Musculoskeletal System

Bones
	Bone shape and structure
	Bone growth
Joints
	Classification of joints
	Joint movement
Muscles
	Muscle classification
	Muscle contraction
Tendons And Ligaments
Pathophysiologic Manifestations
	Alterations in bone
	Alterations of muscle
Disorders
	Bone fracture
	Clubfoot
	Developmental hip dysplasia
	Gout
	Muscular dystrophy
	Osteoarthritis
	Osteogenesis imperfecta
	Osteomalacia and rickets
	Osteomyelitis
	Osteoporosis
	Paget's disease
	Rhabdomyolysis
	Scoliosis
	Sprains
	Strains

T he musculoskeletal system is a complex system of bones, muscles, ligaments, tendons, and other tissues that gives the body form and shape. It also protects vital organs, makes movement possible, stores calcium and other minerals in the bony matrix for mobilization if deficiency occurs, and provides sites for hematopoiesis (blood cell production) in the marrow.

BONES

The human skeleton contains 206 bones, which are composed of inorganic salts (primarily calcium and phosphate), embedded in a framework of collagen fibers.

Bone shape and structure

Bones are classified by shape as either long, short, flat, or irregular. Long bones are found in the extremities and include the humerus, radius, and ulna of the arm; the femur, tibia, and fibula of the leg; and the phalanges, metacarpals, and metatarsals of the hands and feet (See Structure of long bones .) Short bones include the tarsal and carpal bones of the feet and hands, respectively. Flat bones include the frontal and parietal bones of the cranium, ribs, sternum, scapulae, ilium, and pubis. Irregular bones include the bones of the spine (vertebrae, sacrum, coccyx) and certain bones of the skull ― the temporal, sphenoid, ethmoid, and mandible.

Classified according to structure, bone is either cortical (compact) or cancellous (spongy or trabecular). Adult cortical bone consists of networks of interconnecting canals, or canaliculi. Each of these networks, or haversian systems, runs parallel to the bone's long axis and consists of a central haversian canal surrounded by layers (lamellae) of bone. Between adjacent lamellae are small openings called lacunae, which contain bone cells or osteocytes. The canaliculi, each containing one or more capillaries, provide a route for tissue fluids transport; they connect all the lacunae.

Cancellous bone consists of thin plates (trabeculae) that form the interior meshwork of bone. These trabeculae are arranged in various directions to correspond with the lines of maximum stress or pressure. This gives the bone added structural strength. Chemically, inorganic salts (calcium and phosphate, with small amounts of sodium, potassium carbonate, and magnesium ions) comprise 70% of the mature bone. The salts give bone its elasticity and ability to withstand compression.

Bone growth

Bone formation is ongoing and is determined by hormonal stimulation, dietary factors, and the amount of stress put on the bone. It is accomplished by the continual actions of bone-forming osteoblasts and bone-reabsorbing cells osteoclasts. Osteoblasts are present on the outer surface of and within bones. They respond to various stimuli to produce the bony matrix, or osteoid. As calcium salts precipitate on the organic matrix, the bone hardens. As the bone forms, a system of microscopic canals in the bone form around the osteocytes. Osteoclasts are phagocytic cells that digest old, weakened bone section by section. As they finish, osteoblasts simultaneously replace the cleared section with new, stronger bone.

STRUCTURE OF LONG BONES Long bones are the weight-bearing bones of the body. Their structure provides maximal strength and minimal weight. Structure of a long bone in an adult is shown below. <center></center>

Vitamin D supports bone calcification by stimulating osteoblast activity and calcium absorption from the gut to make it available for bone building. When serum calcium levels fall, the parathyroid gland releases parathyroid hormone, which then stimulates osteoclast activity and bone breakdown, freeing calcium into the blood. Parathyroid hormone also increases serum calcium by decreasing renal excretion of calcium and increasing renal excretion of phosphate ion.

STRUCTURE OF A SYNOVIAL JOINT The metacarpophalangeal joint depicted here, permits angular motion between the finger and the hand. A synovial joint is characterized by a synovial pouch full of fluid that lubricates the two articulating bones. <center></center>

Phosphates are essential to bone formation; about 85% of the body's phosphates are found in bone. The intestine absorbs a considerable amount of phosphates from dietary sources, but adequate levels of vitamin D are necessary for their absorption. Because calcium and phosphates interact in a reciprocal relationship, renal excretion of phosphates increases or decreases in inverse proportion to serum calcium levels. Alkaline phosphatase (ALP) influences bone calcification and lipid and metabolite transport. Osteoblasts contain an abundance of ALP. A rise in serum ALP levels can identify skeletal diseases primarily those characterized by marked osteoblastic activity such as bone metastases or Paget's disease. It can also identify biliary obstruction or hyperparathyroidism, or excessive ingestion of Vitamin D.

In children and young adults, bone growth occurs in the epiphyseal plate, a layer of cartilage between the diaphysis and epiphysis of long bones.

Osteoblasts deposit new bone in the area just beneath the epiphysis, making the bone longer, and osteoclasts model the new bone's shape by resorbing previously deposited bone. These remodeling activities promote longitudinal bone growth, which continues until the epiphyseal growth plates, located at both ends, close during adolescence. In adults, bone growth is complete, and this cartilage is replaced by bone, becoming the epiphyseal line.

JOINTS

The tendons, ligaments, cartilage, and other tissues that connect two bones comprise a joint. Depending on their structure, joints either predominantly permit motion or provide stability. Joints, like bones, are classified according to structure and function.

Classification of joints

The three structural types of joints are fibrous, cartilaginous, and synovial.

• Fibrous joints, or synarthroses , have only minute motion and provide stability when tight union is necessary, as in the sutures that join the cranial bones.
• Cartilaginous joints, or amphiarthroses , allow limited motion, as between vertebrae.
• Synovial joints, or diarthroses , are the most common and permit the greatest degree of movement. These joints include the elbows and knees. (See Structure of a synovial joint .)

Synovial joints have distinguishing characteristics:

• The two articulating surfaces of the bones have a smooth hyaline covering (articular cartilage) that is resilient to pressure.
• Their opposing surfaces are congruous and glide smoothly on each other.
• A fibrous (articular) capsule holds them together.
• Beneath the capsule, lining the joint cavity, is the synovial membrane, which secretes a clear viscous fluid called 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.

Joint movement

The two types of synovial joint movement are angular and circular.

Angular movement

Joints of the knees, elbows, and phalanges permit the following angular movements:

• flexion (closing of the joint angle)
• extension (opening of the joint angle)
• hyperextension (extension of the angle beyond the usual arc).

Other joints, including the shoulders and hips, permit:

• abduction (movement away from the body's midline)
• adduction (movement toward the midline).

Circular movements

Circular movements include:

• rotation (motion around a central axis), as in the ball and socket joints of the hips and shoulders
• pronation (downward wrist or ankle motion)
• supination (upward wrist motion to begging position).

Other kinds of movement are inversion (inward turning, as of foot), eversion (outward turning, as of foot), protraction (as in forward motion of the mandible), and retraction (returning protracted part into place).

MUSCLES

The most specialized feature of muscle tissue ― contractility ― makes the movement of bones and joints possible. Normal skeletal muscles contract in response to neural impulses. Appropriate contraction of muscle usually applies force to one or more tendons. The force pulls one bone toward, away from, or around a second bone, depending on the type of muscle contraction and the type of joint involved. Abnormal metabolism in the muscle may result in inappropriate contractility. For example, when stored glycogen or lipids cannot be used because of the lack of an enzyme necessary to convert energy for contraction, the result may be cramps, fatigue, and exercise intolerance.

Muscles permit and maintain body positions, such as sitting and standing. Muscles also pump blood through the body (cardiac contraction and vessel compression), move food through the intestines (peristalsis), and make breathing possible. Skeletal muscular activity produces heat; it is an important component in temperature regulation. Deep body temperature regulators are found in the abdominal viscera, spinal cord, and great veins. These receptors detect changes in the body core temperature and stimulate the hypothalamus to institute appropriate temperature changing responses, such as shivering in response to cold. Muscle mass accounts for about 40% of an average man's weight.

Muscle classification

Muscles are classified according to structure, anatomic location, and function:

• Skeletal muscles are attached to bone and have a striped (striated) appearance that reflects their cellular structure.
• Visceral muscles move contents through internal organs and are smooth (nonstriated).
• Cardiac muscles (smooth) comprise the heart wall.

When muscles are classified according to activity, they are called either voluntary or involuntary. (See Chapter 8 , “Nervous system.”) 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. Some organs contain both voluntary and involuntary muscles.

Muscle contraction

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 into muscles through the fascia to reach the individual muscle fibers. Motor neurons synapse with the motor nerve fibers of voluntary muscles. These fibers reach the membranes of skeletal muscle cells at neuromuscular (myoneural) junctions. When an impulse reaches the myoneural junction, the junction releases the neurotransmitter, acetylcholine, which releases calcium from the sarcoplasmic reticulum, a membranous network in the muscle fiber, which, in turn, triggers muscle contraction. The energy source for this contraction is adenosine triphosphate (ATP). ATP release is also triggered by the impulse at the myoneural junction. Relaxation of a muscle is believed to take place by reversal of these mechanisms.

Muscle fatigue results when the sources of ATP in a muscle are depleted. If a muscle is deprived of oxygen, fatigue occurs rapidly. As the muscle fatigues, it switches to anaerobic metabolism of glycogen stores, in which the stored glycogen is split into glucose (glycolysis) without the use of oxygen. Lactic acid is a by-product of anaerobic glycolysis and may accumulate in the muscle and blood with intense or prolonged muscle contraction.

TENDONS AND LIGAMENTS

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

Ligaments are fibrous connections that control joint movement between two bones or cartilages. Their purpose is to support and strengthen joints.

PATHOPHYSIOLOGIC MANIFESTATIONS

Alterations of the normal functioning of bones and muscles are described next. Most musculoskeletal disorders are caused by or profoundly affect other body systems.

Alterations in bone

Disease may alter density, growth, or strength of bone.

Density

In healthy young adults, the resorption and formation phases are tightly coupled to maintain bone mass in a steady state. Bone loss occurs when the two phases become uncoupled, and resorption exceeds formation. Estrogen not only regulates calcium uptake and release, it also regulates osteoblastic activity. Decreased estrogen levels may lead to diminished osteoblastic activity and loss of bone mass, called osteoporosis. In children, vitamin D deficiency prevents normal bone growth and leads to rickets.

AGE ALERT Bone density and structural integrity decrease after the age of 30 years in women and after the age of 45 years in men. The relatively steady loss of bone matrix can be partially offset by exercise.

CULTURAL DIVERSITY Age, race, and sex affect bone mass, structural integrity (ability to withstand stress), and bone loss. For example, blacks commonly have denser bones than whites, and men typically have denser bones than women.

Growth

The osteochondroses are a group of disorders characterized by avascular necrosis of the epiphyseal growth plates in growing children and adolescents. In these disorders, a lack of blood supply to the femoral head leads to septic necrosis, with softening and resorption of bone. Revascularization then initiates new bone formation in the femoral head or tibial tubercle, which leads to a malformed femoral head.

Bone strength

Both cortical and trabecular bone contribute to skeletal strength. Any loss of the inorganic salts that comprise the chemical structure of bone will weaken bone. Cancellous bone is more sensitive to metabolic influences, so conditions that produce rapid bone loss tend to affect cancellous bone more quickly than cortical bone.

Alterations of muscle

Pathologic effects on muscle include atrophy, fatigue, weakness, myotonia, and spasticity.

Atrophy

Atrophy is a decrease in the size of a tissue or cell. In muscles, the myofibrils atrophy after prolonged inactivity from bed rest or trauma (casting), when local nerve damage makes movement impossible, or when illness removes needed nutrients from muscles. The effects of muscular deconditioning associated with lack of physical activity may be apparent in a matter of days. An individual on bed rest loses muscle strength, as well as muscle mass, from baseline levels at a rate of 3% a day.

Conditioning and stretching exercises may help prevent atrophy. If reuse isn't restored within 1 year, regeneration of muscle fibers is unlikely.

AGE ALERT Some degree of muscle atrophy is normal with aging.

Fatigue

Pathologic muscle fatigue may be the result of impaired neural stimulation of muscle or energy metabolism or disruption of calcium flux. See Chapter 5 , Fluid and electrolytes, for a detailed discussion of these events.

Weakness

AGE ALERT Muscle mass and muscle strength decrease in the elderly, usually as a result of disuse. This can be reversed with moderate, regular, weight-bearing exercise.

Periodic paralysis is a disorder that can be triggered by exercise or a process or chemical (such as medication) that increases serum potassium levels. This hyperkalemic periodic paralysis may be caused by a high-carbohydrate diet, emotional stress, prolonged bed rest, or hyperthyroidism. During an attack of periodic paralysis, the muscle membrane is unresponsive to neural stimuli, and the electrical charge needed to initiate the impulse (resting membrane potential) is reduced from �90 mV to �45 mV.

Myotonia and spasticity

Myotonia is delayed relaxation after a voluntary muscle contraction ― such as grip, eye closure, or muscle percussion ― accompanied by prolonged depolarization of the muscle membrane. Depolarization is the reversal of the resting potential in stimulated cell membranes. It is the process by which the cell membrane “resets” its positive charge with respect to the negative charge outside the cell. Myotonia occurs in myotonic muscular dystrophy and some forms of periodic paralysis.

MANAGING MUSCULOSKELETAL PAIN A patient with a musculoskeletal disorder that causes chronic, nonmalignant pain should be assessed and treated in a stepped approach. Measures include: nonpharmacologic methods, such as heat, ice, elevation, and rest acetaminophen (Tylenol) nonsteroidal anti-inflammatories such as ibuprofen (Motrin) other nonnarcotic analgesics such as tramadol (Ultram) or topical capsaicin cream (Zostrix) tricyclic antidepressants such as amitriptyline hydrochloride (Elavil) may decrease the pain signal at the neurosynaptic junctions opioid analgesics alone or with a tricyclic antidepressant.

Stress-induced muscle tension, or spasticity, is presumably caused by increased activity in the reticular activating system and gamma loop in the muscle fiber. The reticular activating system consists of multiple diffuse pathways in the brain that control wakefulness and response to stimuli. A pathologic contracture is permanent muscle shortening caused by muscle spasticity, seen in central nervous system injury or severe muscle weakness.

DISORDERS

AGE ALERT Patients with musculoskeletal disorders are often elderly, have other concurrent medical conditions, or are victims of trauma. Generally, they face prolonged immobilization. (See Managing musculoskeletal pain .)

Bone fracture

When a force exceeds the compressive or tensile strength (the ability of the bone to hold together) of the bone, a fracture will occur. (For an explanation of the terms used to identify fractures, see Classifying fractures .)

An estimated 25% of the population has traumatic musculoskeletal injury each year, and a significant number of these involve fractures.

The prognosis varies with the extent of disablement or deformity, amount of tissue and vascular damage, adequacy of reduction and immobilization, and patient's age, health, and nutritional status.

AGE ALERT Children's bones usually heal rapidly and without deformity. However, epiphyseal plate fractures in children are likely to cause deformity because they interfere with normal bone growth. In the elderly, underlying systemic illness, impaired circulation, or poor nutrition may cause slow or poor healing.

Causes

Risk factors for fractures are those that involve force to bone, such as:

• falls
• motor vehicle accidents
• sports
• use of drugs that impair judgment or mobility
• young age (immaturity of bone)
• bone tumors
• metabolic illnesses(such as hypoparathyroidism or hyperparathyroidism)
• medications that cause iatrogenic osteoporosis, such as steroids.

AGE ALERT The highest incidence of fractures occurs in young males between the ages of 15 and 24 years (tibia, clavicle, and lower humerus) and are usually the result of trauma. In the elderly, upper femur, upper humerus, vertebrae, and pelvis fractures are often associated with osteoporosis.

CLASSIFYING FRACTURES One of the best-known systems for classifying fractures uses a combination of terms that describe general classification, fragment position, and fracture line ― such as simple, nondisplaced, and oblique ― to describe fractures. GENERAL CLASSIFICATION OF FRACTURES Simple (closed) ― Bone fragments don't penetrate the skin. Compound (open) ― Bone fragments penetrate the skin. Incomplete (partial) ― Bone continuity isn't completely interrupted. Complete ― Bone continuity is completely interrupted. CLASSIFICATION BY FRAGMENT POSITION Comminuted ― The bone breaks into small pieces. Impacted ― One bone fragment is forced into another. Angulated ― Fragments lie at an angle to each other. Displaced ― Fracture fragments separate and are deformed. Nondisplaced ― The two sections of bone maintain essentially normal alignment. Overriding ― Fragments overlap, shortening the total bone length. Segmental ― Fractures occur in two adjacent areas with an isolated central segment. Avulsed ― Fragments are pulled from the normal position by muscle contractions or ligament resistance. CLASSIFICATION BY FRACTURE LINE Linear ― The fracture line runs parallel to the bone's axis. Longitudinal ― The fracture line extends in a longitudinal (but not parallel) direction along the bone's axis. Oblique ― The fracture line crosses the bone at about a 45-degree angle to the bone's axis. Spiral ― The fracture line crosses the bone at an oblique angle, creating a spiral pattern. Transverse ― The fracture line forms a right angle with the bone's axis.

Pathophysiology

When a bone is fractured, the periosteum and blood vessels in the cortex, marrow, and surrounding soft tissue are disrupted. A hematoma forms between the broken ends of the bone and beneath the periosteum, and granulation tissue eventually replaces the hematoma.

Damage to bone tissue triggers an intense inflammatory response in which cells from surrounding soft tissue and the marrow cavity invade the fracture area, and blood flow to the entire bone is increased. Osteoblasts in the periosteum, endosteum, and marrow produce osteoid (collagenous, young bone that has not yet calcified, also called callus), which hardens along the outer surface of the shaft and over the broken ends of the bone. Osteoclasts reabsorb material from previously formed bones and osteoblasts to rebuild bone. Osteoblasts then transform into osteocytes (mature bone cells).

Signs and symptoms

Signs and symptoms of bone fracture may include:

• deformity due to unnatural alignment
• swelling due to vasodilation and infiltration by inflammatory leukocytes and mast cells
• muscle spasm
• tenderness
• impaired sensation distal to the fracture site due to pinching or severing of neurovascular elements by the trauma or by bone fragments
• limited range of motion
• crepitus, or “clicking” sounds on movement caused by shifting bone fragments.

RECOGNIZING COMPARTMENT SYNDROME Compartment syndrome occurs when edema or bleeding increases pressure within a muscle compartment (a smaller section of a muscle), to the point of interfering with circulation. Crush injuries, burns, bites, and fractures requiring casts or dressings may cause this syndrome. Compartment syndrome most commonly occurs in the lower arm, hand, lower leg, or foot. Symptoms include: increased pain decreased touch sensation increased weakness of the affected part increased swelling and pallor decreased pulses and capillary refill. Treatment of compartment syndrome consists of: placing the limb at heart level removing constricting forces monitoring neurovascular status subfascial injection of hyaluronidase (Wydase) emergency fasciotomy.

Complications

Possible complications of fracture are:

• permanent deformity and dysfunction if bones fail to heal (nonunion) or heal improperly (malunion)
• aseptic (not caused by infection) necrosis of bone segments due to impaired circulation
• hypovolemic shock as a result of blood vessel damage (especially with a fractured femur)
• muscle contractures
• compartment syndrome (See Recognizing compartment syndrome .)
• renal calculi from decalcification due to prolonged immobility
• fat embolism due to disruption of marrow or activation of the sympathetic nervous system after the trauma (may lead to respiratory or central nervous system distress).

Diagnosis

Diagnosis of bone fracture includes:

• history of traumatic injury and results of the physical examination, including gentle palpation and a cautious attempt by the patient to move parts distal to the injury
• X-rays of the suspected fracture and the joints above and below (confirm the diagnosis; after reduction, confirm bone alignment).

Treatment

For arm or leg fractures, emergency treatment consists of:

• splinting the limb above and below the suspected fracture to immobilize it
• applying a cold pack to reduce pain and edema
• elevating the limb to reduce pain and edema.

Treatment in severe fractures that cause blood loss includes:

• direct pressure to control bleeding
• fluid replacement as soon as possible to prevent or treat hypovolemic shock.

After confirming a fracture, treatment begins with a reduction. Closed reduction involves:

• manual manipulation
• local anesthetic (such as lidocaine [Xylocaine])
• analgesic (such as morphine IM)
• muscle relaxant (such as diazepam [Valium] I.V.) or a sedative (such as midazolam [Versed]) to facilitate the muscle stretching necessary to realign the bone.

When closed reduction is impossible, open reduction by surgery involves:

• immobilization of the fracture by means of rods, plates, or screws and application of a plaster cast
• tetanus prophylaxis
• prophylactic antibiotics
• surgery to repair soft tissue damage
• thorough wound debridement
• physical therapy after cast removal to restore limb mobility.

When a splint or cast fails to maintain the reduction, immobilization requires skin or skeletal traction, using a series of weights and pulleys. This may involve:

• elastic bandages and sheepskin coverings to attach traction devices to the patient's skin (skin traction)
• pin or wire inserted through the bone distal to the fracture and attached to a weight to allow more prolonged traction (skeletal traction).

Clubfoot

Clubfoot, also called talipes, is the most common congenital disorder of the lower extremities. It is marked primarily by a deformed talus and shortened Achilles tendon, which give the foot a characteristic club-like appearance. In talipes equinovarus, the foot points downward (equinus) and turns inward (varus), while the front of the foot curls toward the heel (forefoot adduction).

Clubfoot occurs in about 1 per 1,000 live births, is usually bilateral and is twice as common in boys as girls. It may be associated with other birth defects, such as myelomeningocele, spina bifida, and arthrogryposis. Clubfoot is correctable with prompt treatment.

Causes

A combination of genetic and environmental factors in utero appears to cause clubfoot, including:

• heredity (mechanism of transmission is undetermined; the sibling of a child born with clubfoot has 1 chance in 35 of being born with the same anomaly, and a child of a parent with clubfoot has 1 chance in 10)
• arrested development during the 9th and 10th weeks of embryonic life when the feet are formed (children without a family history of clubfoot)
• muscle abnormalities leading to variations in length and tendon insertions
• secondary to paralysis, poliomyelitis, or cerebral palsy (older children), in which case treatment includes management of the underlying disease.

Pathophysiology

Abnormal development of the foot during fetal growth leads to abnormal muscles and joints and contracture of soft tissue. The condition called apparent clubfoot results when a fetus maintains a position in utero that gives his feet a clubfoot appearance at birth; it can usually be corrected manually. Another form of apparent clubfoot is inversion of the feet, resulting from the denervation type of progressive muscular atrophy and progressive muscular dystrophy.

Signs and symptoms

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.

Every case includes:

• deformed talus
• shortened Achilles tendon
• shortened and flattened calcaneus bone of the heel
• shortened, underdeveloped calf muscles and soft-tissue contractures at the site of the deformity (depending on degree of the varus deformity)
• foot is tight in its deformed position, resisting manual efforts to push it back into normal position
• no pain, except in elderly, arthritic patients with secondary deformity.

Complications

Possible complications of talipes equinovarius are:

• chronic impairment (neglected clubfoot)
• rarely totally correctable (when severe enough to require surgery).

Diagnosis

Early diagnosis of clubfoot is usually no problem because the deformity is obvious. In subtle deformity, however, true clubfoot must be distinguished from apparent clubfoot (metatarsus varus or pigeon toe), usually by:

• X-rays showing superimposition of the talus and calcaneus and a ladder-like appearance of the metatarsals (true clubfoot).

Treatment

Treatment for clubfoot is done in three stages: correcting the deformity, maintaining the correction until the foot regains normal muscle balance, and observing the foot closely for several years to prevent the deformity from recurring.

Clubfoot deformities are usually corrected in sequential order: forefoot adduction first, then varus (or inversion), then equinus (or plantar flexion). Trying to correct all three deformities at once only results in a misshapen, rocker-bottomed foot.

Other essential parts of management are:

• stressing to parents importance of prompt treatment and orthopedic supervision until growth is completed
• teaching parents cast care and how to recognize circulatory impairment before a child in a clubfoot cast is discharged
• explaining to older child and his parents that surgery can improve clubfoot with good function, but can't totally correct it; the affected calf muscle will remain slightly underdeveloped
• emphasizing the need for long-term orthopedic care to maintain correction; correcting this defect permanently takes time and patience.

Developmental hip dysplasia

Developmental hip dysplasia (DHD), an abnormality of the hip joint present from birth, is the most common disorder affecting the hip joints of children younger than 3 years. About 85% of affected infants are females.

DHD can be unilateral or bilateral. This abnormality occurs in three forms of varying severity:

• Unstable dysplasia: the hip is positioned normally but can be dislocated by manipulation.
• Subluxation or incomplete dislocation: the femoral head rides on the edge of the acetabulum.
• Complete dislocation: the femoral head is totally outside the acetabulum.

Causes

Although the causes of DHD are not clear, it's more likely to occur in the following circumstances:

• dislocation after breech delivery (malposition in utero, 10 times more common than after cephalic delivery)
• elevated maternal relaxin, hormone secreted by the corpus luteum during pregnancy that causes relaxation of pubic symphysis and cervical dilation (may promote relaxation of the joint ligaments, predisposing the infant to DHD)
• large neonates and twins (more common).

Pathophysiology

The precise cause of congenital dislocation is unknown. Excessive or abnormal movement of the joint during a traumatic birth may cause dislocation. Displacement of bones within the joint may damage joint structures, including articulating surfaces, blood vessels, tendons, ligaments, and nerves. This may lead to ischemic necrosis because of the disruption of blood flow to the joint.

Signs and symptoms

Signs and symptoms of hip dysplasia vary with age and include:

• no gross deformity or pain (in newborns)
• the hip rides above the acetabulum, causing the level of the knees to be uneven (complete dysplasia)
• limited abduction on the dislocated side (as the child grows older and begins to walk)
• swaying from side to side (“duck waddle” due to uncorrected bilateral dysplasia)
• limp due to uncorrected unilateral dysplasia.

Complications

If corrective treatment isn't begun until after the age of 2 years, DHD may cause:

• degenerative hip changes
• abnormal acetabular development
• lordosis (abnormally increased concave curvature of the lumbar and cervical spine)
• joint malformation
• soft tissue damage
• permanent disability.

Diagnosis

Diagnostic measures may include:

• X-rays to show the location of the femur head and a shallow acetabulum (also to monitor disease or treatment progress)
• sonography and magnetic resonance imaging to assess reduction.

Observations during physical examination of the relaxed child that strongly suggest DHD include:

• the number of folds of skin over the thighs on each side when the child is placed on his back (a child in this position usually has an equal number of folds, but a child with subluxation or dislocation may have an extra fold on the affected side, which is also apparent when the child lies prone)
• buttock fold on the affected side higher with the child lying prone (also restricted abduction of the affected hip). (See Ortolani's and Trendelenburg's signs of DHD .)

ORTOLANI'S AND TRENDELENBURG'S SIGNS OF DHD A positive Ortolani's or Trendelenburg's sign confirms developmental hip dysplasia (DHD). Ortolani's sign Place infant on his back, with hip flexed and in abduction. Adduct the hip while pressing the femur downward. This will dislocate the hip. Then, abduct the hip while moving the femur upward. A click or a jerk (produced by the femoral head moving over the acetabular rim) indicates subluxation in an infant younger than 1 month. The sign indicates subluxation or complete dislocation in an older infant. Trendelenburg's sign When the child rests his weight on the side of the dislocation and lifts his other knee, the pelvis drops on the normal side because abductor muscles in the affected hip are weak. However, when the child stands with his weight on the normal side and lifts the other knee, the pelvis remains horizontal.

Treatment

The earlier an infant receives treatment, the better the chances are for normal development. Treatment varies with the patient's age.

In infants younger than 3 months, treatment includes:

• gentle manipulation to reduce the dislocation, followed by splint-brace or harness to hold the hips in a flexed and abducted position to maintain the reduction
• splint-brace or harness worn continuously for 2 to 3 months, then a night splint for another month to tighten and stabilize the joint capsule in correct alignment.

If treatment doesn't begin until after the age of 3 months, it may include:

• bilateral skin traction (in infants) or skeletal traction (in children who have started walking) to try to reduce the dislocation by gradually abducting the hips
• Bryant's traction or divarication traction (both extremities placed in traction, even if only one is affected, to help maintain immobilization) for children younger than 3 years and weighing less than 35 lb (16 kg) for 2 to 3 weeks
• gentle closed reduction under general anesthesia to further abduct the hips, followed by a spica cast for 4 to 6 months (if traction fails)
• if closed treatment fails, open reduction, followed by immobilization in a spica cast for an average of 6 months, or surgical division and realignment of bone (osteotomy).

In a child aged 2 to 5 years, treatment is difficult and includes:

• skeletal traction and subcutaneous adductor tenotomy (surgical cutting of the tendon).

Treatment begun after the age of 5 years rarely restores satisfactory hip function.

Gout

Gout, also called gouty arthritis, is a metabolic disease marked by urate deposits that cause painfully arthritic joints. It's found mostly in the foot, especially the great toe, ankle, and midfoot, but may affect any joint. Gout follows an intermittent course, and patients may be totally free of symptoms for years between attacks. The prognosis is good with treatment.

AGE ALERT Primary gout usually occurs in men after age 30 (95% of cases) and in postmenopausal women; secondary gout occurs in the elderly.

Causes

Although the exact cause of primary gout remains unknown, it may be caused by:

• genetic defect in purine metabolism, causing overproduction of uric acid (hyperuricemia), 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), the cause may be:

• breakdown of nucleic acid causing hyperuricemia
• result of drug therapy, especially after the use of hydrochlorothiazide or pyrazinamide (Zinamide), which decrease urate excretion (ionic form of uric acid).

Pathophysiology

When uric acid becomes supersaturated in blood and other body fluids, it crystallizes and forms a precipitate of urate salts that accumulate in connective tissue throughout the body; these deposits are called tophi. The presence of the crystals triggers an acute inflammatory response when neutrophils begin to ingest the crystals. Tissue damage begins when the neutrophils release their lysosomes (see Chapter 12 , Immune System). The lysosomes not only damage the tissues, but also perpetuate the inflammation.

In asymptomatic gout, serum urate levels increase but don't crystallize or produce symptoms. As the disease progresses, it may cause hypertension or urate kidney stones may form.

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 appear hot, tender, inflamed, dusky red, or cyanotic. The metatarsophalangeal joint of the great toe usually becomes inflamed first (podagra), then the instep, ankle, heel, knee, or wrist joints. Sometimes a low-grade fever is present. Mild acute attacks often 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 some attacks, common in those who are untreated, tend to be longer and more severe than initial attacks. Such attacks are also polyarticular, invariably affecting joints in the feet and legs, and 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 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, in internal organs, such as the kidneys and myocardium. The skin over the tophus may ulcerate and release a chalky, white exudate that is composed primarily of uric acid crystals.

Signs and symptoms

Possible signs and symptoms of gout include:

• joint pain due to uric acid deposits and inflammation
• redness and swelling in joints due to uric acid deposits and irritation
• tophi in the great toe, ankle, and pinna of ear due to urate deposits
• elevated skin temperature from inflammation.

Complications

Complications of gout may include:

• eventual erosions, deformity, and disability due to chronic inflammation and tophi that cause secondary joint degeneration
• hypertension and albuminuria (in some patients)
• kidney involvement, with tubular damage from aggregates of urate crystals; progressively poorer excretion of uric acid and chronic renal dysfunction.

Diagnosis

The following test results help diagnose gout:

• needle-like monosodium urate crystals in synovial fluid (shown by needle aspiration) or tissue sections of tophaceous deposits
• hyperuricemia (uric acid greater than 420 μmol/mmol of creatinine)
• elevated 24-hour urine uric acid (usually higher in secondary than in primary gout)
• X-rays initially normal; in chronic gout, damage of articular cartilage and subchondral bone. Outward displacement of the overhanging margin from the bone contour characterizes gout.

Treatment

The goals of treatment are to end the acute attack as quickly as possible, prevent recurring attacks, and prevent or reverse complications. Treatment for acute gout consists of:

• immobilization and protection of the inflamed, painful joints
• local application of heat or cold
• increased fluid intake (to 3 L/day if not contradicted by other conditions to prevent kidney stone formation)
• concomitant treatment with colchicine (oral or I.V.) every hour for 8 hours to inhibit phagocytosis of uric acid crystals by neutrophils, until the pain subsides or nausea, vomiting, cramping, or diarrhea develops (in acute inflammation)
• nonsteroidal anti-inflammatory drugs for pain and inflammation.

AGE ALERT Older patients are at risk for GI bleeding associated with nonsteroidal anti-inflammatory drug use. Encourage the patient to take these drugs with meals, and monitor the patient's stools for occult blood.

Treatment for chronic gout aims to decrease serum uric acid levels, including:

• maintenance dosage of allopurinol (Zyloprim) to suppress uric acid formation or control uric acid levels, preventing further attacks (use cautiously in patients with renal failure)
• colchicine to prevent recurrent acute attacks until uric acid returns to its normal level (doesn't affect uric acid level)
• uricosuric agents (probenecid [Benemid] and sulfinpyrazon [Anturane]) to promote uric acid excretion and inhibit uric acid accumulation (of limited value in patients with renal impairment)
• dietary restrictions, primarily avoiding alcohol and purine-rich foods (shellfish, liver, sardines, anchovies, and kidneys) that increase urate levels (adjunctive therapy).

Muscular dystrophy

Muscular dystrophy is a group of congenital disorders characterized by progressive symmetric wasting of skeletal muscles without neural or sensory defects. Paradoxically, some wasted muscles tend to enlarge (pseudohypertrophy) because connective tissue and fat replace muscle tissue, giving a false impression of increased muscle strength.

The four main types of muscular dystrophy are:

• Duchenne, or pseudohypertrophic; 50% of all cases
• Becker, or benign pseudohypertrophic
• facioscapulohumeral, or Landouzy-Dejerine, dystrophy
• limb-girdle dystrophy.

The prognosis varies with the form of disease. Duchenne muscular dystrophy strikes during early childhood and is usually fatal during the second decade of life. It mostly affects males, 13 to 33 per 100,000 persons. Patients with Becker muscular dystrophy can live into their 40s, and it mostly affects males, 1 to 3 per 100,000 persons. Facioscapulohumeral and limb-girdle dystrophies usually don't shorten life expectancy, and they affect both sexes equally.

Causes

Causes of muscular dystrophy include:

• various genetic mechanisms typically involving an enzymatic or metabolic defect
• X-linked recessive disorders due to defects in the gene coding, mapped genetically to the Xp21 locus, for the muscle protein dystrophin, which is essential for maintaining muscle cell membrane; muscle cells deteriorate or die without it. (Duchenne and Becker dystrophy)
• autosomal dominant disorder (facio-scapulohumeral dystrophy)
• autosomal recessive disorder (limb-girdle dystrophy).

Pathophysiology

Abnormally permeable cell membranes allow leakage of a variety of muscle enzymes, particularly creatine kinase. This metabolic defect that causes the muscle cells to die is present from fetal life onward. The absence of progressive muscle wasting at birth suggests that other factors compound the effect of dystrophin deficiency. The specific trigger is unknown, but phagocytosis of the muscle cells by inflammatory cells causes scarring and loss of muscle function.

As the disease progresses, skeletal muscle becomes almost totally replaced by fat and connective tissue. The skeleton eventually becomes deformed, causing progressive immobility. Cardiac and smooth muscle of the GI tract often become fibrotic. No consistent structural abnormalities are seen in the brain.

Signs and symptoms

Signs and symptoms of Duchenne muscular dystrophy include:

• insidious onset between the ages of 3 and 5 years
• initial effect on legs, pelvis, and shoulders
• waddling gait, toe-walking, and lumbar lordosis due to muscle weakness
• difficulty climbing stairs, frequent falls
• enlarged, firm calf muscles
• confined to wheelchair (usually by 9 to 12 years of age).

Signs and symptoms of Becker (benign pseudohypertrophic) muscular dystrophy are:

• similar to those of Duchenne muscular dystrophy but with slower progression.

Signs of facioscapulohumeral (Landouzy-Dejerine) dystrophy include:

• weakened face, shoulder, and upper arm muscles (initial sign)
• pendulous lip and absent nasolabial fold
• inability to pucker mouth or whistle
• abnormal facial movements and absence of facial movements when laughing or crying
• diffuse facial flattening leading to a masklike expression
• inability to raise arms above the head.

Signs and symptoms of limb-girdle dystrophy include:

• weakness in upper arms and pelvis first
• lumbar lordosis with abdominal protrusion
• winging of the scapulae
• waddling gait
• poor balance
• inability to raise the arms.

Complications

Possible complications of Duchenne muscular dystrophy are:

• weakened cardiac and respiratory muscles leading to tachycardia, electrocardiographic abnormalities, and pulmonary complications
• death commonly due to sudden heart failure, respiratory failure, or infection.

Diagnosis

Diagnosis depends on typical clinical findings, family history, and diagnostic test findings. If another family member has muscular dystrophy, its clinical characteristics can suggest the type of dystrophy the patient has and how he may be affected. The following tests may help in the diagnosis:

• electromyography showing short, weak bursts of electrical activity in affected muscles
• muscle biopsy showing a combination of muscle cell degeneration and regeneration (in later stages, showing fat and connective tissue deposits)
• immunologic and molecular biological techniques (now available in specialized medical centers) to facilitate accurate prenatal and postnatal diagnosis of Duchenne and Becker dystrophies (replacing muscle biopsy and elevated serum creatine kinase levels in diagnosis).

Treatment

No treatment can stop the progressive muscle impairment. Supportive treatments include:

• coughing and deep-breathing exercises and diaphragmatic breathing
• teaching parents to recognize early signs of respiratory complications
• orthopedic appliances, exercise, physical therapy, and surgery to correct contractures (to help preserve mobility and independence)
• genetic counseling regarding risk for transmitting disease for family members who are carriers
• adequate fluid intake, increased dietary bulk, and stool softener for constipation due to inactivity
• low-calorie, high-protein, high-fiber diet (physical inactivity predisposes to obesity).

Osteoarthritis

Osteoarthritis, the most common form of arthritis, is a chronic condition causing the deterioration of joint cartilage and the formation of reactive new bone at the margins and subchondral areas of the joints. It usually affects weight-bearing joints (knees, feet, hips, lumbar vertebrae). Osteoarthritis is widespread (affecting more than 60 million persons in the United States) and is most common in women. Typically, its earliest symptoms manifest in middle age and progress from there.

Disability depends on the site and severity of involvement and can range from minor limitation of finger movement to severe disability in persons with hip or knee involvement. The rate of progression varies, and joints may remain stable for years in an early stage of deterioration.

Causes

The primary defect in both idiopathic and secondary osteoarthritis is loss of articular cartilage due to functional changes in chondrocytes (cells responsible for the formation of the proteoglycans, glycoproteins that act as cementing material in the cartilage, and collagen).

Idiopathic osteoarthritis, a normal part of aging, results from many factors, including:

• metabolic (endocrine disorders such as hyperparathyroidism) and genetic (decreased collagen synthesis)
• chemical (drugs that stimulate the collagen-digesting enzymes in the synovial membrane, such as steroids)
• mechanical factors (repeated stress on the joint).

Secondary osteoarthritis usually follows an identifiable predisposing event that leads to degenerative changes, such as:

• trauma (most common cause)
• congenital deformity
• obesity.

Pathophysiology

Osteoarthritis occurs in synovial joints. The joint cartilage deteriorates, and reactive new bone forms at the margins and subchondral areas of the joints. The degeneration results from damage to the chondrocytes. Cartilage softens with age, narrowing the joint space. Mechanical injury erodes articular cartilage, leaving the underlying bone unprotected. This causes sclerosis, or thickening and hardening of the bone underneath the cartilage.

Cartilage flakes irritate the synovial lining, which becomes fibrotic and limits joint movement. Synovial fluid may be forced into defects in the bone, causing cysts. New bone, called osteophyte (bone spur), forms at joint margins as the articular cartilage erodes, causing gross alteration of the bony contours and enlargement of the joint.

Signs and symptoms

Symptoms, which increase with poor posture, obesity, and occupational stress, include:

• deep, aching joint pain due to degradation of the cartilage, inflammation, and bone stress, particularly after exercise or weight bearing (the most common symptom, usually relieved by rest)
• stiffness in the morning and after exercise (relieved by rest)
• crepitus, or “grating” of the joint during motion due to cartilage damage
• Heberden's nodules (bony enlargements of the distal interphalangeal joints) due to repeated inflammation
• altered gait from contractures due to overcompensation of the muscles supporting the joint
• decreased range of motion due to pain and stiffness
• joint enlargement due to stress on the bone and disordered bone growth
• localized headaches (may be a direct result of cervical spine arthritis).

Complications

Complications of osteoarthritis include:

• irreversible joint changes and node formation (nodes eventually becoming red, swollen, and tender, causing numbness and loss of finger dexterity)
• subluxation of the joint.

Diagnosis

Findings that help diagnose osteoarthritis include:

• absence of systemic symptoms (ruling out inflammatory joint disorder)
• arthroscopy showing bone spurs, narrowing of joint space
• increased erythrocyte sedimentation rate (with extensive synovitis).

X-rays of the affected joint help confirm the diagnosis but may be normal in the early stages. X-rays may require many views and typically show:

• narrowing of joint space or margin
• cyst-like bony deposits in joint space and margins, sclerosis of the subchondral space
• joint deformity due to degeneration or articular damage
• bony growths at weight-bearing areas
• joint fusion.

SPECIFIC CARE FOR ARTHRITIC JOINTS Specific care depends on the affected joint: Hand: hot soaks and paraffin dips to relieve pain, as ordered. Lumbar and sacral spine: a firm mattress or bed board to decrease morning pain. Cervical spine: cervical collar; check for constriction; watch for redness with prolonged use. Hip: moist heat pads to relieve pain and antispasmodic drugs, as ordered. Assist with range-of-motion and strengthening exercises, always making sure the patient gets the proper rest afterward. Check crutches, cane, braces, and walker for proper fit, and teach the patient to use them correctly. For example, the patient with unilateral joint involvement should use an orthopedic appliance (such as a cane or walker) on the unaffected side. Advise use of cushions when sitting and use of an elevated toilet seat . Knee: assist with prescribed range-of-motion exercises, exercises to maintain muscle tone, and progressive resistance exercises to increase muscle strength. Provide elastic supports or braces if needed. To minimize the long-term effects of osteoarthritis, teach the patient to: plan for adequate rest during the day, after exertion, and at night take medication exactly as prescribed and report adverse effects immediately avoid overexertion, take care to stand and walk correctly, minimize weight-bearing activities, and be especially careful when stooping or picking up objects always wear well-fitting supportive shoes and not let the heels become too worn down install safety devices at home, such as guard rails in the bathroom do range-of-motion exercises as gently as possible maintain proper body weight to lessen strain on joints avoid percussive activities.

Treatment

The goal of treatment is to relieve pain, maintain or improve mobility, and minimize disability. Treatment may include:

• weight loss to reduce stress on the joint
• balance of rest and exercise
• medications, including aspirin, phenylbutazone, indomethacin (Indocin), fenoprofen (Nalfon), ibuprofen (Motrin), and other nonsteroidal anti-inflammatory drugs; propoxyphene (Darvon), celecoxib (Celebrex), and glucosamine (See Specific care for arthritic joints .)
• support or stabilization of joint with crutches, braces, cane, walker, cervical collar, or traction to reduce stress
• intra-articular injections of corticosteroids (every 4 to 6 months) to possibly delay node development in the hands (if used too frequently, may accelerate arthritic progression by depleting the normal ground substance of the cartilage).

Surgical treatment, reserved for patients with severe disability or uncontrollable pain, may include:

• arthroplasty (partial or total replacement of deteriorated part of joint with prosthetic appliance)
• arthrodesis (surgical fusion of bones, primarily in spine [laminectomy])
• osteoplasty (scraping and lavage of deteriorated bone from joint)
• osteotomy (change in alignment of bone to relieve stress by excision of wedge of bone or cutting of bone).

Osteogenesis imperfecta

Osteogenesis imperfecta is a genetic disease in which bones are thin, poorly developed, and fracture easily.

The expression of the disease varies, depending on whether the defect is carried as a trait or is clinically obvious. (See Chapter 4 , “Genetics.”) If it's inherited as an autosomal dominant disorder, a heterozygote may eventually express the disease, which occurs in about 1 in 30,000 people. If inheritance is as an autosomal recessive, the homozygous child will likely die before, during, or soon after birth from multiple fractures sustained in utero or during delivery.

Causes

Causes of osteogenesis imperfecta include:

• genetic disease, typically autosomal dominant (characterized by a defect in the synthesis of connective tissue)
• autosomal recessive carriage of gene defects that produce osteogenesis imperfecta in homozygotes (osteoporosis in some).

Pathophysiology

Most forms of the disease appear to be caused by mutations in the genes that determine the structure of collagen. Possible mutations in other genes may cause variations in the assembly and maintenance of bone and other connective tissues. Collectively or alone, these mutated genes lead to pathologic fractures and impaired healing.

Signs and symptoms

In the autosomal dominant disorder, the following symptoms may not be apparent until the child's mobility increases:

• frequent fractures and poor healing due to falls as toddlers begin to walk
• short stature due to multiple fractures caused by minor physical stress
• deformed cranial structure and limbs from multiple fractures
• thin skin and bluish sclera of the eyes; thin collagen fibers of the sclera allowing the choroid layer to be seen
• abnormal tooth and enamel development due to improper deposition of dentine.

Complications

Possible complications of osteogenesis imperfecta include:

• deafness due to bone deformity and scarring of the middle and inner ear
• stillbirth or death within the first year of life (autosomal-recessive disorder).

Diagnosis

Diagnosis involves:

• fractures early in life, hearing loss, and blue sclerae, showing that mutation is expressed in more than one connective tissue
• elevated serum alkaline phosphatase levels (during periods of rapid bone formation and cellular injury)
• skin culture showing reduced quantity of fibroblasts
• echocardiography, possibly showing mitral regurgitation or floppy mitral valves.

Treatment

Possible treatments are:

• prevention of fractures
• internal fixation of fractures to ensure stabilization.

Osteomalacia and rickets

In Vitamin D deficiency, bone cannot calcify normally; the result is called rickets in infants and young children and osteomalacia in adults.

Once a common childhood disease, rickets is now rare in the United States. It does appear occasionally in breast-fed infants who don't receive a vitamin D supplement or in infants fed a formula with a nonfortified milk base. Rickets also occurs in overcrowded, urban areas where smog limits sunlight penetration.

CULTURAL DIVERSITY Incidence of rickets is highest in children with black or dark brown skin, who, because of their pigmentation, absorb less sunlight. In urban Asia, osteomalacia is most prevalent in young women who have had several children, eat a cereal-based diet, and have minimal exposure to sunlight.

With treatment, the prognosis is good. In osteomalacia, bone deformities may disappear; however they usually persist in children with rickets.

Causes

Causes of osteomalacia and rickets include:

• inadequate dietary intake of preformed vitamin D
• malabsorption of vitamin D
• inadequate exposure to sunlight (solar ultraviolet rays irradiate 7-dehydrocholesterol, a precursor of vitamin D, to form calciferol)
• inherited impairment of renal tubular reabsorption of phosphate (from vitamin D insensitivity) in vitamin D-resistant rickets (refractory rickets, familial hypophosphatemia)
• conditions reducing the absorption of fat-soluble vitamin D (such as chronic pancreatitis, celiac disease, Crohn's disease, cystic fibrosis, gastric or small-bowel resections, fistulas, colitis, and biliary obstruction)
• hepatic or renal disease (interfering with hydroxylated calciferol formation, needed to form a calcium-binding protein in intestinal absorption sites)
• malfunctioning parathyroid gland (decreased secretion of parathyroid hormone), contributing to calcium deficiency (normally, vitamin D controls absorption of calcium and phosphorus through the intestine) and interfering with activation of vitamin D in the kidneys.

Pathophysiology

Vitamin D regulates the absorption of calcium ions from the intestine. When vitamin D is lacking, falling serum calcium concentration stimulates synthesis and secretion of parathyroid hormone, causing release of calcium from bone, decreasing renal calcium excretion, and increasing renal phosphate excretion. When the concentration of phosphate in the bone decreases, osteoid may be produced, but mineralization can't proceed normally. Large quantities of osteoid accumulate, coating the trabeculae and linings of the haversian canals and areas beneath the periosteum.

When mineralization of bone matrix is delayed or inadequate, bone is disorganized in structure and lacks density. The result is gross deformity of both spongy and compact bone.

Signs and symptoms

Osteomalacia may be asymptomatic until a fracture occurs. Chronic vitamin D deficiency induces numerous bone malformations due to bone softening. Possible signs and symptoms include:

• pain in the legs and lower back due to vertebral collapse
• bow legs
• knock knees
• rachitic rosary (beading of ends of ribs)
• enlarged wrists and ankles
• pigeon breast (protruding ribs and sternum)
• delayed closing of fontanels
• softening skull
• bulging forehead
• poorly developed muscles (pot belly)
• difficulty walking and climbing stairs.

Complications

Complications of osteomalacia and rickets may include:

• spontaneous multiple fractures
• tetany in infants.

Diagnosis

Physical examination, dietary history, and laboratory tests establish the diagnosis. Test results that suggest vitamin D deficiency include:

• serum calcium less than 7.5 mg/dl
• serum inorganic phosphorus less than 3 mg/dl
• serum citrate less than 2.5 mg/dl, and alkaline phosphatase less than 4 Bodansky units/dl
• X-rays showing characteristic bone deformities and abnormalities such as Looser's zones (radiolucent bands perpendicular to the surface of the bones indicating reduced bone ossification; confirms the diagnosis).

Treatment

Possible treatments include:

• massive oral doses of vitamin D or cod liver oil (for osteomalacia and rickets, except when caused by malabsorption)
• teaching patient on prolonged vitamin D supplementation signs of vitamin D toxicity (headache, nausea, constipation, and, after prolonged use, renal calculi)
• 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, or a synthetic analogue of active vitamin (for rickets refractory to vitamin D or rickets accompanied by hepatic or renal disease)
• foods high in vitamin D (fortified milk, fish liver oils, herring, liver, and egg yolks) and sufficient sun exposure (obtain a dietary history to assess the patient's current vitamin D intake)
• supplemental aqueous preparations of vitamin D for chronic fat malabsorption, hydroxylated cholecalciferol for refractory rickets, and supplemental vitamin D for breast-fed infants (to prevent rickets).

Osteomyelitis

Osteomyelitis is a bone infection characterized by progressive inflammatory destruction after formation of new bone. It may be chronic or acute. It commonly results from a combination of local trauma ― usually trivial but causing a hematoma ― and an acute infection originating elsewhere in the body. Although osteomyelitis often remains localized, it can spread through the bone to the marrow, cortex, and periosteum. Acute osteomyelitis is usually a blood-borne disease and most commonly affects rapidly growing children. Chronic osteomyelitis, which is rare, is characterized by draining sinus tracts and widespread lesions.

AGE ALERT Osteomyelitis occurs more often in children (especially boys) than in adults ― usually as a complication of an acute localized infection. The most common sites in children are the lower end of the femur and the upper ends of the tibia, humerus, and radius. The most common sites in adults are the pelvis and vertebrae, generally after surgery or trauma.

The incidence of both chronic and acute osteomyelitis is declining, except in drug abusers.

With prompt treatment, the prognosis for acute osteomyelitis is very good; for chronic osteomyelitis, prognosis remains poor.

Causes

The most common pyogenic organism in osteomyelitis is:

• Staphylococcus aureus .

Others include:

• Streptococcus pyogenes
• Pneumococcus species
• Pseudomonas aeruginosa
• Escherichia coli
• Proteus vulgaris
• Pasteurella multocida (part of the normal mouth flora of cats and dogs).

Pathophysiology

Typically, these organisms find a culture site in a hematoma from recent trauma or in a weakened area, such as the site of local infection (for example, furunculosis), and travel through the bloodstream to the metaphysis, the section of a long bone that is continuous with the epiphysis plates, where the blood flows into sinusoids. (See Avoiding osteomyelitis .)

Signs and symptoms

Clinical features of chronic and acute osteomyelitis are generally the same and may include:

• rapid onset of acute osteomyelitis, with sudden pain in the affected bone and tenderness, heat, swelling, and restricted movement
• chronic infection persisting intermittently for years, flaring after minor trauma or persisting as drainage of pus from an old pocket in a sinus tract.

Complications

Possible complications of osteomyelitis include:

• amputation (of an arm or leg when resistant chronic osteomyelitis causes severe, unrelenting pain and decreases function)
• weakened bone cortex, predisposing the bone to pathologic fracture
• arrested growth of an extremity (in children with severe disease).

Diagnosis

Diagnosis must rule out septicemia, foreign bodies, poliomyelitis (rare), rheumatic fever, myositis (inflammation of voluntary muscle), and bone fracture. History, physical examination, and laboratory tests that help confirm osteomyelitis may include:

• history of a urinary tract, respiratory tract, ear, or skin infection; human or animal bite; or other penetrating trauma
• white blood cell count showing leukocytosis
• elevated erythrocyte sedimentation rate
• blood cultures showing causative organism
• magnetic resonance imaging to delineate bone marrow from soft tissue (facilitates diagnosis)
• X-rays (may not show bone involvement until the disease has been active for 2 to 3 weeks)
• bone scans to detect early infection.

Treatment

Treatment for acute osteomyelitis should begin before definitive diagnosis and includes:

• large doses of antibiotics I.V. (usually a penicillinase-resistant penicillin, such as nafcillin [Nafcil]or oxacillin [Bactocill]) after blood cultures are taken
• early surgical drainage to relieve pressure and abscess formation
• immobilization of the affected body part by cast, traction, or bed rest to prevent failure to heal or recurrence
• supportive measures, such as analgesics for pain and I.V. fluids to maintain hydration
• incision and drainage, followed by a culture of the drainage (if an abscess or sinus tract forms).

Antibiotic therapy to control infection may include:

• systemic antibiotics
• intracavitary instillation of antibiotics through closed-system continuous irrigation with low intermittent suction
• limited irrigation with blood drainage system with suction (Hemovac)
• packed, wet, antibiotic-soaked dressings.

Chronic osteomyelitis care may include:

• surgery, usually required to remove dead bone and promote drainage (prognosis remains poor even after surgery)
• hyperbaric oxygen to stimulate normal immune mechanisms
• skin, bone, and muscle grafts to fill in dead space and increase blood supply
• teach patient to avoid jerky movements and falls (may threaten bone integrity); report sudden pain, crepitus, or deformity immediately; watch for sudden malposition of the limb (may indicate fracture).

AVOIDING OSTEOMYELITIS Bones are essentially isolated from the body's natural defense system once an organism gets through the periosteum. Bones are limited in their ability to replace necrotic tissue caused by infection, which may lead to chronic osteomyelitis. <center></center>

Osteoporosis

Osteoporosis is a metabolic bone disorder in which the rate of bone resorption accelerates while the rate of bone formation slows, causing a loss of bone mass. Bones affected by this disease lose calcium and phosphate salts and become porous, brittle, and abnormally vulnerable to fractures. Osteoporosis may be primary or secondary to an underlying disease, such as Cushing syndrome or hyperthyroidism. It primarily affects the weight-bearing vertebrae. Only when the condition is advanced or severe, as in secondary disease, do similar changes occur in the skull, ribs, and long bones. Often, the femoral heads and pelvic acetabula are selectively affected.

Primary osteoporosis is often called senile or postmenopausal osteoporosis because it most commonly develops in elderly, postmenopausal women.

CULTURAL DIVERSITY Persons of African origin have a much lower incidence of osteoporosis than those of European or Asian origin.

Causes

The cause of primary osteoporosis is unknown, but contributing factors include:

• mild but prolonged negative calcium balance due to inadequate dietary intake of calcium (may be an important contributing factor)
• declining gonadal and adrenal function
• faulty protein metabolism due to relative or progressive estrogen deficiency (estrogen stimulates osteoblastic activity and limits the osteoclastic-stimulating effects of parathyroid hormones)
• sedentary lifestyle.

The many causes of secondary osteoporosis include:

• prolonged therapy with steroids or heparin (heparin promotes bone resorption by inhibiting collagen synthesis or enhancing collagen breakdown)
• total immobilization or disuse of a bone (as in hemiplegia)
• alcoholism
• malnutrition
• malabsorption
• scurvy
• lactose intolerance
• endocrine disorders such as hyperthyroidism, hyperparathyroidism, Cushing's syndrome, diabetes mellitus (plasma calcium and phosphate concentrations are maintained by the endocrine system)
• osteogenesis imperfecta
• Sudeck's atrophy (localized to hands and feet, with recurring attacks)
• medications (aluminum-containing antacids, corticosteroids, anticonvulsants)
• cigarette smoking.

Pathophysiology

In normal bone, the rates of bone formation and resorption are constant; replacement follows resorption immediately, and the amount of bone replaced equals the amount of bone resorbed. Osteoporosis develops when the remodeling cycle is interrupted, and new bone formation falls behind resorption.

When bone is resorbed faster than it forms, the bone becomes less dense. Men have approximately 30% greater bone mass than women, which may explain why osteoporosis develops later in men.

Signs and symptoms

Osteoporosis is typically discovered suddenly, such as:

• a postmenopausal woman bends to lift something, hears a snapping sound, then feels a sudden pain in her lower back
• vertebral collapse causes back pain that radiates around the trunk (most common presenting feature) and is aggravated by movement or jarring.

In another common pattern, osteoporosis can develop insidiously, showing:

• increasing deformity, kyphosis, loss of height, decreased exercise intolerance, and a markedly aged appearance
• spontaneous wedge fractures, pathologic fractures of the neck and femur, Colles' fractures of the distal radius after a minor fall, and hip fractures (common as bone is lost from the femoral neck).

Complications

Possible complications of osteoporosis include:

• spontaneous fractures as the bones lose volume and become brittle and weak
• shock, hemorrhage, or fat embolism (fatal complications of fractures).

Diagnosis

Differential diagnosis must exclude other causes of bone loss, especially those affecting the spine, such as metastatic cancer or advanced multiple myeloma. History is the key to identify the specific cause of osteoporosis. Diagnosis may include:

• serial height measurements
• dual- or single-photon absorptiometry to measure bone mass of the extremities, hips, and spine
• X-rays showing typical degeneration in the lower thoracic and lumbar vertebrae (vertebral bodies may appear flattened and may look denser than normal; bone mineral loss is evident in only in later stages)
• computed tomography scan to assess spinal bone loss
• normal serum calcium, phosphorus, and alkaline phosphatase, possibly elevated parathyroid hormone.

Since the advent of readily available bone density measurement, the following studies are seldom done:

• bone biopsy showing thin, porous, but otherwise normal-looking bone
• radionuclide bone scans showing diseased areas as darker portions.

Treatment

Treatment to control bone loss, prevent fractures, and control pain may include:

• physical therapy emphasizing gentle exercise and activity and regular, moderate weight-bearing exercise to slow bone loss and possibly reverse demineralization (the mechanical stress of exercise stimulates bone formation)
• supportive devices, such as a back brace
• surgery, if indicated, for hip fracture
• estrogen during 2 years after menopause to slow bone loss
• analgesics and local heat to relieve pain.

Other medications include:

• calcium and vitamin D supplements to support normal bone metabolism
• calcitonin (Calcimar) to reduce bone resorption and slow the decline in bone mass
• biophosphonates (such as etidronate [Didronel] to increase bone density and restore lost bone
• fluoride (such as alendronate [Fosamax]) to stimulate bone formation; requires strict dosage precautions, and can cause gastric distress
• vitamin C, calcium, and protein to support skeletal metabolism (through a balanced diet rich in nutrients).

Other measures include:

• early mobilization after surgery or trauma
• decreased alcohol and tobacco consumption
• careful observation for signs of malabsorption, (fatty stools, chronic diarrhea)
• prompt, effective treatment of the underlying disorder (to prevent secondary osteoporosis)
• safety precautions for frail patients (keeping side rails up, moving the patient gently and carefully at all times, explaining to the patient's family and ancillary health care personnel how easily an osteoporotic patient's bones can fracture)
• advising patient to report new pain immediately, especially after trauma, no matter how slight
• advising patient to sleep on a firm mattress and avoid excessive bed rest
• teaching the patient good body mechanics, such as stooping before lifting and avoiding twisting movements and prolonged bending
• instructing a female patient taking estrogen in the proper technique for breast self-examination, to perform self-examination at least monthly and to report lumps immediately; to have regular gynecologic exams; and to report abnormal bleeding promptly.

Paget's disease

Paget's disease, also called osteitis deformans, is a slowly progressive metabolic bone disease characterized by accelerated patterns of bone remodeling. An initial phase of excessive bone resorption (osteoclastic phase) is followed by a reactive phase of excessive abnormal bone formation (osteoblastic phase). Chronic accelerated remodeling eventually enlarges and softens the affected bones. The new bone structure, which is chaotic, fragile, and weak, causes painful deformities of both external contour and internal structure. Paget's disease usually localizes in one or several areas of the skeleton (most frequently the lumbosacral spine, skull, pelvis, femur, and tibia are affected), but occasionally skeletal deformity is widely distributed.

CULTURAL DIVERSITY Paget's disease occurs worldwide but is extremely rare in Asia, the Middle East, Africa, and Scandinavia.

In the United States, Paget's disease affects about 2.5 million people older than 40 years (mostly men). It can be fatal, particularly when it's associated with heart failure (widespread disease creates a continuous need for high cardiac output), bone sarcoma, or giant-cell tumors.

Causes

Although the exact cause of Paget's disease is unknown, one theory is that early viral infection causes a dormant skeletal infection that erupts many years later as Paget's disease.

Other possible causes include:

• benign or malignant bone tumors
• vitamin D deficiency during the bone-developing years of childhood
• autoimmune disease
• estrogen deficiency

Pathophysiology

Repeated episodes of accelerated osteoclastic resorption of spongy bone occur. The trabeculae diminish, and vascular fibrous tissue replaces marrow. This is followed by short periods of rapid, abnormal bone formation. The collagen fibers in this new bone are disorganized, and glycoprotein levels in the matrix decrease. The partially resorbed trabeculae thicken and enlarge because of excessive bone formation, and the bone becomes soft and weak.

Signs and symptoms

Clinical effects of Paget's disease vary. Early stages may be asymptomatic. When signs and symptoms appear, they may include:

• usually severe and persistent pain intensifying with weight bearing, possibly with impaired movement due to impingement of abnormal bone on the spinal cord or sensory nerve root (pain may also result from the constant inflammation accompanying cell breakdown)
• characteristic cranial enlargement over frontal and occipital areas (hat size may increase) and possibly headaches, sensory abnormalities, and impaired motor function (with skull involvement).

Other deformities include:

• kyphosis (spinal curvature due to compression fractures of vertebrae)
• barrel chest
• asymmetric bowing of the tibia and femur (often reduces height)
• waddling gait (from softening of pelvic bones)
• warm and tender disease sites susceptible to pathologic fractures after minor trauma
• slow and often incomplete healing of pathologic fractures.

Complications

Possible complications of Paget's disease include:

• blindness and hearing loss with tinnitus and vertigo due to bony impingement on the cranial nerves
• pathologic fractures
• hypertension
• renal calculi
• hypercalcemia
• gout
• heart failure due to high blood flow demands of remodeling bones
• respiratory failure due to deformed thoracic bones
• malignant changes in involved bone (1% of the patients).

Diagnosis

Diagnosis of Paget's disease may include:

• X-rays, computed tomography scan, and magnetic resonance imaging taken before overt symptoms develop showing increased bone expansion and density
• radionuclide bone scan (more sensitive than X-rays) clearly showing early Paget's lesions (radioisotope concentrates in areas of active disease)
• bone biopsy showing characteristic mosaic pattern.

Other laboratory findings include:

• anemia
• elevated serum alkaline phosphatase (an index of osteoblastic activity and bone formation)
• elevated 24-hour urine levels for hydroxyproline (amino acid excreted by kidneys and an index of osteoclastic hyperactivity) and pyridinolines.

Treatment

Primary treatment consists of drug therapy and includes one of the following medications:

• bisphosphonate (alendronate [Fosamax], etidronate [Didronel]) to inhibit osteoclast-mediated bone resorption
• calcitonin (Calcimar, a hormone, and etidronate [Didronel]) to retard bone resorption and reduce serum alkaline phosphate and urinary hydroxyproline secretion (Calcitonin requires long-term maintenance therapy, but improvement is noticeable after the first few weeks of treatment; etidronate produces improvement after 1 to 3 months)
• mithramycin (Mithracin), a cytotoxic antibiotic, to decrease serum calcium, urinary hydroxyproline, and serum alkaline phosphatase levels; produces remission of symptoms within 2 weeks and biochemical improvement in 1 to 2 months, but may destroy platelets or compromise renal function.

Other treatment varies according to symptoms:

• surgery to reduce or prevent pathologic fractures, correct secondary deformities, and relieve neurologic impairment; drug therapy with calcitonin and etidronate or mithramycin must precede surgery to decrease the risk for excessive bleeding from hypervascular bone
• joint replacement (difficult because bonding material [methyl methacrylate] doesn't set properly on pagetic bone)
• aspirin, indomethacin (Indocin), or ibuprofen (Motrin) to control pain
• monitoring for new areas of pain or restricted movements (may indicate new fracture sites) and sensory or motor disturbances, such as difficulty in hearing, seeing, or walking
• instructing the patient to follow specific instructions when taking etidronate or alendronate, to minimize adverse affects and avoid neutralizing effects of drug, and to watch for and report stomach cramps, diarrhea, fractures, and increasing or new bone pain
• instructing the patient taking mithramycin to watch for signs of infection, easy bruising, bleeding, and temperature elevation, and to report for regular follow-up laboratory tests.

Rhabdomyolysis

Rhabdomyolysis, the breakdown of muscle tissue, may cause myoglobinuria, in which varying amounts of muscle protein (myoglobin) appear in the urine. Rhabdomyolysis usually follows major muscle trauma, especially a muscle crush injury.

Long-distance running, certain severe infections, and exposure to electric shock can cause extensive muscle damage and excessive release of myoglobin. Prognosis is good if contributing causes are stopped or disease is checked before damage has progressed to an irreversible stage. Unchecked, it can cause renal failure.

Causes

Possible causes of rhabdomyolysis include:

• familial tendency
• strenuous exertion
• infection
• anesthetic agents (halothane) causing intraoperative rigidity
• heat stroke
• electrolyte disturbances
• cardiac arrhythmias
• excessive muscular activity associated with status epilepticus, electroconvulsive therapy, or high-voltage electrical shock.

Pathophysiology

Muscle trauma that compresses tissue causes ischemia and necrosis. The ensuing local edema further increases compartment pressure and tamponade; pressure from severe swelling causes blood vessels to collapse, leading to tissue hypoxia, muscle infarction, and neural damage in the area of the fracture, and release of myoglobin from the necrotic muscle fibers into the circulation.

Signs and symptoms

Signs and symptoms of rhabdomyolysis include:

• tenderness, swelling, and muscle weakness due to muscle trauma and pressure
• dark, reddish-brown urine from myoglobin.

Complications

Possible complications of rhabdomyolysis are:

• renal failure as myoglobin is trapped in renal capillaries or tubules
• amputation if muscle necrosis is substantial.

Diagnosis

Diagnosis may include:

• urine myoglobin greater than 0.5 μg/dl (evident with only 200 g of muscle damage)
• elevated creatinine kinase (0.5 to 0.95 mg/dl) due to muscle damage
• elevated serum potassium, phosphate, creatinine, and creatine levels
• hypocalcemia in early stages, hypercalcemia in later stages
• computed tomography, magnetic resonance imaging, and bone scintigraphy to detect muscle necrosis
• intracompartmental venous pressure measurements using a wick catheter, needle, or slit catheter inserted into the muscle.

Treatment

Treatment of rhabdomyolysis may include:

• treating the underlying disorder
• preventing renal failure
• bed rest
• anti-inflammatory agents
• corticosteroids (in extreme cases)
• analgesics for pain
• immediate fasciotomy and debridement (if compartment venous pressure is greater than 25 mm Hg).

Scoliosis

Scoliosis is a lateral curvature of the thoracic, lumbar, or thoracolumbar spine. The curve may be convex to the right (more common in thoracic curves) or to the left (more common in lumbar curves). Rotation of the vertebral column around its axis may cause rib cage deformity. Scoliosis is often associated with kyphosis (humpback) and lordosis (swayback).

About 2% to 3% of adolescents have scoliosis. In general, the greater the magnitude of the curve and the younger the child at the time of diagnosis, the greater the risk for progression of the spinal abnormality. Favorable outcomes are usually achieved with optimal treatment.

Types of structural scoliosis are:

• congenital, such as wedge vertebrae, fused ribs or vertebrae, or hemivertebrae
• paralytic or musculoskeletal, developing several months after asymmetric paralysis of the trunk muscles due to polio, cerebral palsy, or muscular dystrophy
• idiopathic (most common), may be transmitted as an autosomal dominant or multifactorial trait (appears in a previously straight spine during the growing years).

Idiopathic scoliosis can be further classified according to age at onset:

• infantile (affects mostly male infants between birth and 3 years and causes left thoracic and right lumbar curves)
• juvenile (affects both sexes between the ages of 4 and 10 years and causes varying types of curvature)
• adolescent (generally affecting girls from the age of 10 years until skeletal maturity and causing varying types of curvature).

Causes

Scoliosis may be functional or structural. Possible causes include:

• functional: poor posture or a discrepancy in leg lengths, not fixed deformity of the spinal column (postural scoliosis)
• structural: deformity of the vertebral bodies leading to curvature.

Pathophysiology

Differential stress on vertebral bone causes an imbalance of osteoblastic activity; thus the curve progresses rapidly during adolescent growth spurt. Without treatment, the imbalance continues into adulthood.

Signs and symptoms

Scoliosis rarely produces subjective symptoms until it's well established. When symptoms occur, they include:

• backache
• fatigue
• dyspnea.

The most common curve in functional or structural scoliosis arises in the thoracic segment, with convexity to the right and compensatory curves (S curves) in the cervical and lumbar segments, both with convexity to the left. As the spine curves laterally, compensatory curves develop to maintain body balance. Subtle signs include:

• uneven hemlines or pant legs that appear unequal in length
• one hip that appears higher than the other.

Physical examination shows:

• unequal shoulder heights, elbow levels, and heights of iliac crests
• asymmetric thoracic cage and misalignment of the spinal vertebrae when the patient bends over
• asymmetric paraspinal muscles, rounded on the convex side of the curve and flattened on the concave side
• asymmetric gait.

Complications

Without treatment, curves greater than 40 degrees progress. Untreated scoliosis may result in:

• pulmonary insufficiency (curvature may decrease lung capacity)
• back pain
• degenerative arthritis of the spine
• vertebral disk disease
• sciatica.

Diagnosis

Diagnosis of scoliosis includes:

• anterior, posterior, and lateral spinal X-rays, taken with the patient standing upright and bending (confirm scoliosis and determine the degree of curvature [Cobb method] and flexibility of the spine)
• scoliometer to measure the angle of trunk rotation.

Treatment

The severity of the deformity and potential spine growth determine appropriate treatment, which may include:

• close observation
• exercise
• brace
• surgery
• a combination of these.

To be most effective, treatment should begin early, when spinal deformity is still subtle. For a curve less than 25 degrees, or mild scoliosis, treatment includes:

• X-rays to monitor curve
• examination every 3 months
• exercise program to strengthen torso muscles and prevent curve progression.

For a curve of 30 to 50 degrees:

• spinal exercises and a brace (may halt progression but doesn't reverse the established curvature); braces can be adjusted as the patient grows and worn until bone growth is complete)
• transcutaneous electrical stimulation (alternative therapy).

A lateral curve continues to progress at the rate of 1 degree a year even after skeletal maturity. For a curve of 40 degrees or more, treatment includes:

• surgery (supportive instrumentation, with spinal fusion in severe cases)
• periodic postoperative checkups for several months to monitor stability of the correction.

Sprains

A sprain is a complete or incomplete tear of the supporting ligaments surrounding a joint. It usually follows a sharp twist. An immobilized sprain may heal in 2 to 3 weeks without surgical repair, after which the patient can gradually resume normal activities. A sprained ankle is the most common joint injury, followed by sprains of the wrist, elbow, and knee.

Causes

Causes of sprains include:

• sharply twisting with force stronger than that of the ligament, inducing joint movement beyond normal range of motion
• concurrent fractures or dislocations.

Pathophysiology

When a ligament is torn, an inflammatory exudate develops in the hematoma between the torn ends. Granulation tissue grows inward from the surrounding soft tissue and cartilage. Collagen formation begins 4 to 5 days after the injury, eventually organizing fibers parallel to the lines of stress. With the aid of vascular fibrous tissue, the new tissue eventually fuses with surrounding tissues. As further reorganization takes place, the new ligament separates from the surrounding tissue, and eventually becomes strong enough to withstand normal muscle tension.

Signs and symptoms

Possible signs and symptoms of sprain are:

• localized pain (especially during joint movement)
• swelling and heat due to inflammation
• loss of mobility due to pain (may not occur until several hours after the injury)
• skin discoloration from blood extravasating into surrounding tissues.

Complications

Possible complications of sprain include:

• recurring dislocation due to torn ligaments that don't heal properly, requiring surgical repair (occasionally)
• loss of function in a ligament (if a strong muscle pull occurs before it heals and stretches it, it may heal in a lengthened shape with an excessive amount of scar tissue).

Diagnosis

Sprain may be diagnosed by:

• history of recent injury or chronic overuse
• X-ray to rule out fractures
• stress radiography to visualize the injury in motion
• arthroscopy
• arthrography.

MUSCLE-TENDON RUPTURES Perhaps the most serious muscle-tendon injury is a rupture of the muscle-tendon junction. This type of rupture may occur at any such junction, but it's most common at the Achilles tendon, which extends from the posterior calf muscle to the foot. An Achilles tendon rupture produces a sudden, sharp pain and, until swelling begins, a palpable defect. This rupture typically occurs in men between the ages of 35 and 40 years, especially during physical activities such as jogging or tennis. To distinguish an Achilles tendon rupture from other ankle injuries, perform this simple test: With the patient prone and his feet hanging off the foot of the table, squeeze the calf muscle. The response establishes the diagnosis: plantar flexion, the tendon is intact ankle dorsiflexion, it's partially intact no flexion of any kind, the tendon is ruptured. An Achilles tendon rupture usually requires surgical repair, followed by a long leg cast for 4 weeks, and then a short cast for an additional 4 weeks.

Treatment

Treatment to control pain and swelling includes:

• immobilizing the injured joint to promote healing
• elevating the joint above the level of the heart for 48 to 72 hours (immediately after the injury)
• intermittently applying ice for 12 to 48 hours to control swelling (place a towel between the ice pack and the skin to prevent a cold injury)
• an elastic bandage or cast, or if the sprain is severe, a soft cast or splint to immobilize the joint
• codeine or another analgesic (if injury is severe)
• crutch and gait training (sprained ankle)
• immediate surgical repair to hasten healing, including suturing the ligament ends in close approximation (some athletes)
• tape wrists or ankles before sports activities to prevent sprains (athletes).

Strains

A strain is an injury to a muscle or tendinous attachment usually seen after traumatic or sports injuries. Strain is a general term for muscle or tendon damage that often results from sudden, forced motion causing it to be stretched beyond normal capacity. Injury ranges from excessive stretch (muscle pull) to muscle rupture. (See Muscle-tendon ruptures .) If the muscle ruptures, the body of the muscle protrudes through the fascia. A strained muscle can usually heal without complications.

AGE ALERT Tendon rupture is more common in the elderly; muscle rupture, in the young.

Causes

Possible causes of strain include:

• vigorous muscle overuse or overstress, causing the muscle to become stretched beyond normal capacity, especially when the muscle isn't adequately stretched before the activity (acute strain)
• knife or gunshot wound causing a traumatic rupture (acute strain)
• repeated overuse (chronic strain).

Pathophysiology

Bleeding into the muscle and surrounding tissue occurs if the muscle is torn. When a tendon or muscle is torn, an inflammatory exudate develops between the torn ends. Granulation tissue grows inward from the surrounding soft tissue and cartilage. Collagen formation begins 4 to 5 days after the injury, eventually organizing fibers parallel to the lines of stress. With the aid of vascular fibrous tissue, the new tissue eventually fuses with surrounding tissues. As further reorganization takes place, the new tendon or muscle separates from the surrounding tissue and eventually becomes strong enough to withstand normal muscle strain. If a muscle is chronically strained, calcium may deposit into a muscle, limiting movement by causing stiffness, and muscle fatigue.

Signs and symptoms

Signs and symptoms of acute strain include:

• sharp, transient pain (myalgia)
• snapping noise
• rapid swelling that may continue for 72 hours
• limited function
• tender muscle (when severe pain subsides)
• ecchymoses (after several days).

Signs and symptoms of chronic strain include:

• stiffness
• soreness
• generalized tenderness.

Complications

Possible complications of strain include:

• complete muscle rupture requiring surgical repair
• myositis ossificans (chronic inflammation with bony deposits) due to scar tissue calcification (late complication).

Diagnosis

Diagnosis of strain may include:

• history of a recent injury or chronic overuse
• X-ray to rule out fracture
• stress radiography to visualize the injury in motion
• biopsy showing muscle regeneration and connective tissue repair (rarely done).

Treatment

Possible treatments for acute strain includes:

• compression wrap to immobilize the affected area
• elevating the injured part above the level of the heart to reduce swelling
• analgesics
• application of ice for up to 48 hours, then application of heat to enhance blood flow, reduce cramping, and promote healing
• surgery to suture the tendon or muscle ends in close approximation.

Chronic strains usually don't need treatment. Discomfort may be relieved by:

• heat application
• nonsteroidal anti-inflammatory drugs (such as ibuprofen [Motrin])
• analgesic muscle relaxant.