Musculoskeletal Disorders

Musculoskeletal Disorders


A complex system of bones, muscles, ligaments, tendons, and other connective tissue, the musculoskeletal system gives the body its form and shape. It also protects vital organs, makes movement possible, stores calcium and other minerals, and provides sites for hematopoiesis. A fibrous layer called the periosteum covers all bones, except at joints, where they’re covered by articular cartilage.

The human skeleton contains 206 bones, which are composed of inorganic salts, such as calcium and phosphate, embedded in a framework of collagen fibers. Bones are classified by shape as long, short, flat, or irregular.


Long bones, which are found in the limbs, include the humerus, radius, and ulna of the arm; the femur, tibia, and fibula of the leg; and the phalanges, metacarpals, and metatarsals in the hands and feet. These bones have a long shaft, or diaphysis, and widened, bulbous ends, called epiphyses. A long bone is made up mainly of compact bone, which surrounds the medullary cavity (also called the yellow marrow), a storage site for fat. The lining of the medullary cavity (the endosteum) is a thin layer of connective tissue. The outer layer is the periosteum. (See Long-bone structure, page 296.)

In children and young adults, lengthwise growth occurs at the epiphyseal cartilage between the diaphysis and epiphysis. In adults, in whom bone growth is complete, this cartilage is ossified and forms the epiphyseal line. The epiphysis also has a surface layer made up of compact bone, but its center is made of spongy or cancellous bone. Cancellous bone contains open spaces between thin threads of bone, called trabeculae, which are arranged in various directions to correspond with the lines of maximum stress or pressure. This configuration gives the bone added structural strength.

Unlike cancellous bone, adult compact bone consists of numerous orderly networks of interconnecting canals that run parallel to the bone’s long axis. Each of these networks, called a haversian system, consists of a central haversian canal surrounded by layers (lamellae) of bone. Between adjacent lamellae are small openings (lacunae), which contain bone cells (osteocytes). All lacunae are joined by an interconnecting network of tiny canals (canaliculi), each of which contains one or more capillaries and provides a route for movement of tissue fluids. The haversian system carries blood to the bone through blood vessels that enter the system through channels called Volkmann’s canals.


Short bones include the tarsal and carpal bones; flat bones, the frontal and parietal bones of the cranium, ribs, sternum, scapulae, ilium, and pubis; and irregular bones, the bones of the spine (vertebrae, sacrum, and coccyx) and certain bones of the skull (sphenoid, ethmoid, and mandible).

Short, flat, and irregular bones have an outer layer of compact bone and an inner portion of spongy bone. In the sternum and certain areas in the flat bones of the skull, the spongy bone contains red marrow.


The tissues connecting two bones make up a joint, which permits motion between the bones and provides stability. Joints, like bones, have varying forms.

  • Fibrous joints (synarthroses) have only minute motion and provide stability when tight union is necessary, as in the seams, called sutures, that join the cranial bones.

  • Cartilaginous joints (amphiarthroses) have limited motion, as between vertebrae and symphysis pubis.

  • Synovial joints (diarthroses) are the most common and have the greatest degree of movement. Such joints include the elbows, shoulders, and knees. Synovial joints have special characteristics: the articulating surfaces of each bone have a smooth hyaline covering (articular cartilage), which is resilient to pressure; their opposing surfaces are congruous and glide smoothly on each other without touching each other; a fibrous (articular) capsule holds them together. Beneath the capsule and lining the joint cavity, the synovial membrane secretes the clear, viscous synovial fluid. This fluid lubricates the two opposing surfaces during motion and also nourishes the articular cartilage. Surrounding a synovial joint are ligaments, muscles, and tendons, which strengthen and stabilize the joint but allow free movement.

In some synovial joints, the synovial membrane forms two additional structures—bursae and tendon sheaths—which reduce friction that normally accompanies movement. Bursae are small, cushionlike sacs lined with synovial membranes and filled with synovial fluid; most are located between tendons and bones. Tendon sheaths wrap around the tendon and cushion it as it crosses the joint.

The synovial joints permit angular and circular movements. Angular movements include flexion (decrease in joint angle), extension (increase in the joint angle), and hyperextension (increase in the angle of extension beyond the usual arc). Joints of the knees, elbows, and phalanges permit such movement. Other angular movements are abduction (movement away from the body’s midline) and adduction (movement toward the body’s midline).

Circular movements include rotation (motion around a central axis), as in the ball-and-socket joints of the hips and shoulders; pronation (wrist motion to place palmar surface of the hand down, with the thumb toward the body); supination (begging position, with palm up). Other kinds of movement are inversion (movement facing inward), eversion (movement facing outward), protraction (as in forward motion of the mandible), and retraction (returning protracted part into place).


Muscle tissues’ most specialized feature— contractility— makes movement of bones and joints possible. Muscles also pump blood through the body, move food through the intestines, and make breathing possible. Muscular activity produces heat, so it’s an important component in temperature regulation. Muscles maintain body positions, such as sitting and
standing. Muscle mass accounts for about 40% of the body weight of a person of average size.

Muscles are classified in many ways. Skeletal muscles are attached to bone, visceral muscles permit function of internal organs, and cardiac muscles make up the heart wall. Also, muscles may be striated or nonstriated (smooth), depending on their cellular configuration.

Muscles classified according to activity are called voluntary or involuntary. Voluntary muscles can be controlled at will and are under the influence of the somatic nervous system; these are the skeletal muscles. Involuntary muscles, controlled by the autonomic nervous system, include the cardiac and visceral muscles.

Each skeletal muscle consists of many elongated muscle cells, called muscle fibers, through which run slender threads of protein, called myofibrils. Muscle fibers are held together in bundles by sheaths of fibrous tissue, called fascia. Blood vessels and nerves pass through the fascia to reach the individual muscle fibers.

Skeletal muscles are attached to bone directly or indirectly by fibrous cords called tendons. The least movable end of the muscle attachment is called the point of origin; the most movable end is the point of insertion.


To stimulate muscle contraction and movement, the brain sends motor impulses through the peripheral motor nerves to motor nerve fibers in the voluntary muscle. These nerve fibers reach membranes of skeletal muscle cells at neuromuscular (myoneural) junctions. When an impulse reaches the myoneural junction, it triggers the following sequence: release of the neurochemical acetylcholine, transient release of calcium from the sarcoplasmic reticulum (a membranous network in the muscle fiber), and muscle contraction. The arriving impulse at the myoneural junction also triggers release of adenosine triphosphate, the energy source for muscle contraction. Muscle relaxation is believed to take place by reversal of the above mechanisms.


Most patients with musculoskeletal disorders are elderly, have concurrent medical conditions, or have experienced trauma. Younger patients tend to experience more benign, self-limited conditions. Generally, they face prolonged immobilization. These factors make thorough assessment essential. Your assessment should include a complete history and a careful physical examination to determine a possible cause of the symptoms.

Interview the patient carefully to obtain a complete medical, social, and personal history. Ask about general activity (does he jog daily, or is he sedentary?), which may be significantly altered by musculoskeletal disease or trauma. Does the patient have any systemic symptoms, such as fever, chills, weight loss, or skin rashes? Obtain information about occupation, diet, sexual activity, and elimination habits, drugs taken, and use of safety devices, and try to assess how the problem will affect body image. Also, ask how he functions at home. Can he perform activities of daily living? Does he have difficulty getting around? Are there stairs where he lives? Where are the bathroom and bedroom? Does he use any prosthetic devices? Ask if other family members can help with his care.

Get an accurate account of the musculoskeletal problem. Ask the patient if it has caused him to change his everyday routine. When did symptoms begin and how did they progress? Has the patient received treatment for this problem? If he’s experienced trauma, find out how he was hurt.

Assess the level of pain. Is the patient in pain at the moment? Ask what makes the discomfort worse or better (movement, position, and so forth). Evaluate past and present responses to treatment. For instance, if the patient has arthritis and uses corticosteroids, ask him about their effectiveness. Does he require more or less medication than before? Did he comply with the prescribed treatment?

The physical examination helps to determine the diagnosis and reveals any existing disabilities. (These baseline data will help when the effects of treatment are evaluated.) Observe the patient’s appearance. Look for localized edema, pigmentation, redness and tenderness at pressure points, and other deformities such as atrophy. Note mobility, strength, and gait. To check range of motion, ask the patient to abduct, adduct, or flex the muscles in question. Obtain height, weight, and vital signs. Check neurovascular status, including motion sensation and circulation. Measure and record discrepancies in muscle circumference or leg length. Compare one side or limb to the other. If a neck injury is suspected, don’t force range of motion.


  • X-rays are a useful diagnostic tool to evaluate musculoskeletal diseases. They can help to
    identify joint disruption, bone deformities, calcifications, and bone destruction and fractures. X-rays also measure bone density.

  • Myelography is an invasive procedure used to evaluate abnormalities of the spinal canal and cord. It entails injection of a radiopaque contrast medium into the subarachnoid space of the spine. Serial X-rays visualize the progress of the contrast medium as it passes through the subarachnoid space. Displacement of the medium indicates a space-occupying lesion, such as a herniated disk or a tumor.

  • Magnetic resonance imaging is useful in evaluating soft-tissue injuries or ligament tears, such as rotator cuff tears or meniscal tears.

  • Computed tomography scan can be used to identify injuries to bones, soft tissue, ligaments, tendons, and muscles.

  • Arthroscopy is the visual examination of the interior of a joint with a fiber-optic endoscope.

Other useful tests include bone and muscle biopsies, electromyography, microscopic examination of synovial fluid, and multiple laboratory studies of urine and blood to identify systemic abnormalities.


Each patient with musculoskeletal disease needs an individual care plan formulated early in his hospital stay by the entire clinical team, including the physician, physical therapist, and occupational therapist. Develop this plan with short- and long-term goals, during and after hospitalization.

Caring for the patient with a musculoskeletal disease usually includes at least one of the following: traction, casts, braces, splints, crutches, intermittent range-of-motion devices, prolonged immobilization, physical therapy, occupational therapy, and self-care measures; adequate vitamin D intake, weight loss, dietary modifications, and drugs.

Traction is the manual or mechanical application of a steady pulling force to reduce a fracture, minimize muscle spasms, or immobilize or align a joint.

  • Skin traction is the indirect application of traction to the skeletal system through skin and soft tissues.

  • Skeletal traction is the direct application of traction to bones by means of a pin (Steinmann pin) or wire (Kirschner wire) through the affected bone or by calipers or a tonglike device (Gardner-Wells tongs) that grips the bone.

  • Manual traction, for emergency use, is the direct application of traction to a body part by hand.

During the use of all types of traction:

  • Explain to the patient how traction works, and advise him about permissible amounts of activity and elevation of the head of the bed. Inform him of the anticipated duration of traction and whether or not the traction is removable. Teach active range-of-motion (ROM) exercises.

  • Check neurovascular status to prevent nerve damage. Also, make sure the mattress is firm, that the traction ropes aren’t frayed, that they’re on the center track of the pulley, and that traction weights are hanging free. Thoroughly investigate any complaint the patient makes.

  • Check for signs of infection (odor, local inflammation and drainage, or fever) at pin sites if the patient is in skeletal traction. Also, check with the physician’s or the facility’s procedure regarding pin-site care, such as use of peroxide or povidone-iodine.

Ideally, a cast immobilizes without adding too much weight. It’s snug-fitting but doesn’t constrict and has a smooth inner surface and smooth edges to prevent pressure or skin irritation. Casts require comprehensive patient education.

  • A plaster cast takes 24 to 48 hours to dry. To prevent indentations, tell the patient not to squeeze the cast with his fingers, not to cover or walk on the cast until it has dried, and not to bump a damp cast on hard surfaces because dents can cause pressure areas. Warn the patient that while the cast is drying, he’ll feel a temporary sensation of heat under the cast.

  • If fiberglass is used, the cast may feel dry and the patient may be able to bear weight immediately. Advise the patient, however, not to get the cast wet. Although the fiberglass won’t disintegrate as plaster would, the padding will become wet and potentially cause maceration of the skin.

  • Emphasize the need to keep the cast above heart level for 24 hours after its application to reduce swelling in the limb.

  • While the cast is drying and after drying is complete, the patient should watch for and immediately report persistent pain in the limb inside or distal to the cast as well as edema, changes in skin color, coldness, or tingling or numbness in this area. If any of these signs occur, tell the patient to position the casted body part above heart level and notify his physician.

  • The patient should also report drainage through the cast or an odor that may indicate infection. Warn against inserting foreign objects under the cast, getting it wet, pulling out its padding, or scratching inside it. Tell the patient to seek immediate attention for a broken cast.

  • Instruct the patient to exercise the joints above and below the cast to prevent stiffness and contracture.

Braces, splints, and slings also provide alignment, immobilization, and pain relief for musculoskeletal diseases. Slings and splints are usually used for short-term immobilization. Explain to the patient and his family why these appliances are necessary, and show them the proper way to apply the sling, splint, or brace for optimal benefit. Tell the patient how long the appliance will have to be worn, and advise him of any activity limitations that must be observed. If the patient has a brace, check with his orthotist (orthopedic appliance specialist) about proper care. Encourage the patient to refer additional questions to his physician. Teach proper crutch walking.


Immobilized patients require meticulous care to prevent complications. Without constant care, the bedridden patient becomes susceptible to pressure ulcers, caused by the increased pressure on tissue over bony prominences, and is especially vulnerable to cardiopulmonary complications.

  • To prevent pressure ulcers, turn the patient every 2 hours and, if possible, position him in a 30-degree side-lying position for short periods. In addition, place a flotation pad or sheepskin pad under bony prominences, or use an alternating-air-current, convoluted foam, or foam mattress. Show the patient how to use a Balkan frame with a trapeze to move about in bed.

  • Keep the patient’s skin dry and clean.

  • Keep the sheets wrinkle-free.

  • Increase fluid intake to minimize risk of renal calculi.

  • Provide adequate nutrition; a high-protein diet is preferred, if tolerated.

  • Perform passive ROM exercises on the affected side, as ordered, to prevent contractures, and instruct the patient in active ROM exercises on the unaffected side. Apply footboards or high-topped sneakers to prevent footdrop. Keep the patient’s heels off the bed to prevent heel breakdown. Also, watch for reddened elbows.

  • Because most bedridden patients involuntarily perform a Valsalva maneuver when using the upper arms and trunk to move, instruct the patient to exhale (instead of holding his breath) as he turns. This will prevent possible cardiac complications that result from increased intrathoracic pressure.

  • Emphasize the importance of coughing and deep breathing, and teach the patient how to use the incentive spirometer if ordered.

  • Because constipation is a common problem in bedridden patients, establish a bowel program (fluids, fiber, laxatives, stool softeners), as needed.


Restoring the patient to his former state of health isn’t always possible. When it isn’t, help the patient adjust to a modified lifestyle. During hospitalization, promote independence by letting him finish difficult tasks by himself. If necessary, refer the patient to a community facility for continued rehabilitation.



Clubfoot, or talipes, is the most common congenital disorder of the lower limbs. It’s marked primarily by a deformed talus and shortened Achilles tendon, which give the foot a characteristic clublike appearance. In talipes equinovarus, the foot points downward (equinus) and turns inward (varus), whereas the front of the foot curls toward the heel (forefoot adduction).


It is no longer believed that clubfoot is caused by fetal position in utero. Heredity is a definite factor in some cases, although the mechanism of transmission is undetermined. In children without a family history of clubfoot, this anomaly seems linked to arrested development during the 9th and 10th weeks of embryonic life, when the feet are formed. Researchers also suspect muscle abnormalities, leading to variations in length and tendon insertions, as possible causes of clubfoot. Environmental factors play a role. Studies strongly link clubfoot to cigarette smoking during pregnancy, especially if there is a family history of clubfoot.

Clubfoot, which has an incidence of about 1 per 1,000 live births, usually occurs bilaterally and is twice as common in boys. It may be associated with other birth defects, such as myelomeningocele, spina bifida, and arthrogryposis. However, most cases are sporadic occurrences.


Talipes equinovarus varies greatly in severity. Deformity may be so extreme that the toes
touch the inside of the ankle, or it may be only vaguely apparent. In every case, the talus is deformed, the Achilles tendon shortened, and the calcaneus somewhat shortened and flattened. Depending on the degree of the varus deformity, the calf muscles are shortened and underdeveloped, and soft-tissue contractures form at the site of the deformity. The foot is tight in its deformed position and resists manual efforts to push it into normal position. Clubfoot is painless, except in elderly, arthritic patients. In older children, clubfoot may be secondary to paralysis, poliomyelitis, or cerebral palsy, in which case treatment must include management of the underlying disease.

Developmental dysplasia of the hip

Developmental dysplasia of the hip (DDH), an abnormality of the hip joint present from birth, is the most common disorder affecting hip joints of children younger than age 3. DDH can be unilateral or bilateral. (See Characteristics of developmental hip dysplasia.) This abnormality occurs
in three forms of varying severity: unstable hip dysplasia, in which the hip is positioned normally but can be dislocated by manipulation; subluxati on or incomplete dislocation, in which the femoral head rides on the edge of the acetabulum; and complete or true congenital dislocation, in which the femoral head is totally outside the acetabulum.

Developmental hip subluxation or dislocation can cause abnormal acetabular development and permanent disability.


Experts are uncertain about the causes of DDH. Dislocation is 10 times more common after breech delivery (malpositioning in utero) than after cephalic delivery, and it’s also more common among large neonates and twins. It’s a lot more common in firstborn children. Girls are affected more often than boys and white children more than black children. Genetic factors may also play a role.

Although DDH is found throughout the world, incidence is particularly high among Native Americans.


Clinical effects of hip dysplasia vary with age. In neonates, dysplasia doesn’t cause gross deformity or pain. However, in complete dysplasia, the hip rides above the acetabulum, causing the level of the knees to be uneven. As the child grows older and begins to walk, the abduction on the dislocated side is limited. Uncorrected bilateral dysplasia may cause him to sway from side to side, a condition known as “duck waddle”; unilateral dysplasia may produce a limp. If corrective treatment isn’t begun until after age 2, DDH may cause degenerative hip changes, lordosis, joint malformation, and softtissue damage.

Muscular dystrophy

Muscular dystrophy is actually a group of congenital disorders characterized by progressive symmetrical wasting of skeletal muscles without neural or sensory defects. Paradoxically, these wasted muscles tend to enlarge because of connective tissue and fat deposits, giving an erroneous impression of muscle strength. The main types of muscular dystrophy are Duchenne’s (pseudohypertrophic), Becker’s (benign pseudohypertrophic), facioscapulohumeral (Landouzy-Dejerine), limb-girdle dystrophy,
Emery-Dreifuss muscular dystrophy, and myotonia congenita.

The prognosis varies. Duchenne’s muscular dystrophy generally strikes during early childhood and usually results in death in the 20s or early 30s. Patients with Becker’s muscular dystrophy typically live into their 40s. Facioscapulohumeral and limb-girdle dystrophies usually don’t shorten life.


Muscular dystrophy is caused by various genetic mechanisms. Duchenne’s and Becker’s muscular dystrophies are X-linked recessive disorders. Both result from defects in the gene coding for the muscle protein dystrophin; the gene has been mapped to the Xp21 locus.

The incidence of muscular dystrophy is about 1 in 651,450 persons in the United States. Duchenne’s and Becker’s muscular dystrophies affect males almost exclusively.

Facioscapulohumeral dystrophy is an autosomal dominant disorder. Limb-girdle dystrophy is usually autosomal recessive. These two types affect both sexes about equally.


Although all four types of muscular dystrophy cause progressive muscular deterioration, the degree of severity and age of onset vary.

Duchenne’s muscular dystrophy begins insidiously, between ages 2 and 3. Initially, it affects leg and pelvic muscles but eventually spreads to the involuntary muscles. Muscle weakness produces a waddling gait, toe walking, and lordosis. Children with this disorder have difficulty climbing stairs, fall down often, can’t run properly, and their scapulae flare out (or “wing”) when they raise their arms. Calf muscles especially become enlarged and firm. Muscle deterioration progresses rapidly, and contractures develop. Some have abrupt intermittent oscillations of the irises in response to light (Gower’s sign). Usually, these children are confined to wheelchairs by ages 9 to 12. Late in the disease, progressive weakening of cardiac muscle causes tachycardia, electrocardiogram abnormalities, and pulmonary complications. Death commonly results from sudden heart failure, respiratory failure, or infection.

Signs and symptoms of Becker’s muscular dystrophy resemble those of Duchenne’s muscular dystrophy, but they progress more slowly. It generally affects older boys and young men. Children affected usually walk through their teens and into adulthood—sometimes into their 40s. Cardiac involvement is much less frequent.

Facioscapulohumeral dystrophy is a slowly progressive and relatively benign form of muscular dystrophy that commonly occurs before age 10 but may develop during early adolescence. The earlier the disease occurs, the more rapid and progressive it is. Initially, it weakens the muscles of the face, shoulders, and upper arms but eventually spreads to all voluntary muscles, producing a pendulous lower lip and absence of the nasolabial fold. Early symptoms include the inability to pucker the mouth or whistle, abnormal facial movements, and the absence of facial movements when laughing or crying. Other signs consist of diffuse facial flattening that leads to a masklike expression, winging of the scapulae, the inability to raise the arms above the head and, in infants, the inability to suckle.

Limb-girdle dystrophy follows a similarly slow course and commonly causes only slight disability. Usually, it begins between ages 6 and 10; less commonly, in early adulthood. The later the onset, the more rapid the progression. Muscle weakness first appears in the upper arm and pelvic muscles. Other symptoms include winging of the scapulae, lordosis with abdominal protrusion, waddling gait, poor balance, and the inability to raise the arms.


Septic arthritis

Septic, or infectious, arthritis is a medical emergency that occurs when bacterial invasion of a joint causes inflammation of the synovial lining, effusion and pyogenesis, and destruction of bone and cartilage. Septic arthritis can lead to ankylosis and even fatal septicemia. However, prompt antibiotic therapy and joint aspiration or drainage cures most patients.


In most cases of septic arthritis, bacteria spread from a primary site of infection—usually in adjacent bone or soft tissue—through the bloodstream to the joint. Common infecting organisms in children are group B Streptococcus and Haemophilus influenzae. Adults are usually infected by Staphylococcus, Streptococcus, Neisseria gonorrhoeae (pneumonia), and group B Streptococcus, whereas chronic septic arthritis is caused by Mycobacterium tuberculosis and Candida albicans.

Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as malignancy, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, elderly people and those who abuse I.V. drugs run a higher risk of developing septic arthritis. Of course, diseases that depress the immune system and immunosuppressant therapy increase susceptibility. Other predisposing factors include recent articular trauma, joint arthroscopy or other surgery, intra-articular injections, local joint abnormalities, animal or human bites, and nail puncture wounds.


Acute septic arthritis begins abruptly, causing intense pain, inflammation, and swelling of the affected joint and low-grade fever. It usually affects a single joint. It most commonly develops in the large joints but can strike any joint, including the spine and small peripheral joints. The hip is a frequent site in infants. Systemic signs of inflammation may not appear in some patients. Migratory polyarthritis sometimes precedes localization of the infection. If the bacteria invade the hip, pain may occur in the groin, upper thigh, or buttock or may be referred to the knee.


Gout, also called gouty arthritis, is a metabolic disease marked by urate deposits, which cause painfully arthritic joints. (See Gouty deposits, page 308.) It can strike any joint but favors those in the feet and legs. Gout follows an intermittent course and typically leaves patients totally free from symptoms for years between attacks. It can cause chronic disability or incapacitation and, rarely, severe hypertension and progressive renal disease. The prognosis is good with treatment.


Although the exact cause of primary gout remains unknown, it appears to be linked to a genetic defect in purine metabolism, which causes elevated blood levels of uric acid (hyperuricemia) due to overproduction of uric acid, retention of uric acid, or both. In secondary gout, which develops during the course of another disease (such as obesity, diabetes mellitus, hypertension, sickle cell anemia, and renal disease), hyperuricemia results from the breakdown of nucleic acids. Myeloproliferative and lymphoproliferative diseases, psoriasis, and hemolytic anemia are the most common causes. Primary gout usually occurs in men and in postmenopausal women; secondary gout occurs in elderly people.

Secondary gout can also follow drug therapy that interferes with uric acid excretion. Increased concentration of uric acid leads to urate deposits (tophi) in joints or tissues and
consequent local necrosis or fibrosis. The risk is greater in men, postmenopausal women, and those who use alcohol.


Gout develops in four stages: asymptomatic, acute, intercritical, and chronic. In asymptomatic gout, serum urate levels rise but produce no symptoms. As the disease progresses, it may cause hypertension or nephrolithiasis, with severe back pain. The first acute attack strikes suddenly and peaks quickly. Although it generally involves only one or a few joints, this initial attack is extremely painful. Affected joints are hot, tender, inflamed, and appear dusky-red or cyanotic. The metatarsophalangeal joint of the great toe usually becomes inflamed first (podagra), followed by the instep, ankle, heel, knee, or wrist joints. Sometimes a low-grade fever is present. Mild acute attacks usually subside quickly but tend to recur at irregular intervals. Severe attacks may persist for days or weeks.

Intercritical periods are the symptom-free intervals between gout attacks. Most patients have a second attack within 6 months to 2 years, but in some the second attack doesn’t occur for 5 to 10 years. Delayed attacks are more common in untreated patients and tend to be longer and more severe than initial attacks. Such attacks are also polyarticular, invariably affecting joints in the feet and legs, and are sometimes accompanied by fever. A migratory attack sequentially strikes various joints and the Achilles tendon and is associated with either subdeltoid or olecranon bursitis.

Eventually, chronic polyarticular gout sets in. This final, unremitting stage of the disease is marked by persistent painful polyarthritis, with large, subcutaneous tophi in cartilage, synovial membranes, tendons, and soft tissue. Tophi form in fingers, hands, knees, feet, ulnar sides of the forearms, helix of the ear, Achilles tendons and, rarely, internal organs, such as the kidneys and myocardium. The skin over the tophus may ulcerate and release a chalky, white exudate or pus. Chronic inflammation and tophaceous deposits precipitate secondary joint degeneration, with eventual erosions, deformity, and disability. Kidney involvement, with associated tubular damage, leads to chronic renal dysfunction. Hypertension and albuminuria occur in some patients; urolithiasis is common.

Aug 27, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Musculoskeletal Disorders
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