondylitis.

Back pain and stiffness—diffuse idiopathic skeletal hyperostosis (DISH)

Asymmetric osteophytes develop at multiple levels of the spine leading to bridging of multiple intervertebral spaces and irregular ankylosis with decreased spinal motion, especially in the cervical and lumbar regions. The disk spaces are preserved. Men are affected more often than men.

Back pain and stiffness—rigid spine syndrome

The clinical syndrome of rigid spine, proximal muscle weakness, scoliosis, and joint contractures can have several different etiologies. The combination of restrictive chest disease and muscle weakness can lead to respiratory failure [Janssen WJ, Collard HR, Saint S, Weinberger SE. A perfect storm. N Engl J Med. 2005;353:1956–1961].

Low back pain—lumbosacral strain

Mechanical injury commonly occurs to the soft tissues (muscles, tendons, and ligaments) of the low back where the mobile lumbar spine meets the fixed sacrum, concentrating mechanical forces at the transition zone. Injury can be the result of a single, large loading force or of a repetitive loading with lesser forces. Usually the patient complains of aching pain near L5 and S1. The pain may radiate laterally or to the lateral aspect of the thigh. There is an increased lumbar lordosis and attempted spinal motion is accompanied by muscle spasm. Spinal flexion is limited and painful. The patient cannot lie flat without flexing the knees and hips to relieve pain. The straight-leg-raising test is negative except that lumbosacral pain occurs at extreme flexion. Have the patient lie prone with the pelvis resting on four pillows to separate the spinous processes. In this position, palpation of the spines and supraspinous ligament may reveal tenderness above or below the spine of L5; sometimes a depression is found indicating spondylolisthesis.

Low back pain—sciatica

Compression or direct injury to the sciatic nerve produces pain, altered sensation (dermatomes L4-S2), loss of muscle reflexes (ankle jerk), and, if severe, muscle power in the distribution of the nerve (e.g., ankle flexion, extension, inversion and eversion, great toe extension). Sciatica is pain in the distribution of the sciatic nerve. Pain is initially felt in the buttock and posterior thigh, and may extend to involve the posterolateral aspect of the leg to the lateral malleolus, the lateral dorsum of the foot and the entire sole. When nerve function is compromised, paresthesias are felt in the same distribution. Pain and paresthesias are intensified by coughing or straining. The nerve trunk is tender when palpated at the sciatic notch or stretched when the leg is extended while the thigh is flexed (Lasègue sign, straight-leg raising). Rectal examination should always be done to look for pelvic masses. A pulsating rectal mass associated with sciatica suggests aneurysm of the internal iliac or common iliac artery. Most cases are caused by herniated intervertebral disk.

Low back pain—herniated intervertebral disk

Herniation of a desiccated nucleus pulposus through tears in the annulus fibrosa produces pressure on nerve roots in the neural foramina laterally or directly on the cauda equina, conus or spinal cord if the extrusion is directly posterior (Fig. 13-26B). The onset of pain may be gradual or sudden and is partially relieved in recumbency. Sciatica may be the presenting symptom with pain in the buttock radiating to the thigh. In severe cases, the pain involves the leg, usually the lateral aspect, and some or all of the toes (dermatomes L4 to S2). Coughing, sneezing, or the Valsalva maneuver accentuates the pain. Chronic herniated disk is attended by symptom-free periods; continuous back pain is usually caused by some other lesion. On examination, the spine may be flexed, frequently with a lateral deviation toward the affected side. Active flexion and extension of the spine are limited, more so than lateral bending and rotation. Muscle spasm is most severe over the ipsilateral sacrospinalis with rigidity and tenderness, most pronounced on the affected side 5 cm lateral to the midline. Palpate for muscle rigidity, and other areas of tenderness including trigger points and fibrositis tender points. Have the patient heel-and-toe walk and extend the great toe against resistance. Pain with the straight leg test often occurs at less than 40 degrees with a prolapsed disk; when pain occurs only at much greater angles, there may be another cause. If the straight-leg-raising test is positive, repeat it and as the painful angle is approached, dorsiflex the foot sharply stretching the sciatic nerve to test its irritability. Check sensation noting the dermatome involved. [Vroomen PC, de Krom MC, Knottnerus JA. Diagnostic value of history and physical examination in patients suspected of sciatica due to disc herniation. J Neurol. 1999;246:899–906; Vroomen PC, de Krom MC, Knottnerus JA. Consistency of history taking and physical examination in patients with suspected lumbar nerve root involvement. Spine. 2000;25:91–96].

Low back pain—spinal stenosis

Compression of the lower lumbar and sacral roots occurs from overgrowth of bony tissue, from congenital narrowing, or degenerative disk disease that narrows the spinal canal. Pseudoclaudication is pain in the buttocks, bilateral posterior thighs, and calves while standing or walking upright, that is relieved by sitting or bending forward (reversing the lumbar lordosis and decreasing the degree of stenosis). DDX: Unlike intermittent claudication from vascular insufficiency, pain occurs while standing without walking. Sitting gives relief, in contrast to lumbar disk disease. Osteoporosis, spondylolisthesis, trauma, laminectomy, spinal fusion, spondylosis, scoliosis, acromegaly, and Paget disease are all potential contributors. Congenital narrowing of the canal is not uncommon.

Sacral pain—lesions of the cauda equina

Compression of the cauda equina (“horse’s tail”: the spinal roots below the level of the spinal cord termination, or conus) results in compromise of nerve function in one or more lumbar or spinal nerves, often accompanied by pain. Pain is localized to the sacrum and inner thigh, and the skin may be anesthetic. Bladder symptoms (including decreased urinary stream, hesitancy, and urinary retention), anal sphincter laxity, absent anal wink, and impotence are common. Compression occurs from a herniated intervertebral disk with posterior protrusion, epidural hematoma or abscess, and neoplasms.

Sacroiliac pain—sacroiliac arthritis

On arising, there is painful stiffness in the upper medial buttocks, which improves with exercise. Pain may be referred to the upper outer quadrant of the buttock, or the posterolateral aspect of the thigh. Sometimes there is a limp. Spinal rotation accentuates pain. The joint is tender to palpation or percussion. SI arthritis is characteristic of spondyloarthritis.

Sacroiliac pain—sacroiliac strain

Mechanical strain or postpartum relaxation of the ligaments about the joint is followed by inflammation. The patient complains of pain in the joint or in the upper inner quadrant of the buttock or the posterolateral aspect of the thigh (dermatomes L4, L5, S1). The joint is tender. The pain is accentuated by compressing the anterior iliac crests while the patient lies supine. The tendon reflexes in the lower limbs are normal.

Ischial tuberosity pain—ischiogluteal bursitis

The gluteal muscles cover the ischial tuberosities when standing. With thigh flexion, such as sitting, the muscles slide upward exposing the tuberosities and their tendon insertions to pressure, protected only by intervening skin, subcutaneous tissue, and the ischiogluteal bursa. Irritation of the bursa and/or tendon insertions can lead to secondary sciatic nerve irritation. This is more common with occupations characterized by sitting on a poorly cushioned seat. The pain is aggravated by sitting, coughing, walking, and standing on tiptoe. The patient lists toward the affected side with standing and walking, and the stride is shortened with circumduction of the affected foot. The patient sits with the affected buttock elevated and on lying supports the pelvis on that side. There is point tenderness on the ischial tuberosity. The straight-leg-raising test causes pain. The FABER sign is present. On rectal examination a region of tender, bulging, doughy tissue may be palpated in the lateral rectal wall. DDX: Patients with herniated disk and lumbosacral disease lie quietly and lack the FABER sign. This bursa may also be affected by gout. Pain is referred to the tuberosity from intramedullary lesions of the femoral head.

Upper Extremity Syndromes

Finger snapping or locking—trigger finger

A nodular thickening forms in the long flexor tendon just proximal to the metacarpal head as a result of inflammation or repetitive trauma. In extension, the nodule lies within the flexor tendon sheath; during flexion, it is easily pulled from the proximal end of the sheath. The constricted mouth of the sheath resists reentry of the nodule during extension until it is suddenly achieved with a noticeable click. The middle or ring finger is usually involved (Fig. 13-28D). Flexion of the finger feels normal, but extension is accompanied by a snap that the patient sometimes refers to the region of the PIP joint. The nodule can be palpated moving with the tendon on active or passive flexion–extension. Triggering may or may not be painful.

Finger infections

It is essential to distinguish superficial from deep tissue infections in the fingers. The latter are initially limited to specific tissue compartments giving characteristic signs.

Paronychia

The skin over the matrix of the nail and the lateral nail folds is swollen, reddened, painful, and tender (Fig. 13-38A). When infection is over the nail root, light palpation of the inflamed area provokes exquisite pain. Pain from pressure on the nail plate indicates subungual abscess, which occurs between the nail plate and periosteum.

Chronic paronychia

Candida paronychia is minimally tender and does not drain. Chronic ulceration of the nail mantle and lateral folds occurs in occupations requiring frequent immersion of the hands in water or contaminated oil. The ulcers are indolent; abscess formation is rare.

Abscess of the apical space

Symptoms follow a puncture wound beneath the nail. The distal nail bed becomes red and extremely painful without much swelling (Fig. 13-38B). Maximum tenderness is proximal to the free edge of the plate, unlike a felon, which produces tenderness at the fingertip. When the abscess ruptures, drainage is at the free edge of the nail plate.

Abscess of the terminal pulp space (Felon)

Infection of the finger pad is confined within small fascial compartments attached to the periosteum (Fig. 13-38C). There is swelling of the fingertip and dull pain that becomes intense and throbbing with exquisite tenderness. Induration of the pulp indicates the presence of pus. The abscess may drain through the volar surface of the finger pad; osteomyelitis may occur.

Abscess of the middle volar pulp space

The finger is held in partial flexion to reduce the pain. A tender swelling occurs on the volar aspect of the finger between the PIP and DIP joints (Fig. 13-38D). The symptoms resemble those of a felon. Osteomyelitis may occur or the abscess may drain after burrowing to the distal flexor crease.

Abscess of the proximal volar pulp space

An abscess forms on the volar aspect between the MCP and PIP joints (Fig. 13-38D). The symptoms and signs are similar to those in the middle space, except the infection burrows proximally to involve the web space.

Barber’s pilonidal sinus

Short hair shafts may penetrate the soft skin in the finger webs producing inflammation. One or more nodules are felt which are drained by sinuses; seen as black dots between the fingers.

Localized thickening of palmar fascia—Dupuytren contracture

There is a painless nodular thickening of the palmar aponeurosis from hyalinization of collagen fibers beginning near the base of the digit. It extends to form a plaque or band adhering to the palmar fascia and producing retraction and dimpling of the palmar skin and flexion contracture of the fingers. The condition occurs exclusively in Caucasians, predominately men and 40% have a positive family history. It is more common in patients with alcoholism, epilepsy, or diabetes mellitus; the cause for these associations is unknown. It usually begins after age 40 years as an inconspicuous hard nodule fixed to the skin in the distal palm. Both hands may be involved. The ring finger is more often affected than the little, long, index or thumb. Fascial retraction pulls the finger(s) into partial flexion (Fig. 13-30I). Palpation reveals a hard cord over the tendon that is raised in extension making it readily seen. With progression, a painless contracture of the digit(s) results requiring surgical correction. Other fibrosing conditions that may be part of the same diathesis, occurring singly or in combination, are plantar fibrosis (Lederhosen syndrome) and fibrosis of the corpus cavernosum (Peyronie disease).

Hand infections

Infections in the hand can be trivial or tragic depending upon the site of infection and the organism. Care must be taken in evaluation to identify deep space infections resulting from puncture or bite wounds that can rapidly destroy hand function.

Painful palmar swelling—web space infection

Fever, malaise, and diffuse pain in the hand and dorsal edema occur early. The two involved fingers are separated at their bases by a tender erythematous swelling; tenderness is maximal on the palmar surface (Fig. 13-39A).

Painful palmar swelling—infection of the thenar space

The thenar eminence is swollen, tender, and may have erythema and warmth. DDX: Deep hematoma gives similar symptoms and signs but with a history of blunt trauma. Extension at the IP joint is not painful as it is in tenosynovitis of the flexor pollicis longus.

Painfully swollen palm—deep abscess of the palm

There is usually a history of penetrating trauma, often minor. There is pain, swelling and limited motion. In addition to severe dorsal edema, the concavity of the palm is obliterated, or even elevated; the raised area is tender and erythematous; the erythema may extend to the volar wrist extending under the flexor retinaculum. This is a surgical emergency.

Painful palm and finger swelling—acute suppurative flexor tenosynovitis

Throbbing pain begins in a finger, progressing toward the palm. The finger and dorsum of the hand are swollen. The finger is held slightly flexed; the patient resists moving it. Passive extension of adjacent fingers is painful, of the affected finger, exquisitely so. Test for the point of maximum tenderness by gently palpating the palm and flexor surface of the finger with the blunt end of an applicator or tongue depressor. If it is located at the proximal end of the tendon sheath of the index, middle, or ring finger, involvement of the sheath is certain. If there is no localization, the sheath may have ruptured.

Painfully swollen palm—infection of the ulnar bursa

There is dorsal edema and fullness on the ulnar side of the palm (Fig. 13-39A). The point of maximum tenderness is halfway between the lunate and the fifth MCP joint.

Painfully swollen palm—infection of the radial bursa

The interphalangeal joint of the thumb is flexed and passive extension produces pain. There is tenderness and swelling over the sheath of the flexor pollicis longus.

Painfully swollen palm—metacarpal fracture

In a transverse fracture, the fragments of the metacarpal bone are bowed into the palm to produce a painful prominence (Fig. 13-39B). The prominence may be obscured by soft-tissue swelling, but dorsal palpation will localize tenderness at the fracture site. In a spiral fracture, proximal slippage of the distal fragment produces shortening revealed by loss of prominence in the corresponding knuckle when the fist is closed. Rotation of the distal fragment is present if the affected finger is not aligned with the unaffected fingers when the tips are flexed onto the base of the thenar eminence. Bennett fracture is an oblique break through the base of the first metacarpal, frequently with subluxation of the carpal-metacarpal joint. The thumb is semiflexed, and it cannot be opposed to the ring or little finger and the fist cannot be clenched.

Painful swelling in the anatomic snuffbox—tenosynovitis

Inflammation in the tendon sheaths of the extensor pollicis longus and brevis as they pass under a fibrous band near the radial styloid causes pain and tenderness. Pain is felt in the region of the snuffbox. The patient has pain with pinching, thumb extension and ulnar deviation of the wrist. When the fist is clenched over the flexed thumb, gentle but firm ulnar deviation of the hand by the examiner elicits pain at the radial styloid process, Finkelstein test (Fig. 13-40B). This pain may be transmitted down the thumb or toward the elbow. Passive extension of the thumb is painless. Crepitus may be felt or auscultated over the tendon sheath during thumb flexion–extension.

Acute tenosynovitis

A sausage-like swelling approximately 4 cm long (Fig. 13-40C), involves the tendon sheaths at the radial border of the snuffbox. The cause is usually trauma, although inflammation can be produced by gout, pseudogout, or gonococcal infection.

Chronic stenosing tenosynovitis—de Quervain tenosynovitis

The symptoms are similar to the acute process and are frequently chronic and recurrent, exacerbated by repetitive movements of the wrist and thumb. Chronic inflammation involves all layers of the tendon sheath.

Forearm pain and weakness—flexor compartment syndrome and Volkmann ischemic contracture

See compartment syndrome). Volkmann contracture, the fibrosis and shortening of the muscles, is a late finding. Passive extension of the fingers produces pain in the forearm. The fingers may be cyanotic and are often edematous. The radial pulse is absent, the skin over the hands is cool, and median nerve sensation is diminished. Emergent surgical consultation is required. In Volkmann contracture, the fingers are fixed in flexion by shortening of the fibrotic bellies of the digital flexors in the forearm. Because the flexor tendons are free to move in their sheaths, slight extension of the fingers is permitted when the wrist is held in flexion. This distinguishes it from adhesions of flexor tendons to their sheaths. Precipitating events are forearm and supracondylar fractures and circumferential bandages or casts applied shortly after trauma.

Elbow pain—lateral and medial epicondylitis, tennis elbow

Repetitive forceful wrist and/or finger flexion and extension focus tension on the common proximal tendon insertions at the lateral (extensors) and medial (flexors) humeral epicondyles. Lateral Epicondylitis causes pain in the lateral aspect of the elbow, accentuated by use of the hand during a power grip (when the wrist extensors are also contracting), as in lifting objects. Palpation discloses tenderness over the lateral epicondyle and 1 cm distally. Having the patient hold the long finger in full extension against resistance reliably reproduces the pain. In the Cozen test (resisted wrist extension), the patient is asked to keep the fist clenched while extending the wrist against resistance reproducing the patient’s lateral epicondylar pain. In the Mill maneuver, have the elbow held in extension with the wrist flexed; when you pronate the forearm against the patient’s resistance, epicondylar pain is elicited. Medial Epicondylitis is less common. The pain is located just distal to the medial epicondyle in the flexor tendons and is reproduced by maneuvers requiring wrist and finger flexion or arm pronation against resistance.

Pain in the upper arm—bicipital tenosynovitis

Inflammation in the tendon sheath of the biceps where it emerges anteriorly from the capsule of the shoulder joint is usually the result of overuse. Pain is located near the insertion of the pectoralis major on the humerus and may shoot down the arm. Shoulder motions are somewhat limited, especially flexion of the arm. Palpation of the bicipital groove reproduces the pain. Yergason Sign: With the elbow flexed to 90 degrees and the forearm pronated, ask the patient to supinate against resistance; pain in the anteromedial aspect of the shoulder is a positive test.

Pain in the shoulder—coracoiditis

Repeated acute or chronic arm work produces inflammation at the origin of the short head of the biceps and the coracobrachialis muscles on the tip of the coracoid process. There is a history of trauma with pain and tenderness at the tip of the coracoid process. The pain is reproduced by adduction and external rotation of the humerus, or having the patient perform against resistance either supination of the forearm with the elbow flexed, forward flexion of the shoulder, or adduction of the flexed shoulder.

Painful arc and impingement sign—rotator cuff injury

During arm abduction the supraspinatus tendon and its insertion on the proximal greater humeral tuberosity must pass beneath the acromion. The subacromial bursa is positioned to decrease the friction, or impingement, which occurs with this motion. Repetitive forceful motion causes mechanical irritation to the tissues eliciting inflammation of the tendon and bursa. Sudden or severe loading of the shoulder may result in incomplete or complete tears of the tendon. Three conditions present with similar signs and symptoms. A history of sudden onset favors partial tear of the tendon, whereas repetitive shoulder motion and subacute or chronic symptoms favor tendonitis or bursitis. All have painful abduction between 60 and 120 degrees, often prohibiting full active range of motion. Less painful passive range of motion is preserved (Fig. 13-41). Precise distinction between the three is not possible with physical examination. Partial Rupture of the Supraspinatus Tendon. When the tendon is only incompletely torn, the rotator cuff is intact. Pain is referred to the humeral insertion of the deltoid muscle, but there is no tenderness at that point. Sometimes the pain extends down the arm to the elbow or beyond. Tenderness is elicited just beneath the acromial tip or in the notch between greater and lesser humeral tubercles. DDX: If weakness of the supraspinatus, weak external rotation and impingement signs are all present, a rotator cuff tear is likely [Murrell GA, Walton JR. Diagnosis of rotator cuff tears. Lancet. 2001;357:769–770]. Acute Supraspinatus Tendinitis: This usually occurs in a person 25 to 45 years of age, with a dull ache developing in the shoulder without antecedent trauma. The pain steadily worsens and may be excruciating. The diagnostic test is abduction to 90 degrees and then full internal rotation, which reproduces pain. Tenderness is pronounced beneath the acromial tip. Chronic Supraspinatus Tendinitis: Dull shoulder pain develops in a patient who is usually between 45 and 60 years old and without preceding trauma. Abduction is painless to 60 degrees, where the patient feels a jerk with pain in the region of the deltoid muscle. Pronounced tenderness can be elicited in the notch between the greater and lesser tubercles of the humeral head or beneath the acromial tip. Crepitus may also be present. Lying on the shoulder produces pain that prevents sleeping on the affected side for months. Subacromial Bursitis: This can be acute or chronic and often accompanies supraspinatus tendonitis. The pain is constant and aggravated by elevation in abduction. There is often a history of heavy arm use.

Minimal arm elevation—complete rupture of the supraspinatus tendon, torn rotator cuff

The supraspinatus muscle initiates arm abduction from 0 to 45 degrees, where the deltoid engages. Inability to initiate elevation in 90° abduction indicates rupture of the supraspinatus tendon. This usually occurs after age 40. The patient cannot elevate the arm against minimal resistance at 30 degrees elevation and 90 degrees abduction, but passive motion is free and painless. Initial shoulder motion is mostly with the scapula. There is resistance to external rotation when the arm is held at the side with elbow flexed. As the arm is moved forward, one may palpate a jerk, fine crepitus, or an indentation in the subacromial region between the greater and lesser humeral tubercles (Fig. 13-18D). Wasting of the supraspinatus and infraspinatus occurs after 3 weeks.

Adhesive capsulitis—frozen shoulder

Chronic inflammation of the rotator cuff and joint capsule leads to shortening of the usually loose tendinous cuff and to progressive loss of motion. All types of arthritis may involve the shoulder. In the early stages of inflammatory processes, motions are inhibited by pain; later, adhesions restrict motion. This often follows unresolved subacromial bursitis or supraspinatus tendinitis. At onset, pain is that of the original injury. Progressive limitation of motion ensues until capsular contraction and fibrosis abate the pain with associated muscle wasting. Osteoarthritis may be associated with crepitus in the joint, but effusions are relatively rare. Over time, there is progressive loss of glenohumeral motion. With chronically limited motion, generalized muscle wasting occurs. Joint effusion suggests rheumatoid arthritis, crystal arthritis, or less-common disorders such as villonodular synovitis.

Conditions of the entire upper limb

Flail arm

Lower motor neuron or peripheral nerve injuries produce muscular denervation with flaccid paralysis and muscle wasting. After injuries to the brachial plexus or poliomyelitis, the arm may hang limply at the side with the flexed palm facing backward (Fig. 13-32B).

Spastic arm

Injury to upper motor neurons leads to uninhibited muscular contraction with the antigravity flexors overpowering the weaker extensors. With hemiplegia, the arm is carried with flexion of the elbow, wrist, and fingers (Fig. 13-32C).

Lower extremity syndromes

Painless limp—osteonecrosis, aseptic hip necrosis

Ischemia of the femoral head leads to bone necrosis with collapse and mushrooming of the femoral head. It may be unilateral or bilateral. Although the cause may be unknown, use of corticosteroids, diabetes, obesity, and alcohol are each associated with an increased risk. Osteonecrosis of the epiphysis in childhood (Legg–Calvé–Perthes disease) is relatively painless, whereas osteonecrosis in adults may be painful. Usually it begins with a painless limp and all motions of the hip are slightly impaired. Later, there is severe limitation of abduction and rotation. Muscle wasting and shortening of the limb are common. The Trendelenburg gait suggests hip dislocation.

Painful hip—septic arthritis

Usually, there is groin pain, fever, leukocytosis, and prostration. The thigh may be held in slight abduction and lateral rotation to best accommodate the joint effusion. All motion of the hip is painful. Rarely, fluctuation can be felt in the joint. Because pain may be referred only to the knee, knee pain should always prompt examination of the hip. Early diagnosis is urgent because the joint cartilage may be irreparably damaged in a few hours without proper drainage and antibiotics. Tuberculous arthritis is more insidious, often presenting with a limp and pain only after exertion.

Painful hip—slipped capital femoral epiphysis

The femoral head dislocates on the femoral neck at the relatively weak growth plate during rapid growth in adolescence. Patients walk with a limp accompanied by pain. The distinguishing feature is painful limitation of internal rotation when thigh and knee are both flexed. This may be succeeded by shortening and outward rotation from anterosuperior displacement of the femoral neck.

Painful hip—torn labrum

A tear in the acetabular labrum occurs because of trauma. Patients are usually young men with persistent hip pain without limitation of motion. There may be no history of specific injury, or only of injury thought to be minor at the time. Instability of the hip is increased. DDX: Hip impingement syndrome is being recognized more frequently and should be considered in the differential diagnosis.

Painful hip—osteoarthritis

Boring pain in the groin and buttocks, sometimes with referral to the knee is frequent. Initially, stiffness on arising disappears with exercise, but later walking is limited by pain. The thigh is held in adduction. Passive motion is restricted in internal rotation and abduction and may be painful. Palpable and audible crepitus may be present.

Painful hip and limping—chronic hip dislocation

Dislocation of the hip may be congenital or acquired. Weakness of the supporting muscles (from nerve or muscle injury), joint infections, and trauma lead to dislocation in adults. Prosthetic hips are especially susceptible to dislocation with flexion and external rotation. For congenital hip dislocation, consult pediatric texts. In adults, Trendelenburg gait (Thigh and leg girth) is present. With the patient supine and the hips and knees flexed, the knee of the affected leg will be lower when observed from the foot of the bed. Inspect the buttocks with the patient standing on one leg at a time; normally, the pelvis tilts upwards on the nonweightbearing side (Fig. 13-33A). In the Trendelenburg sign, when standing on the affected leg, the pelvis tilts downwards on the nonweightbearing side because the muscles are not strong enough to support the pelvis when the femur is not engaged in the acetabulum. The sign is also positive with disease of the glutei, fracture of the femoral head, and in severe degrees of coxa vara. In adults, there is hip pain and premature OA of the affected joint.

Medial knee pain—anserine bursitis

The anserine bursa lies superficial to the tibial collateral ligament and deep to the pes anserina (goose foot) formed by the tendons of the sartorius, gracilis, and semitendinosus (Fig. 13-34). The patient complains of pain in the anterior medial aspect of the knee 2 to 3 cm distal to the joint line. Pain is aggravated by walking; especially while climbing stairs. Tenderness, usually without swelling, is palpated on the medial aspect of the knee.

Anterior knee pain—chondromalacia patellae

Degeneration of the articular surface of the patella occurs from unknown cause. It is more common in women than men. Pain is felt anteriorly and is aggravated by prolonged sitting and walking down stairs. A small effusion may be present. Passive joint motion is painless. Rocking the patella in the femoral groove frequently elicits pain, often with palpable crepitation.

Anterior knee pain—quadriceps and patellar tendonitis

Pain is felt in the anterior knee either above (quadriceps) or below (patellar) the patella. It occurs following an unusual level of activity such as running, lifting, climbing, up and down squatting); it may occur as a result of chronic overuse. Pain is well localized to the involved tendon and reproduced by direct pressure and resisted knee extension.

Anterior knee pain after exercise—osteochondritis of tibial tubercle (Osgood–Schlatter disease)

Before closure of the epiphysis of the tibial tubercle during adolescence, vigorous exercise produces chronic traction injury with partial avulsion of the tubercle. Pain occurs after exercise and a tender, hard swelling is seen and felt at the attachment of the patellar tendon.

Tibial pain after exercise—stress fracture of the tibia

An incomplete cortical fracture of the tibia results from repeated strenuous use of the leg. Dull aching pain begins gradually with progressively shortening intervals after exercise and persists for hours. There is localized tenderness over the tibia, frequently along the medial border. Pain at the fracture site may be elicited by springing the tibia: with the patient supine, place one hand on the knee and the other on the heel; pull the tibia laterally against your knee as a fulcrum.

Exertional calf pain—intermittent claudication

See Chapter 8.

Anterior leg pain after exercise—tibial compartment syndrome

See Compartment syndrome. Several hours after unusually strenuous leg exercise, stiffness followed by severe pain occurs in the anterior tibial muscular compartment. The region becomes swollen, tense, tender, and warm. Ischemic necrosis of the muscles may occur if the pressure is not relieved by fasciotomy.

Foot pain—tarsal tunnel syndrome

The tarsal tunnel is behind and inferior to the medial malleolus of the tibia. Its bony floor is roofed by the flexor retinaculum extending from the medial malleolus to the calcaneus. Through the tunnel pass several tendons and the posterior tibial nerve, which divides into the calcaneal nerve to the skin of the heel, the medial plantar nerve to the skin and muscles of the medial aspect of the sole, and the lateral plantar nerve to the lateral portion of the sole. Compression of the nerves in the tunnel causes numbness, burning pain, or paresthesias in portions of the sole. Paresis or paralysis of some small muscles of the foot may occur. Occasionally, a tender area is palpated at the posterior margin of the medial malleolus. The diagnosis is confirmed by nerve conduction studies. Precipitating conditions include fracture or dislocation of the bones near the tunnel, traumatic edema, tenosynovitis, chronic stasis of the posterior tibial vein and foot strain.

Forefoot pain—metatarsalgia

Loss of the normal transverse metatarsal arch from the first to the fifth metatarsal heads leads to abnormal weight bearing on the second to fourth metatarsal heads, which are insufficiently cushioned. Ask the patient to point to the site of the pain. Pain occurs in the region of the distal metatarsal heads. Examination may show callus under the second to fourth metatarsals and decreased callus under the first and fifth. Pressure on the callus reproduces the pain. Symmetrical bilateral metatarsalgia may be an early symptom of RA. Fibroneuroma gives similar pain, so squeeze the foot transversely to see if the pain is reproduced.

Forefoot pain—metatarsal stress fracture

Excessive walking or standing may cause a stress fracture of the metatarsal shaft (Fig. 13-36C). Pain develops gradually. Muscle cramps and slight swelling may occur. Motion of the corresponding toe is painful. Pain is usually localized several centimeters proximal to the metatarsal head.

Forefoot pain—infection in the interdigital space

Puncture of the sole may cause infection in one of the four interdigital subcutaneous spaces. The abscess may point between two metatarsals causing swelling on the dorsum of the foot. Walking produces pain between the metatarsals. Tenderness is localized to the interdigital space.

Chronic painless enlargement of the legs

Several causes must be distinguished. Although some evidence of obesity is present elsewhere in the body, adipose tissue about the ankles may be disproportionately great, while the feet are spared. The tissue has the consistency of fat, and pitting edema is absent. Chronic deep venous obstruction usually is preceded by a history suggesting thrombophlebitis. The venous deficit may produce pain in the legs. Some pitting edema is usually present, although it may be obscured by thickening of the skin from chronic inflammation (dermatoliposclerosis). The skin is stained with hemosiderin and may be cyanotic. Superficial veins may be dilated. Postphlebitic syndrome results from previous occlusion of the deep veins either without recanalization or resulting in destruction of the valves with persistent venous incompetence. One-third of patients with acute deep vein thrombosis will develop postphlebitic syndrome (Post-phlebitic syndrome). The leg is persistently enlarged, usually with pitting edema. Sensations of fullness and pain occur with prolonged sitting or standing and chronic stasis changes are common. Early treatment decreases long-term disability. Varicose veins are readily recognized when they are associated with edema. Chronic edema from any cause leads to subcutaneous and cutaneous fibrosis with woody induration that does not pit (dermatoliposclerosis). Lymphedema causes firm, uniform, nonpitting swelling which extends to the feet, without venous engorgement or cyanosis.

Muscle Syndromes

Fibromyalgia

See Tender Points,. Fibromyalgia is at the extreme end of an ill-defined group of disorders variously described as polysomatic distress or functional somatic disorders [Barsky AJ, Borus JF. Functional somatic syndromes. Ann Intern Med. 1999;130:910–921]. It is characterized by chronic widespread pain (CWP) involving both sides of the body above and below the waist, and the axial skeleton. The pain is described as diffuse aching and is accompanied by stiffness, nonrestorative sleep, and fatigue, and must have been present for at least 3 months and not explained by another disorder. Fibromyalgia is more common in women than men. The 1990 American College of Rheumatology (ACR) diagnostic criteria included at least 11 of 18 paired, bilateral tender points elicited on physical examination (Fig. 13-42). In 2010 new ACR criteria were proposed that eliminated the tender points. The new criteria are based on a Symptom Severity (SS) scale and the Widespread Pain Index (WPI) [Wolfe F, Hauser W. Fibromyalgia diagnosis and diagnostic criteria. Ann Med. 2011;43:495–502]. Each specific symptom (fatigue, waking unrefreshed, and cognitive symptoms) and the widespread somatic symptoms are each scored 0 to 3. The WPI and SS are combined to form a polysymptomatic distress scale that is continuous rather than dichotomous. Worksheets and supportive materials can be obtained at www.arthritis-research.org/research/fibromyalgia-criteria.

Myofascial pain syndrome

Afferent signals from the trigger areas are believed to remodel spinal and possibly thalamic pain pathways to cause reflex muscle spasm and diminished blood flow, which, in turn, increase the sensitivity of the trigger area. See Trigger Points. Chronic recurrent pain occurs roughly in the distribution of one or more muscles and their distribution of referred pain. The pain may be lancinating, aching, boring, or a feeling of muscular stiffness. Often, the patient relates the onset to some specific trauma or activity. The distinguishing feature is the presence of one or more trigger points, with or without palpable muscle spasm. The examiner should palpate the entire region carefully with firm pressure of the fingertips. Often, the trigger point is discovered some distance from the referred pain area. The diagnosis is confirmed when the pain is relieved by injection of the primary trigger point with a local anesthetic.

Polymyalgia rheumatica

This inflammatory disease of unknown origin is characterized by pain in proximal muscle groups, with inflammation demonstrable by MRI in the shoulder girdle tendon sheaths and bursae, and less commonly the shoulder joint itself. It usually occurs after the sixth decade and is most common in women. Pronounced morning stiffness of the neck, shoulder, and upper back muscles usually begins gradually. Some patients have sudden onset and can note the day and time of their first symptoms. Muscles of the low back, pelvic girdle, and thighs are less prominently involved and/or may develop later. It is common in patients with temporal arteritis, but only 15% of patients presenting with PMR develop temporal arteritis. Although spontaneously painful, the muscles are seldom very tender, trigger points are not characteristic, and the stiffness is improved by activity. The erythrocyte sedimentation rate is usually markedly elevated; symptoms are promptly relieved by low-dose corticosteroids.

Compartment syndrome

Edema, hemorrhage, and inflammation from injury to muscle enclosed within a constricting fascial compartment lead to increasing pressure within the compartment sufficient to occlude venous drainage further increasing swelling. Eventually the pressure exceeds arteriolar pressure and ischemic necrosis supervenes. A high index of suspicion is required to recognize this before irreversible muscle injury with contractures occurs. The patient complains of severe pain often disproportionate to apparent injury. The onset of ischemia is indicated by the five P’s: Pain, Puffiness, Pallor, Pulselessness, and Paralysis. Palpation of the affected compartment reveals tense distention of the fascia with severe pain. If major arteries or nerves pass through the compartment, distal pulses may be diminished and sensation impaired. Without relief of pressure, muscle necrosis leads to fibrosis, shortening, and loss of function. Diagnosis is made by measuring compartment pressure; treatment is surgical fasciotomy.

Trichinosis

Heavy infection with Trichinella spiralis after ingestion of incompletely cooked infected meat (pork, bear meat) may cause severe and, infrequently, death. The organisms localize in muscle. One to four days after ingestion, the patient complains of nausea and vomiting, diarrhea, and abdominal pain. Within 10 days, there are fever, dyspnea, anorexia, myalgia, and asthenia. Physical findings include periorbital edema, scarlatiniform rash, splinter hemorrhages under nails, tremors, and involuntary movements.

STOP: Fractures are discussed in this section only for the purpose of illustrating relatively common physical findings. This text should not be used as a guide for the definitive diagnosis of traumatic musculoskeletal injuries. Orthopedic texts should be consulted for details, differential diagnosis, and as a guide to diagnosis and management.

• Fat embolism. After trauma to large bones, and especially after fractures, fat globules embolize via the veins to the lungs, brain, and other tissues. The pathogenesis remains controversial. The onset of fat embolism is sudden, with restlessness and vague pain in the chest. Symptoms reach a maximum in approximately 48 hours. Dyspnea and cyanosis are common and purulent sputum occasionally containing diagnostic fat droplets may be produced. Fever occurs with a disproportionately high pulse rate. Cerebral symptoms and signs are extremely variable; delirium and coma indicate a grave prognosis. Fat droplets may be seen in retinal or conjunctival vessels. On the second or third day, petechiae may appear over the shoulders and chest as well as in the conjunctivae and retinae. Fat embolism should be considered in acutely ill patients with trauma to long bones or skull, insertion of prosthetic joints, chronic alcoholism, diabetes mellitus, and sickle cell disease.

Traumatic neck pain

STOP: Following trauma or suspected cervical injury, the cervical spine must ALWAYS be immediately IMMOBILIZED in a rigid collar PRIOR TO ANY MOVEMENT or examination of the patient.

• Fracture of the atlas (C1) or the odontoid process (C2). Disruption of the ring of bone and ligament restraining the odontoid process or fracture at the base of the odontoid produces instability of C1 on C2 leading to compression of the cervical spinal cord. If immediate death does not result, the patient supports his head with his hands; he is unwilling to nod his head. There is severe occipital headache. The patient cannot rotate the head. If the clinical diagnosis is not made immediately and the neck completely immobilized, sudden death may ensue. In RA, pannus may erode the transverse ligament of C1 that supports the posterior odontoid leading to C1–C2 instability with trivial trauma. A high index of suspicion is required to make the diagnosis.

Flexion fracture of the neck

The C5 vertebral body is most frequently fractured when there is forceful hyperflexion of the neck, for example, when a diver strikes his head on the bottom. The patient who escapes immediate death or quadriplegia may be unable to walk without supporting his head with his hands. Pain restricts all motions of the neck. The spinous process of the affected vertebra is tender and may be somewhat prominent.

Partial dislocation from hyperextension

A fall or blow on the forehead may hyperextend the neck and rupture the anterior longitudinal ligament. There is intense pain in the neck. One spinous process may seem more prominent. Paraplegia frequently occurs.

Whiplash cervical injury

Sudden, forceful hyperextension of the neck with flexion recoil commonly occurs to a passenger in an automobile that is struck from behind (Fig. 13-43). Posterior neck pain develops slowly over hours or days. Nerve-root irritation produces spasm of the neck muscles and torticollis. Occipital headache develops, sometimes with blurring of vision. The chin is turned toward the painful side of the neck. Palpation over the lower cervical spinous processes elicits tenderness. An effusion with soft crepitus can sometimes be felt over the lowest part of the ligamentum nuchae. The biceps reflex may be diminished or absent on one or both sides. Occasionally, the pupil is dilated on the affected side.

Fracture of a spinous process

The long, thin, spinous process of vertebrae near the cervicothoracic junction breaks readily from a direct blow or from violent muscular contraction, such as raising a heavy load with a shovel. Sudden, severe pain extends from the neck to the shoulder, accentuated by flexion and rotation of the neck. Tenderness is exquisite over the fracture site. Sometimes the fractured process is mobile laterally and crepitus can be felt.

Traumatic mid-back pain

Traumatic back pain—stable vertebral compression fracture with intact spinal ligaments

The thoracic or lumbar vertebrae are fractured by trauma that crushes their bodies, such as forceful hyperflexion of the spine, falling and landing on the feet or buttocks, or a downward blow on the shoulders (Fig. 13-26C). Pain and tenderness at the fracture site may be mild or even absent for weeks, so fracture may not be suspected until a radiograph is obtained. Occasionally, slight kyphosis is present.

Traumatic back pain—unstable vertebral compression fracture with torn spinal ligaments

Rupture of the interspinal and supraspinal ligaments, accompanying the compression fracture, permits the articular facets of two adjacent vertebrae to slide apart; on recoil, they may interlock (Fig. 13-26E). This dangerous condition may be suggested clinically by palpating a gap between two spinous processes (Fig. 13-26D).

Traumatic back pain—dislocation of vertebrae

Violent hyperflexion of the spine, in addition to fracturing the vertebrae, may tear the supporting ligaments, permitting vertebral dislocation and consequent damage to the spinal cord. This is a potentially unstable condition requiring immediate immobilization and evaluation. This should be suspected when the palpating finger finds a gap between two spinous processes.

Fracture of a transverse process

The transverse process of a vertebra, usually lumbar, is fractured from violent contraction of the attached muscles. There is severe pain in the lumbar region, with intense muscle spasm. The spinous processes are not tender. If caused by a direct blow, look for blood in the urine to identify a concomitant kidney injury.

Traumatic wrist, arm, and shoulder pain

Wrist silver-fork deformity—Colles fracture

The most common cause is a fall on the outstretched hand. The radius is fractured within 2.5 cm of its distal end (Fig. 13-44A). Fracture of the ulnar styloid process occurs in half the cases. When the pronated arm is laid on the table, its profile resembles a dinner fork lying horizontally with the tines pointing downward, so the base of the tines forms an upward curve. The corresponding hump in the fractured arm occurs from dorsal displacement of the distal radial fragment.

Wrist reversed silver-fork deformity—Smith fracture, reversed Colles fracture

Like the Colles fracture, this is a break of the distal end of the radius, but the distal fragment is displaced volarward, making a deformity somewhat resembling the silver fork with its tines pointing upward (Fig. 13-44B). The fracture usually results from a blow or fall on the hyperflexed hand.

Pain and tenderness in the forearm—radial and ulnar fractures

In fractures of the ulnar shaft, the bone is well splinted by the radius, so displacement and deformity are rare (Fig. 13-44D). The only physical signs are localized tenderness and swelling. Ulnar fractures accompanied by volar dislocation of the radial head (Monteggia fracture/dislocation), especially common in children, permit considerable bowing of the fractured ulna. A fractured radial shaft presents variable degrees of bowing, especially with concomitant dislocation of the lower radioulnar joint.

Painful angular forearm deformity—fractures of both forearm bones

Greenstick fractures produce little deformity, but complete fractures of the radius and ulna present easily recognizable deformity.

Traumatic elbow pain—fracture of the ulnar coronoid process

Fracture of the ulnar coronoid process, which forms the distal elbow joint, is easily missed if not considered and searched for.

Traumatic elbow pain—fracture of the olecranon process

Pronounced swelling results, particularly around the dorsum of the elbow. The olecranon process is tender. When the fracture is complete, the patient cannot extend the flexed forearm (Fig. 13-45A). The bony equilateral triangle may be flattened.

Traumatic elbow pain—subluxation of the radial head

This usually occurs in childhood (the “pulled elbow”). There is no elbow deformity and tenderness is maximal at the radial head. Flexion–extension is painful; pronation and supination are not.

Traumatic elbow pain—radial head fracture

Usually this results from a fall on the outstretched hand. Swelling is minimal and there is no deformity; the bony equilateral triangle is normal. Flexion and extension are painless, but there is severe restriction of pronation-supination and the radial head is tender.

Traumatic painful shoulder immobility—fracture of the humeral shaft

These are painful injuries, and the arm is useless, being held in the opposite hand. Transverse fracture is usually caused by a direct blow and there is unmistakable deformity. Spiral fracture, commonly from a fall on the hand, may not cause deformity. Lacking deformity, gently palpate the lateral and medial aspects of the humerus for local tenderness and swelling. Shaft fractures can lacerate the radial nerve and distal brachial artery where they are in contact with the posterior upper third of the humerus. In all cases of fractured humerus, feel the radial arterial pulse and test for radial nerve injury. Test the motor function of the nerve by having the patient flex the elbow with the forearm pronated and look for wrist-drop. Anesthesia on the radial dorsum of the hand is evidence of sensory loss of the radial nerve.

Traumatic painful shoulder immobility—shoulder dislocation

When the hand or arm are forcefully abducted and externally rotated, the humeral head dislocates out of the glenoid tearing through the anterior rotator cuff. The humeral head is usually displaced anteriorly and medially to lie under the coracoid process (Fig. 13-46A). The shoulder profile in anterior dislocations is flattened and the bony triangle is disrupted. The humeral head can be palpated medially in the normally soft belly of the deltoid. With the ruler test of Hamilton, a straight edge can rest simultaneously on the acromial tip and the lateral epicondyle of the elbow; normally, the humeral head intervenes. The test is also positive in fracture of the humeral neck. The Calloway test, useful in obese patients, consists of measuring the girth of the two shoulder joints. A tape measure is looped through the axilla and the girth measured at the acromial tip; the girth of the affected joint is increased. In the Dugas test, the patient cannot adduct the arm sufficiently to place the hand on the opposite shoulder. Posterior dislocations are rare. The humeral head is felt posteriorly under the spine of the scapula near the base of the acromial process. A common cause of this uncommon dislocation is a major motor seizure. Shoulder dislocation can be identified by a scapular Y-view X-ray without manipulation of the shoulder. Dislocation of the humeral head can damage adjacent structures including the labrum of the glenoid and the axillary nerve (causing paralysis and later wasting of the deltoid). Palpate the pulses of the arm to detect compression of the axillary vessels.