28

Orthopedic Surgery: Diseases of the Musculoskeletal

System
John J. Murnaghan and Justin Siebler

The musculoskeletal system is composed of connective tissue of mesodermal origin. Bones, joints, muscles,
tendons, ligaments, and aponeurotic fascia constitute 70% of total body mass. Although disorders of the
musculoskeletal system do not usually affect longevity, they frequently interfere with the quality of life and
consume a significant portion of U.S. health care resources. Musculoskeletal problems are the second most
frequent cause of visits to a physician and are second in the consumption of health care dollars. Forty percent
of emergency room visits are related to musculoskeletal problems. It is estimated that osteoporosis affects
more than 20 million postmenopausal women and that associated hip fractures occupy almost 20% of surgical
hospital beds. Back pain is the most common cause of time lost from work and disability in patients younger
than 45 years. The annual cost of treatment and compensation for back conditions is greater than $14 billion.
These statistics make it is clear that a working understanding of the musculoskeletal system is necessary to all
physicians, especially those who practice primary care.

TRAUMA

FRACTURES, SUBLUXATIONS, AND DISLOCATIONS

A fracture is a break or loss of structural continuity in a bone. In a subluxation, the normally apposing joint
surfaces are partially out of contact (Figure 28-1A). In a dislocation, those surfaces are completely out of
contact (see Figure 28-1B). Joint subluxation may be a transient phenomenon in which the joint surfaces
approach dislocation but reduces spontaneously.

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Figure 28-1 A, Subluxation is a partial displacement of apposing joint surfaces. This phenomenon may be
transient and reduce itself. B, Dislocation is complete displacement of apposing joint surfaces. A reduction
maneuver is often needed to restore joint alignment. (Modified with permission from Rockwood C, Green D.
Fractures in Adults. 3rd ed. Philadelphia, PA: JB Lippincott; 1982:1193.)

Fractures

Description
Knowledge of the accepted fracture nomenclature allows for communication between medical colleagues and
may affect decision making. It is essential to describe fractures in a precise and detailed manner. Fractures are
described according to type, site, pattern, amount of displacement, and angulation. In children, injuries can
affect the growth plate and are described according to the Salter-Harris classification.

Type
Fractures are either open or closed. A fracture is open when there is a break in the surrounding skin or
mucosa that allows the fracture to communicate with the external environment. Although most open fractures
are obvious to cursory inspection, others, such as pelvic fractures, may communicate with the rectum or vagina
and are discovered only in the course of a thorough physical examination. All open fractures are, by definition,
contaminated and require emergency treatment to prevent infection. A fracture is closed when the skin or
overlying mucosa is intact.
Fractures usually are the result of a single forceful impact. However, repeated submaximal stress can
produce microscopic fractures, which, if not allowed to heal, will coalesce into a stress fracture. Stress
fractures are frequently seen in army recruits or in insufficiently conditioned patients who participate in
vigorous athletic training routines. A fracture produced by minimal trauma through abnormal bone is termed
a pathologic fracture. Pathologic fractures occur in bone that is weakened by metabolic bone diseases (e.g.,

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osteoporosis) or in bone weakened by primary or metastatic tumors.

Site
When describing the location of a fracture, the bone affected is identified, as well as the specific site involved,
such as the proximal or distal epiphysis, metaphysis, or diaphysis (Figure 28-2). A fracture in the epiphyseal
region suggests intra-articular fracture extension that would violate the joint surface and could result in
traumatic arthritis. By convention, the diaphysis of a long bone is described in thirds: proximal, middle, or
distal (Figure 28-2). Fracture location has implications for healing and treatment. Fractures of metaphyseal or
cancellous (spongy) bone with a rich blood supply and high bone turnover rates usually heal quite rapidly. In
contrast, cortical, diaphyseal bone heals more slowly. Diaphyseal fractures, therefore, require lengthier periods
of stress protection by immobilization or protection from weight bearing.

Figure 28-2 Anatomic regions of a long tubular bone. (From Lawrence PF. Essentials of Surgical Specialties. 3rd
ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

Pattern
The fracture pattern suggests the type and amount of kinetic energy imparted to the bone. A transverse
fracture (Figure 28-3A) is a low-energy injury, usually the result of either a direct blow to a long bone or a
ligament avulsion. A “nightstick” fracture is a transverse fracture of the ulna that occurs when the forearm
receives a direct blow. Stress and pathologic fractures usually have a transverse pattern. Spiral or oblique
fractures (see Figure 28-3B and C) result from a rotatory, twisting injury. These fractures have a tendency to
displace and shorten after reduction and immobilization. A fracture with more than two fragments is termed
comminuted or multifragmented. The middle fragment may be triangular and is called a butterfly fragment

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(Figure 28-4A); when cylindrical in configuration, it is described as segmental (Figure 28-4B). Comminuted
fractures occur as a result of larger forces and imply greater degrees of damage to the intramedullary blood
supply to the bone and surrounding soft tissues, which may compromise the healing of one or both fracture
sites. An impacted fracture (Figure 28-5A; also see Figure 28-15) is commonly seen in metaphyseal bone,
such as with femoral neck, distal radius, or tibial plateau fractures. These are low-energy injuries in which two
bone fragments are jammed together. A compression fracture signifies that trabecular or cancellous bone is
crushed; it often occurs in vertebral bodies (Figure 28-5B). Although most bone fractures are complete, an
incomplete buckling of only one cortex is seen in children and is known as a greenstick fracture (Figure 28-6).

Figure 28-3 Common fracture patterns. A, Transverse fracture. B, Spiral fracture. C, Oblique fracture. (From
Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2007.)

Figure 28-4 Comminuted fractures. A, Triangular butterfly fragment. B, Cylindrical segmental fracture. (From
Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins;

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2007.)

Figure 28-5 A, Impacted femoral neck fracture. B, Anterior compression fracture of vertebral body. (From
Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2007.)

Figure 28-6 Greenstick fracture of the ulna in which only one cortex is broken (arrowd with its apex anterior.
The fracture must be completed (the other cortex broken) to prevent angular deformity. Greenstick fractures
typically occur in children whose bones are more plastic and less brittle than those of adults. (From Lawrence
PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

Displacement
Fractured bone fragments may be displaced by the force of an injury, gravity, or muscle pull. Displacement is
described in terms of distance or bone diameters in the anterior–posterior (AP), medial–lateral, and length
(either shortening or distraction).
Displacement is measured in both the mediolateral (coronal) and the anteroposterior (sagittal) planes. The
position of the distal fragment is always named relative to the proximal fragment. This naming convention is
helpful, because most fractures are aligned by reducing the displaced distal fragment to the proximal one.
Fracture displacement is customarily quantified as a percentage (Figure 28-7). This description can be
misleading because 50% posterior (Figure 28-7B) and 50% lateral displacement (Figure 28-7A), may, when
viewed in three dimensions, represent only 25% bone apposition (Figure 28-7C). Angulation is the
relationship between the long axis of the distal fragment to the long axis of the proximal fragment. It may be

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described by one of two conventions. In the first convention, the direction to which the distal fragment is
inclined is identified (Figure 28-8). In the second convention, the location of the fracture angle apex is
described. Reference to either the distal fragment or apical angulation should be mentioned in reports of
fracture alignment. For example, in Figure 28-8, the distal fragment is inclined in the posterior and lateral
directions, or the fracture apex is angled anteromedially.

Figure 28-7 Fracture displacement. A, The anterior–posterior (AP) view shows approximately 50% lateral
displacement of the distal fragment. B, The lateral view shows 50% posterior displacement of the distal femur.
C, Additively in three dimensions, the amount of bone apposition is approximately 25%, an amount that is
underestimated by either view (A or B) in isolation. (From Lawrence PF. Essentials of Surgical Specialties. 3rd
ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

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Figure 28-8 A, On the anterior–posterior view (coronal plane), the distal fragment is angulated laterally, and the
fracture angle apex is medial. B, On the lateral view (sagittal plane), the distal fragment is angulated
posteriorly, and the angle apex is anterior. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

The terms varus and valgus are also used in the descriptions of fractures and limb deformity. These terms
refer to the direction of an angular deformity in relation to the midline of the body. If the deformity apex is
pointed away from the midline (Figure 28-9A), the term varus is used. If the deformity apex is directed
toward the midline (Figure 28-9B), it is called valgus. Thus, bowlegs in which the deformity apex at the knee
(genu) is away from the midline are called genu varum, whereas knock-knees are called genu valgum.

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Figure 28-9 The terms varus and valgus refer to the relation of a deformity to the midline of the body. A, Genu
varum, or bowlegs, occurs when the deformity apex is pointing away from the midline. B, Genu valgum, or
knock-knees, occurs when the deformity apex is directed toward the midline; it is called valgus. In knock-
knees, the knee resembles the letter L, which is a helpful mnemonic in distinguishing between these confusing
terms.

Fracture apposition, angulation, and shortening are quantified in percentage, degrees, and centimeters,
respectively, from radiographs. Rotation describes angular shifts around the long axis of the bone. It is best
judged clinically. Rotational deformity is expressed by identifying the position of the distal fragment as it
relates to the proximal one. For example, if the foot is twisted outward, the fracture is externally rotated.

The Salter-Harris Classification of Growth Plate Fractures

In children, the growth plate (physis) is the growing zone of cartilage situated between the epiphysis and the
metaphysis of long bones. Cartilage is weaker than bone, and thus it is a common site of injury. The Salter-
Harris classification of growth plate injuries is descriptive, is generally recognized, and has important
prognostic implications (Figure 28-10).

Figure 28-10 Salter-Harris classification of pediatric growth plate fractures. The greater the classification

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number is, the more violent the injury is to the epiphyseal plate and the greater the risk is for long bone
growth and healing problems. (Reprinted with permission from Rang MC. Children’s Fractures. 2nd ed.
Philadelphia, PA: JB Lippincott; 1983.)

The Salter-Harris type I fracture is a separation of the epiphysis from the metaphysis (Figure 28-10). If
the periosteum is not torn, the fracture remains undisplaced. In this injury, there is tenderness over the growth
plate. The Salter-Harris type II fracture passes through the growth plate and exits through the metaphysis.
This fracture is due to a bending movement that tears periosteum on the side opposite the triangular
metaphyseal fragment. In a Salter-Harris type III injury, the fracture extends from the growth plate through
the epiphysis to enter the joint. This fracture is intra-articular and requires a perfect reduction to avoid
arthritic sequelae. The Salter-Harris type IV fracture line extends from the metaphysis through the growth
plate cartilage into the epiphysis. This fracture pattern is also intra-articular. These fractures must be
operatively fixed to prevent nonunion and joint surface incongruity. Salter-Harris types III and IV fractures
have the highest incidence of growth disturbance if not properly managed. A Salter-Harris type V fracture
involves a crushing of the epiphyseal growth plate. These injuries may not be apparent on radiographs and are
therefore difficult to identify prospectively. The type V injury causes a bony bar to replace the injured section
of the growth plate, which will result in asymmetrical, angular growth.
Growth plate injuries, no matter how trivial, have the potential to cause growth disturbance of the
involved long bone. The larger Salter-Harris numbers represent greater degrees of injury to the growth plate.
Consequently, the type IV fracture has a poorer prognosis and higher incidence of growth disturbance than
the type I injury. The possibility of a growth disturbance requires that all growth plate fractures be followed
radiographically for at least 1 year after injury.

Evaluation of Patients with Musculoskeletal Trauma

The patient usually has a history of injury, although in pathologic fractures the injury may be minimal. In
children, either a limp or the refusal to use an extremity suggests a possible fracture. Symptoms of
musculoskeletal injury include pain, swelling, and deformity. Bony tenderness, crepitus, or deformity strongly
suggests a fracture. The examiner should inspect the extremity circumferentially for small puncture wounds.
Vascular integrity (pulses, capillary return) and neurologic status (sensory, motor, and reflex functions) must
be assessed and documented. Active motion of articulations distal to the fracture site implies an element of
soft tissue integrity and neurologic function. The two most important clinical features of the fracture (whether
it is open or not and whether the neurovascular status is compromised) are determined by clinical examination
before x-ray films are obtained.
A complete radiologic evaluation includes the following:

1. Two views of the affected bone or joint at right angles to each other must be taken. Because fractures
occur in three dimensions, a single radiographic view will not permit an accurate description (i.e.,
displacement and angulation) of the injury (see Figure 28-7). Two views taken perpendicular to each
other, usually an AP and a lateral view, meet these requirements.
2. The joint above and the joint below the injured area must be visualized. It is not uncommon for a knee
injury or hip fracture to be associated with a fracture of the femoral shaft.

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 3. Known injury associations warrant special radiographic examination. Cervical spine radiographs are
mandatory in all patients with facial and head injuries; hip dislocations are associated with high-energy
injuries to the knee. Fractures of the axial skeleton (spine and pelvis) occur with injuries to the thoracic,
abdominal, or pelvic viscera, as well as neural structures.
4. If a fracture is not evident radiographically but is suspected clinically (e.g., scaphoid fracture), the patient
will not be harmed if the extremity is immobilized and reassessed. Repeated radiographs, stress views, or
other imaging techniques—such as bone scan, computed tomography (CT), or magnetic resonance
imaging (MRI)—may be needed to establish the diagnosis.

Although rare, trauma patients with long bone fractures are prone to fat embolism. Clinical examination
should watch for petechiae in conjunction with alteration of mental status. Patients are often dyspneic and
have low oxygen saturation. Chest x-ray films reveal diffuse opacification without focal findings. Fat
embolism syndrome is a clinical diagnosis because there is no specific laboratory finding. Treatment is
supportive and in severe cases may require intubation and positive pressure ventilation with up to 100% O2.

Principles of Fracture Management

A patient with a fracture should be initially managed as a trauma patient (see Chapter 9) with life-threatening
conditions treated first. All musculoskeletal injuries must be splinted in the field, and splints should remain in
place whenever the patient is transported. Splinting prevents fracture motion, thus minimizing further
damage to the surrounding soft tissues (nerves, blood vessels, and muscle; see Figure 28-16), limits blood loss,
and decreases the pain of injury. Proper splinting requires that the joint above and the one below the fracture
site be immobilized. Similarly, with a dislocation, the bone above and the bone below the joint should be
splinted. It is essential to check the integrity of neural and vascular structures distal to any fracture site. Repeat
evaluation of these clinical exam findings should be performed after any reduction or manipulations of the
fractured extremity.
All open fractures are considered contaminated with bacteria, and treatment is aimed at preventing
subsequent infection. The wound is examined once, covered with a sterile dressing, and the extremity is
splinted. Tetanus prophylaxis is administered if necessary (see Chapter 8) and antibiotic treatment initiated.
Intravenous first-generation cephalosporin is used for mildly contaminated wounds. Extensive open wounds
or those that occurred in barnyards should receive an aminoglycoside and metronidazole (Flagyl) in addition.
If needed, surgical debridement and irrigation is usually performed in the operating room under general
anesthesia. All tissue layers are examined, foreign material and devitalized tissue are removed, and the wound
is copiously irrigated. The severity of the wound determines the closure technique: primary versus
orthoplastics soft tissue reconstruction; however, not until a clean healthy wound is achieved can fracture
treatment be performed.
Fracture management requires knowledge of the stages of fracture healing (Table 28-1). The two
principles of fracture care are obtaining a reduction and maintaining this reduction until the bone heals while
preserving the bone’s blood supply.

TABLE 28-1 Stages of Fracture Healing

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Hematoma formation (immediate)

Inflammation and cellular proliferation (hours to weeks)

Soft callus formation (2 d–6 wk)

Chondrogenic and osteogenic cell proliferation; formation of woven or fibrous bone

Hard callus formation (10 d–4 mo)

Consolidation; transformation of woven bone to lamellar bone

Bone remodeling (2–24 mo)

Callus remodeling and resorption, with reconstitution of the medullary cavity

Reduction
Fracture deformity is reduced to restore bone apposition and alignment and can be achieved by either closed
or open methods. Closed reduction involves the manipulation of the fracture into a functional position with
traction applied to the distal segment to separate the impacted fragments and force applied to provide
realignment. When an open reduction is required, the fracture is surgically exposed, and bone fragments are
manipulated directly. Open reduction is indicated when closed reduction methods fail, with most displaced
fractures in weight-bearing bones, or with intra-articular fractures in which the joint surface must be perfectly
restored to prevent the development of posttraumatic arthritis.

Maintenance of Reduction
Once the fracture has been reduced, alignment must be maintained until the process of bone healing is
completed. Maintaining alignment requires some form of fracture immobilization, which may include casting,
traction, functional bracing, and internal or external fixation. The type of immobilization employed depends
on fracture stability or its propensity for displacement, with the traditional method of immobilization most
commonly being a circumferential plaster or fiberglass cast. A cast protects and maintains fracture alignment
until healing occurs. Early clinical and radiographic follow-up is necessary to ensure that fracture reduction is
not lost as swelling diminishes.
Continuous traction applied through the skin, the skeleton, or by gravity is a technique that can both
effect and maintain reduction. Skin traction is useful in small children or to temporarily splint an adult with a
hip fracture before surgery. Skeletal traction requires that a pin be inserted through bone distal to the fracture
site. Large distraction forces can then be applied directly to the bone and can overcome the contractile forces
of large muscles in patients with pelvic, femoral, or tibial fractures (Figure 28-11). Gravity acting through a
dependent extremity can also act as a traction force. In humeral fractures, the weight of the distal arm applies
traction if the body is kept upright (Figure 28-12A). Application of a forearm cast can augment this type of
traction (Figure 28-12B). This technique is rarely used and largely replaced by functional bracing.

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Figure 28-11 A, Skeletal traction applied through a pin placed in the tibia is useful for treating femur or pelvic
fractures. B, The leg is supported in a suspension apparatus, and the foot of the bed is raised to permit body
weight and gravity to act as countertraction. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

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Figure 28-12 Gravity traction. A, With the weight of the arm supported by a collar and cuff. B, With a hanging
cast. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2007.)

Several complications are associated with casts and traction. Circumferential bandages may cause
circulatory impairment in acutely traumatized limbs in which further swelling is expected. To prevent this
complication, a splint is generally used in the acute treatment of fractures, which is then replaced by a
circumferential cast after initial swelling subsides. A cast or dressing that is too tight must be completely
released to the level of skin. Excessive traction can cause nonunion and peripheral nerve injury. Ulcerative skin
problems may occur with both skin and skeletal traction. Skeletal traction causes frictional shearing forces
between the patient’s sacrum and the bed, which can result in a sacral decubitus ulcer. A poorly applied cast
can cause a pressure ulcer over an inadequately padded bony prominence or a displaced bone end. Joint
stiffness and muscle atrophy are common problems after prolonged immobilization.
Functional braces that are used most often for humeral shaft fractures allow for early joint motion while
maintaining fracture alignment through a compressive hydraulic effect on the soft tissues. Conversion from a
cast or splint to a functional brace after early evidence of fracture healing hastens both healing and
rehabilitation.
Internal fixation devices include pins, screws, plates (Figure 28-13), circumferential wires or bands, and
intramedullary rods (see Figure 28-19). Indications for internal fixation are listed in Table 28-2. Metallic
fracture fixation implants may appear sturdy on radiographs. However, like a cast, they simply position the
fracture until healing is complete. Fracture fixation hardware should be considered an internal splint that must
respect the biology of fracture healing. The mere presence of an internal fixation device does not guarantee
fracture healing. If the fracture does not unite, repetitive (cyclic) loading of a fracture implant will ultimately

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lead to its loosening or to breakage. Whenever internal fixation is employed, there is a race between fracture
healing and implant failure. Although internal fixation enhances early patient mobility, it has a number of
potential complications. Internal fixation requires a surgical exposure that itself can devitalize tissue and adds
to the risk of infection and nonunion. A second surgical procedure may be needed if the implant is to be
removed. Finally, after hardware removal, the bone can refracture through screw holes, especially when they
are in cortical, diaphyseal bone.

TABLE 28-2 Indications for Internal Fixation of a Fracture

Failure of nonoperative reduction methods

Anatomic reduction of intra-articular fractures

Fractures not amenable to traction or cast immobilization (e.g., femoral neck fractures, intertrochanteric fractures in the elderly)

Pathologic fractures

Multiple fractures in the same extremity or same patient

Fractures in paraplegics (to assist nursing care)

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Figure 28-13 Radiographs of a comminuted ankle fracture. A, Anterior–posterior radiograph. B, Lateral
radiograph. C, Intra-articular fracture treated with a complex array of internal fixation plates and screws.
(From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2007.)

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 External fixation is a minimally invasive method of maintaining fracture alignment. Threaded pins are
placed into the bone above and below the fracture site and are attached to an external frame to immobilize the
fracture (Figure 28-14). Indications for external fixation are listed in Table 28-3. Complications include pin
track infection and delayed union.

TABLE 28-3 Indications for External Fixation of a Fracture

Open, unstable fractures (to allow access to and care of the wound and to avoid the use of internal fixation devices in contaminated
wounds)

Infected fractures

Unstable pelvic fractures

Severely comminuted or unstable fractures not amenable to internal fixation

Fractures involving bone loss in which bone length must be maintained until a bone graft can be performed

Figure 28-14 Severely comminuted open tibia fracture treated with an external fixator. This form of fixation
immobilizes the fracture yet permits access to the wound for observation and care. (From Lawrence PF.
Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

Rehabilitation of Function
Rehabilitation planning begins with the initial phases of fracture management. To avoid joint stiffness
common to periarticular and intra-articular fractures, the limb is immobilized in a position of maximum
function. Isometric exercises of immobilized muscles are started to avoid excessive atrophy. Range-of-motion
exercises for adjacent joints that are not immobilized are encouraged from the onset of care. After a cast or
brace is removed, active range-of-motion and resistive muscle strengthening exercises are initiated.
The speed of rehabilitation depends on the rate and quality of fracture healing. Exuberant rehabilitative
activities or exercises may result in delayed healing, implant failure, and loss of reduction. A rational
rehabilitation plan incorporates those factors that influence the speed and success of fracture healing. These
factors include the amount of energy imparted to the bone during injury (open, multifragmented, and
displaced fractures heal slowly), the type of bone involved (cancellous or cortical), the integrity of the soft
tissue envelope, and the patient’s general health or nutritional status and age (children heal more rapidly than

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adults).
Bone healing is evaluated clinically and radiologically. Clinically, healing is evident when the fracture is no
longer tender to palpation or mobile when stressed. Radiographically, healing is evident when distinct bony
trabeculae are seen crossing the fracture site on radiographic images.

Complications of Fracture Healing

Local Complications
Local complications of fracture healing include infection, delayed union, nonunion, malunion, avascular
necrosis, and, in children, growth disturbances. Fractures that are open, either from injury or surgical
intervention, have a higher incidence of infection than closed fractures. Delayed union is characterized by
fracture healing that appears to be taking longer than usual. Nonunion is characterized by incomplete fracture
healing. The nonunited fracture gap may be filled with fibrous tissue or, if subjected to significant motion,
may form a synovial membrane with joint fluid called a pseudarthrosis (a “false joint”). Delayed unions and
nonunions are caused by fracture separation, soft tissue interposition, excessive fracture motion, inadequate
vascularization of the fracture segments, or infection. When a fracture heals with a deformity that causes
cosmetic or functional impairment, it is called a malunion. Malunited fractures can be shortened, angulated,
or rotated. A corrective osteotomy may be required to regain alignment and function.
Avascular necrosis occurs when the blood supply to a bone is injured by the traumatic event (see section on
Bone Necrosis later in this chapter). Bones that are extensively covered by articular cartilage and have a
minimal muscular envelope are particularly vulnerable to osteonecrosis (e.g., the femoral head, the scaphoid,
or the talus).
Growth disturbance is a fracture complication specific to children. The epiphyseal plate is composed of
cartilage and is the site of longitudinal growth in bones. Because cartilage is weaker than bone, the growth
plate is often involved in pediatric fractures. Fractures in children may damage the growth plate, especially by
compressive or shearing mechanisms. When the entire growth plate is damaged, growth will cease, and the
affected limb will be shorter than the unaffected limb by the end of growth. If only part of the epiphyseal plate
is damaged, the bone may grow asymmetrically and cause an angular deformity. A growth plate injury can be
detected only by serial radiographs. Most growth plate problems can be identified by radiographs taken at the
1-year anniversary of the injury, a date that parents should mark down so they are reminded to present for
follow-up radiographs. Lower limb shortening of less than 1 cm is well tolerated; shortening between 1 and 2
cm can be managed by a shoe lift. A leg length discrepancy of more than 2 cm can be corrected by fusion of
the opposite growth plate, a procedure known as epiphysiodesis. The timing of this procedure is calculated
from growth tables. Angular deformity from a partial growth plate arrest is managed surgically and is best
handled when diagnosed early.
Posttraumatic arthritis is a complication of displaced intra-articular fractures. Articular cartilage has no
blood supply and depends on synovial fluid for nourishment. When injured, articular cartilage has minimal
healing potential. If intra-articular fractures are not anatomically reduced, the irregular surface may cause
rapid arthritic change.
Arthritis can also develop indirectly from a severe angular deformity. Weight-bearing forces can be
concentrated in the part of the joint causing abnormal stress concentration and joint wear. Depending on the

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magnitude of injury, posttraumatic arthritis can occur rapidly or slowly over a decade or more. Patients who
have had a traumatic hip dislocation, for example, usually have hip arthritis in 10 to 20 years later.

Systemic Complications
Systemic complications are unusual following a fracture and usually result from trauma in general and not
from the fracture itself. These complications include shock, sepsis, tetanus (in open injuries), gas gangrene,
venous thrombosis, and fat embolism. The emergent stabilization of spine, pelvic, and long bone fractures is
necessary to minimize blood loss and to allow a patient to sit upright and receive proper pulmonary
physiotherapy. Accomplishing this can significantly decrease the incidence of respiratory insufficiency in
multisystem trauma patients.

Joint Subluxation and Dislocation

Diagnosis and Evaluation

Subluxation of a joint is usually a transient phenomenon, when articular surfaces of a joint become partially
separated. When a joint is dislocated, the articular surfaces of a joint are no longer in contact with each other,
and the patient is reluctant to move it. The limb may be held in a typical posture (e.g., when a hip is
posteriorly dislocated, the thigh is held in flexion, adduction, and internal rotation). Neurovascular structures,
in close proximity to joints, can be injured with dislocations, especially in older patients whose arteries may be
thickened by atherosclerotic plaque. Not all vascular injuries are acute occlusive phenomena. An intimal tear
of the artery may slowly cause thrombus formation, delaying the presentation of vascular compromise.
Therefore, serial neurovascular evaluations are essential after the reduction of a dislocated joint. Asymmetry in
pulses, which is detected by palpation, Doppler ultrasonography, or ankle–brachial index (ABI)
determination, warrants further vascular workup, especially in young patients who have had little stimulus to
develop collateral circulation.
Radiographs of the involved joint are obtained in the dislocated posture. This radiograph demonstrates the
pathology and allows the treating physician to infer which specific ligamentous structures are damaged. Like a
fracture, a dislocation can be described as open or closed and according to the position of the distal fragment
relative to the proximal fragment. If radiographic assessment will be delayed and if skin is compromised (e.g.,
ankle fracture or dislocation) or if neurovascular integrity is in question (e.g., knee dislocations), then
reduction should be attempted immediately.

Treatment
Dislocations are usually realigned by traction along the normal axis of the extremity. Occasionally, bone or
soft tissue may be interposed between joint surfaces and will require a surgical (open) reduction. Postreduction
radiographs must be taken to ensure the adequacy of reduction and rule out an associated fracture.

Common Musculoskeletal Injuries

Upper Extremity

Carpal Scaphoid Fracture

The scaphoid is the bone most frequently fractured of the carpal bones. A fracture through the waist of the

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scaphoid usually occurs after a fall on the outstretched hand, with the wrist positioned in dorsiflexion and
radial deviation. If a fracture is suspected from the mechanism of injury and tenderness in the anatomic snuff
box, the patient should be treated as if there were a fracture (even if radiographic views do not indicate a
fracture). A bone scan, CT scan, or follow-up radiographs at 7 to 14 days will confirm or disprove the
diagnosis. The scaphoid bone is extensively covered by hyaline cartilage and has limited soft tissue
attachments and blood supply. Complications of avascular necrosis, delayed union, and nonunion are
increased by failure to treat a scaphoid fracture initially. Undisplaced fractures are treated in a thumb spica cast
(a forearm cast extended to incorporate the thumb in the pinch position). Displaced scaphoid fractures are
treated by open reduction and internal fixation.

Distal Radius Fracture

A distal radius fracture is also caused by falling on an outstretched hand. When this injury causes a transverse
fracture of the distal radius just proximal to the wrist, it is referred to as a Colles fracture. It is a common
fracture in elderly, osteoporotic patients. Radiographically, dorsal comminution can be noted, and the distal
fragment is impacted and shortened with apex palmar angulation (Figure 28-15), and the ulnar styloid is often
fractured as well.

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Figure 28-15 Colles fracture of the distal radius is common to osteoporotic patients. The fracture occurs from a
fall on an outstretched dorsiflexed hand. A, The anterior–posterior view demonstrates the impaction and
shortening of the distal fragment (arrows). B, The lateral radiograph shows the dorsal cortex of the radius to
be comminuted and impacted, which results in apex palmar angulation. (From Lawrence PF. Essentials of
Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

Reduction is obtained by longitudinal traction applied to the hand, disimpacting the fracture. The wrist
and distal fragment are manipulated into flexion and ulnar deviation to correct the dorsal and radial
displacement. After reduction, a splint is applied from the elbow to the palm. A repeat radiograph should be
taken following reduction at approximately 10 days to assess whether the reduction has been maintained. If it
has not, a repeat manipulation or external fixation is required. The deformity tends to recur because of dorsal
cortical comminution. Occasionally, Kirschner wires, or K-wires, are inserted percutaneously to prevent loss of
fracture alignment.
The median nerve is in proximity to the volar aspect of the wrist. Its function must be documented before
and after fracture manipulation. The shoulder–hand syndrome is a common complication of a Colles fracture
in the elderly. In this syndrome, shoulder and finger stiffness results from disuse during the treatment period.
Patients are encouraged to exercise the shoulder and fingers during the early phases of fracture healing.

Olecranon Fracture
An olecranon fracture is usually caused by a fall in which there is a direct blow to the point of the elbow. The
fracture is displaced by contraction of the triceps muscle. Thus, there is loss of active elbow extension. The
fracture also involves the elbow joint surface, and any displacement of the fracture fragments requires an open
reduction to restore the articular surface and triceps integrity.

Pulled Elbow
This is a painful condition that affects young children aged 1 to 4 years. It occurs frequently when the child
has been pulled forcibly by the hand. The child tends to hold the elbow slightly flexed and avoids moving it.
The pain is believed to be due to impingement of the annular ligament of the radial neck. Treatment is to flex
the elbow slightly and supinate the child’s hand, which repositions the annular ligament around the radial

1062
neck and relieves the symptoms.

Supracondylar Humerus Fracture

A supracondylar humerus fracture is commonly seen in children 5 to 10 years of age. It occurs from a fall on
an outstretched hand with the elbow extended. The distal fragment is usually displaced posteriorly. It can
cause significant neurovascular complications by entrapping the brachial artery and the median and radial
nerves, either at the time of injury or during reduction (Figure 28-16). This fracture is a frequent cause of a
forearm compartment syndrome because of ischemia (Volkmann’s ischemic contracture). It must be treated
with great care and vigilance. Usual management of displaced fractures is with prompt reduction and
percutaneous pin fixation in the operating room.

Figure 28-16 The dangerous supracondylar distal humerus fracture may entrap the brachial artery and the
median and radial nerves. This fracture is associated with forearm compartment syndrome and warrants
cautious and frequent neurovascular monitoring. (Reprinted with permission from American Academy of
Orthopaedic Surgeons. Athletic Training and Sports Medicine. 2nd ed. Park Ridge, IL: American Academy
of Orthopaedic Surgeons; 1991:277.)

A forearm compartment syndrome can be caused by kinking of the brachial artery at the site of the
supracondylar fracture. If the flow of blood with the delivery of oxygen and removal of metabolic waste from
the muscles is not restored, severe and even permanent muscle injury can occur. If muscle is ischemic at
normal body temperature for more than 2 hours, there is some permanent muscle damage. If the warm
ischemia time exceeds 8 hours, then the muscle is likely dead, and revascularizing the limb can lead to
systemic complications from hyperkalemia and release of myoglobin. The flexor compartment of the forearm
is completely dependent on the blood supply from the brachial artery. If the muscles die, the fibers contract
and leave a nonfunctional hand because of fingers and thumb being flexed into the palm. There is no effective

1063
tendon transfer to restore hand and wrist function when the entire flexor compartment has stiffened and
scarred.

Shoulder Dislocation
The shoulder is the most frequently dislocated joint in the body. In more than 90% of traumatic dislocations,
the humeral head is anterior to the scapular glenoid fossa (Figure 28-17A), which can endanger the axillary
nerve and artery. The integrity of the axillary nerve should be documented by testing sensation over the
deltoid patch and motor function of the deltoid muscle before and after reduction of the shoulder dislocation.
An anterior shoulder dislocation occurs with forced external rotation of the abducted arm. This type of injury
may be caused by an arm tackle in football or by blocking a basketball shot.

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Figure 28-17 A, Axillary lateral radiograph of an anterior shoulder dislocation. The humeral head lies out of the
glenoid fossa (G). The coracoid process (C) is an anterior scapular structure and orients the film. B, Closed
reduction of an anterior shoulder dislocation via traction countertraction. a, acromion; cl, clavicle. (Reprinted
with permission from Rockwood C, Green D. Fractures in Adults. 3rd ed. Philadelphia, PA: JB Lippincott;
1982:1092.)

Reduction can be achieved by gradual shoulder abduction while longitudinal traction is placed on the arm
and countertraction is placed through the axilla with a sheet (Figure 28-17B). Sedation and muscle relaxation
facilitate the manipulation.
Posterior shoulder dislocations, although rare, are often missed because of improper interpretation of the
AP radiograph, which appears to show the humeral head aligned with the glenoid. An axillary view shows the
humeral head to lie posterior to the glenoid, which should reinforce the principle that two radiographs taken
in perpendicular planes are needed for proper radiographic evaluation of any bony structure. Clinically, the
arm is held internally rotated and cannot be externally rotated beyond the neutral position. A posterior
dislocation should be considered in all patients with shoulder symptoms after an electrocution or a seizure
caused by epilepsy, alcohol withdrawal, electroconvulsive therapy, or electrocution.

Lower Extremity

Hip Fractures
Low-energy hip fractures are common in elderly, osteoporotic patients. They account for about 33% of
admissions to large orthopedic centers. The common types are femoral neck (see Figure 28-5A) and
intertrochanteric hip fractures (Figure 28-18). In both fractures, the affected limb is externally rotated and

1065
shortened. The patient cannot bear weight, and slight amounts of hip motion cause pain.

Figure 28-18 A, Intertrochanteric hip fracture. The bone is osteopenic and rarefied. B, This fracture has been
reduced and internally fixed with a screw and sideplate device. This type of fixation will permit early patient

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mobilization. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2007.)

The blood supply to the femoral head comes from vessels that run along the posterior femoral neck. These
vessels can be damaged by a femoral neck fracture. If the femoral head is rendered avascular, the bone cells
die. When dead bone is subjected to repetitive weight-bearing loads, it will collapse and fragment. Femoral
neck fractures have a higher incidence of nonunion because the fracture is within the hip joint (intracapsular),
with a thin periosteum and no muscle envelope. Femoral neck fractures are either reduced and surgically fixed
or, because of attendant complications, replaced with a metal hemiarthroplasty. An intertrochanteric hip
fracture occurs outside the hip joint (extracapsular). There is a good blood supply, and the fracture usually
heals (Figure 28-18A). Intertrochanteric fractures are reduced under radiographic guidance and fixed with a
sliding screw and sideplate device (Figure 28-18B). Surgical treatment allows for early patient mobilization
and decreases problems related to prolonged bed confinement (e.g., pneumonia, thrombophlebitis, decubitus
ulcers).

Femoral Shaft Fractures

The femoral shaft is the strongest bone in the body. In young patients, femur fractures require high-energy
trauma and are incurred by motor vehicle accidents and falls from heights. Blood loss may be considerable. In
a closed fracture, 1 to 3 units of blood may be lost into the thigh, and the patient may present in hypovolemic
shock. Other sources of hypovolemia (such as intra-abdominal and intrathoracic injuries or pelvic fractures)
must be excluded. In all patients with a fractured femur, the pelvis and hip must be assessed radiologically to
rule out associated fractures or dislocations. Knee stability should be evaluated.
Closed, interlocked intramedullary nailing is the preferred treatment (Figure 28-19). Because the nail can
be locked proximally and distally, the fracture can be rendered quite stable and allow early ambulation. This
approach prevents the lengthy periods of bed rest required with skeletal traction (see Figure 28-11) and
minimizes the risks of venous thrombosis, knee stiffness, quadriceps contracture, muscle atrophy, and disuse
osteoporosis.

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Figure 28-19 Comminuted femoral shaft fracture after internal fixation with an interlocked intramedullary nail.
(From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2007.)

Hip Dislocation
Hip dislocation often occurs in motor vehicle accidents when the knee strikes the dashboard. Seated posture
places the hip in adduction and 90° of flexion. The longitudinal load of unrestrained dashboard impact drives
the hip posteriorly out of the acetabular socket and may stretch the sciatic nerve. All patients with posterior
hip dislocations should be assessed for a foot drop. The hip should be reduced urgently and associated
fractures repaired to restore stability of the hip joint. Delays in treatment beyond 8 to 12 hours from injury
can increase the risks for avascular necrosis of the femoral head and posttraumatic arthritis of the hip.

Tibia and Fibular Shaft Fracture

Shaft fractures of the tibia and fibula occur nine times more often than femoral shaft fractures. Almost 33% of
the tibial surface is subcutaneous. For this reason, tibia fractures are often open and contaminated. The
limited blood supply to the tibia causes fractures of this bone to have delayed union and nonunion. Tibia
fractures are at risk for compartment syndrome (discussed later), which requires attentive observation and
early diagnosis. The key clinical sign in a conscious patient is pain that is out of proportion to the injury.
Complications associated with tibia fracture management are the most frequent cause of trauma-related
orthopedic malpractice suits.
Closed reduction and above-the-knee cast immobilization are the standard treatment for uncomplicated
closed fractures of the tibia and fibula. Open reduction and internal fixation are considered only when an
acceptable reduction cannot be achieved by closed means or the reduction cannot be maintained by a plaster

1068
cast. External fixation (see Figure 28-14) is frequently used in managing open fractures of the tibia: stability
and alignment of the fracture fragments are maintained while allowing access to treat the soft tissue wound.
Current trends are toward adequate surgical debridement at the time of injury followed by internal fixation.
The implant of choice is a reamed intramedullary nail.

Ankle Injuries
Ankle injuries are common in young, athletic individuals and may involve both ligamentous and bony
structures. The ankle is a mortise and tenon joint. The three-sided mortise is composed of the tibial malleolus,
the tibial plafond (ceiling), and the fibular malleolus. The talus represents the tenon. The mechanism of injury
can be inferred from the plane of the fracture line (Figure 28-20). A transverse fracture line occurs from a
tensile or “pulling off” force. Thus, when the medial malleolus fracture is transverse, it suggests an abduction
(eversion or pronation) force of the foot on the leg (Figure 28-20B and C). If the lateral malleolus fracture is
transverse, the force applied to the foot is adduction (inversion or supination; Figure 28-20A). A spiral
fracture configuration implies a rotatory force. A coronal plane spiral fracture is a common lateral malleolar
fracture pattern and is seen when the foot is externally rotated on the leg and body (Figure 28-20C).
Bimalleolar ankle fractures are common. When a posterior tibial fragment is seen on the lateral radiograph, it
is called a trimalleolar fracture, and it results from vertical loading of the plantar flexed ankle (Figure 28-20D).

Figure 28-20 Ankle fractures. The basic mechanism of injury can be identified by the characteristic fracture
patterns. A transverse fracture line implies that tensile, avulsive force was applied to the bone and is usually
the first fracture to occur in the injury pattern. A, Adduction (inversion), in which the lateral malleolus is
pulled off transversely and the medial malleolus is pushed off obliquely by the talus. B, Pure abduction
(eversion) in which the medial malleolus is pulled off transversely, the fibula pushed off obliquely by the talus.
The lateral malleolus is fractured in the sagittal plane. In some cases, the fibula is fractured above the joint
line, indicating a tear in the interosseous membrane. C, Abduction (eversion) and external rotation
(common), in which the medial malleolus is pulled off transversely, whereas the lateral malleolus is obliquely
fractured by the talus as it externally rotates and abuts the fibula. The fibular fracture is in the coronal plane.
D, Vertical load, in which the posterior malleolus, seen best on a lateral x-ray film, can be fractured by a
vertical compression load as the talus impacts the posterior tibia. The addition of this fracture fragment to any
of the above constitutes a trimalleolar fracture. (Reprinted with permission from Rockwood C, Green D.
Fractures in Adults. 3rd ed. Philadelphia, PA: JB Lippincott; 1982.)

Because ankle fractures are intra-articular, anatomic restoration of the joint congruity is an essential

1069
treatment principle. One millimeter of ankle displacement can reduce joint surface contact by 40%. Anatomic
open reduction with internal fixation is the ideal treatment for displaced ankle fractures.

Spinal and Pelvic Fractures

Spinal and pelvic fractures in young people result from high-velocity trauma and are associated with
intrathoracic, intra-abdominal, and extremity injuries. In the elderly, spine fractures may occur after minimal
trauma in bone that is weakened by osteoporosis or tumor.

Spinal Fractures
Spinal stability is the critical concept in the treatment of spinal fractures. The spine is unstable if unprotected
movement causes fracture displacement that can compromise the integrity of neural structures. In all cases of
suspected spinal injury, a complete and detailed baseline neurologic assessment should be performed and
documented as soon as the patient’s condition permits. In unconscious patients or in those with any injuries
above the level of the clavicle (facial), the cervical spine is presumed to be injured until proven otherwise (see
Chapter 9). Patients with minor wedge compression fractures (see Figure 29-5B) of the lower thoracic or
lumbar spine often develop an ileus from retroperitoneal bleeding and should not be fed enterally until the
ileus has resolved. If paraplegia results from a catastrophic spinal column injury, the signs of other injuries are
masked by the lack of sensation. A systematic and thorough examination of all vital structures must therefore
be carried out in patients with paraplegia. The patient with suspected spine trauma is properly splinted at the
site of injury in a cervical collar with the head secured by taped sandbags. The thorax, abdomen, and
extremities are strapped to a spine board. Consultation with a neurosurgeon or an orthopedic surgeon is
indicated if the physician has any doubt about the stability of the spine injury.

Pelvic Fractures
The pelvis transfers body weight through the sacroiliac joints and acetabula in stance and through the ischial
tuberosities in seated postures. The pelvis also protects the lower abdominal and genitourinary tracts. The
pelvis houses the extensive vascular arborizations of the iliac vessels and the lumbosacral plexus of nerves.
Pelvic fractures usually occur after high-velocity blunt trauma and can be associated with massive blood loss
and multiorgan system injuries (Figure 28-21). Therefore, in a hemodynamically unstable patient, emergency
pelvic stabilization with external fixation is considered essential to the trauma resuscitation. The two goals of
acute pelvic fracture surgery are to stop bleeding and permit sitting stability to facilitate pulmonary
physiotherapy.

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Figure 28-21 A, Anterior–posterior (AP) pelvis radiograph depicting diastasis of the symphysis pubis. The
retrograde cystogram demonstrates bladder compression from a large pelvic hematoma. This type of pelvic
injury can cause massive amounts of internal hemorrhage. B, AP pelvis radiograph after internal fixation with
a plate and screws. Fracture reduction decreases pelvic volume, which both stabilizes and facilitates tamponade
of bleeding fracture surfaces. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2007.)

Almost one in five pelvic fractures has a concomitant bladder or urethral injury in males. When blood is
seen at the external urethral meatus or when the patient cannot pass urine, a retrograde urethrogram is
obtained to evaluate the integrity of the urethra before an indwelling catheter is placed. With hematuria, an
intravenous pyelogram is performed to show renal function. If blood is detected in the rectum or vagina, the
pelvic fracture may be open. Open pelvic fractures are treated with a diverting colostomy after debridement
and external fixation to prevent ongoing fecal soilage of the fracture.

TRAUMATIC AMPUTATIONS AND REPLANTATION

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With the advent of microsurgical techniques, completely severed digits and limbs can be surgically reattached.
Limb replantation is most successful if the part is amputated cleanly with a minimum of crushed tissue.
Children enjoy better nerve regeneration than adults and are ideal candidates for replantation. A general rule
applies to replantation: Because muscle tissue is sensitive to ischemic injury, the greater the amount of muscle
attached to the amputated part, the poorer is the prognosis for its function after replantation.
The best amputation levels for replantation in adults are the thumb, multiple digits, and the wrist or
metacarpal level of the hand. In children, amputations at any level have a good chance of successful
replantation. Contraindications to replantation include amputations with large crush or avulsive components;
body parts that have been amputated at multiple levels; individual digit amputations (other than the thumb),
especially proximal to the middle phalanx; and amputation in older patients who have concurrent disease or
mental instability.
An amputated part may remain viable for approximately 6 hours of warm (36°C) ischemia. Cooling
decreases tissue metabolism and increases the duration of viability. Amputated tissues can tolerate up to 16
hours of cold (10°C) ischemia. Thus, preparation of a severed part for transportation should include cleansing
of superficial contamination, wrapping in moist gauze, and placement in an air-tight plastic bag that is then
immersed in ice water. Dry ice is never used because it causes frostbite and further tissue damage.
Of digital replants, 85% remain viable. Joint motion is usually about 50% of normal, and two-point
sensory discrimination is protective (>10 mm) in half of adults yet almost normal (>5 mm) in children. All
digits are cold intolerant for a period of at least 2 years, and 80% of epiphyses will continue to grow after
replantation.

COMPARTMENT SYNDROME

Muscles are surrounded by a relatively stiff fascial membrane composed of fibrous collagen. These fibrous
envelopes separate various muscles into anatomically distinct compartments (Figure 28-22). Bleeding and
tissue swelling inside these membranes cause increased pressure within the fascial compartment. Under these
circumstances, capillary blood flow to muscle and nerve is thus reduced, causing local acidosis, cell injury, and
further edema. Compartment pressures can become so elevated that muscle and nerve necrosis result. Dead
fibrotic muscle will cause joint contractures, and the limb function will be severely impaired.

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Figure 28-22 Four distinct leg compartments are separated by thick, unyielding fascial planes. (From Lawrence
PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

A compartment syndrome can be caused by fractures, severe muscle contusions, crush injuries, and acute
vascular occlusion followed by revascularization. They may be aggravated by casts. Fractures that cause the
most compartment syndromes are supracondylar distal humerus (see Figure 28-16), both bones (radius and
ulna) of the forearm, and proximal third tibia fractures.
The classic signs of a compartment syndrome caused by tissue ischemia are described by the four Ps: pain,
paresthesia, paralysis, and pallor. Pain is the most useful clinical sign. It is intense and usually disproportionate
to the injury. In addition, the pain is intensified on passive stretching of the muscles within the suspected
compartment. If these symptoms and signs occur in the presence of one of the high-risk injuries, an urgent
orthopedic consultation should be obtained regarding possible fasciotomy. It is important to remember that a
compartment syndrome can occur in the presence of normal pulses and sensation. Systolic arterial pulse
pressures are usually much higher than the 30 mm Hg interstitial compartment pressure at which myonecrosis
begins.
A high index of suspicion and pain out of proportion to the injury should lead to the removal of all circular
bandages or casts. The clinician should not wait for paresthesia, paralysis, or pallor. Decompression by open
fasciotomy is indicated if compartment pressure is greater than 30 to 40 mm Hg in an unconscious or
paralyzed patient. (Compartment syndrome is also discussed in Chapters 10 and 26.)

SPORTS-RELATED INJURIES

The recent emphasis on physical fitness has led to an increase in sports-related injuries. These injuries can be

1073
classified as those caused by acute trauma or repetitive stress. All musculoskeletal tissues are composed of
living cells that are stimulated by physical stress to become stronger. When these tissues are not stressed,
bones, ligaments, muscles, and tendons will atrophy. The goal of exercise is to produce beneficial increases in
physical strength and endurance through the controlled application of stress. Tissues gain strength following
stress-induced microscopic breakdown by a process of hypertrophic repair. When the stresses of exercise
overwhelm the normal reparative process, tissues become chronically injured and inflamed and ultimately fail.
There is much to be learned about the proper duration, frequency, and intensity of physical training. For
example, the “no pain, no gain” attitude toward exercise often exacerbates many injuries. Although pain may
be an annoyance, it is also appropriate biofeedback signifying injury and the need for rest.
It has been calculated that, while running, the foot strikes the ground between 800 and 2,000 times per
mile at a force of 2 to 4 times body weight. An average 140-lb man generates between 110 and 560 tons of
ground reaction force per mile. This tremendous amount of force is dissipated by the shoe, the small joints of
the foot, and the bones and muscles of the leg. Any of these tissues can and do fail with injudicious exercise.
This section describes the more common injuries related to acute trauma and chronic, repetitive overuse.
Many of these syndromes can occur as occupational injuries in which a given task is repeated with great
frequency and without adequate periods of restorative rest.

Stress Fractures

Stress fractures are the classic overuse injury. They occur when individuals are subjected to increased activity
levels or changes in habits and training methods. Historically, stress fractures were first identified in the
metatarsals of military recruits who were expected to endure arduous marches (march fracture syndrome).
Stress fractures have been identified in most bones of the body, including femur, tibia, calcaneus, and
metatarsals in runners; humerus in throwers; ribs in oarsmen; and wrists and L5 vertebrae in gymnasts.
Stress fractures are postulated to occur as a consequence of muscle fatigue. Not only do muscles cause
locomotion, they also absorb shock. Eccentric muscle contraction, or controlled muscle lengthening,
decelerates the body, absorbs shock, and diffuses stress away from bone. When muscles tire, this stress-
shielding effect is negated and stress is transferred directly to bone. Repeated submaximal stress will cause
bone as a material to fatigue. Microfractures result and may cause an achy discomfort. The traditional
treatment of rest and stress protection permits these microscopic fractures to heal. Normal cellular bone
healing mechanisms permit the bone to strengthen in response to increasing demands. If the bone’s ability to
heal itself is overwhelmed by repeated, unremitting stress, these microfractures will coalesce, resulting in a
gross, macroscopic fracture. Because stress fractures are initiated on a microscopic level, radiographs lack
diagnostic sensitivity and have high false-negative rates, missing as many as 70% of these injuries.
Radioisotope-labeled technetium pyrophosphate bone scans, which detect cellular bone formation, can
identify a stress fracture at an earlier stage of its pathogenesis (Figure 28-23).

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Figure 28-23 A, Femoral neck stress fracture detected by increased radioisotopic uptake on bone scan (arrow) 2
weeks before B, radiographic evidence of the fracture (arrow). (From Lawrence PF. Essentials of Surgical
Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

Lateral Epicondylitis (Tennis Elbow)

Lateral epicondylitis, or tennis elbow, is an overuse injury of the wrist extensor muscle origin. This condition
affects players of racquet sports, as well as laborers who use their hand in repetitive forceful gripping. Wrist
extension is necessary for power grip (try to grip with your wrist flexed!).
The wrist extensor muscles also dissipate force when a handheld object is used in striking. In tennis elbow,
the common wrist extensors are damaged and inflamed at their lateral humeral epicondyle origin. The
majority of these injuries respond to nonoperative methods that include rest, heat, anti-inflammatory agents,
wrist extensor muscle stretching, and antagonist (wrist flexor) strengthening exercises. In the few cases that
are managed operatively, chronic granulation tissue is found in the origin of the extensor carpi radialis brevis
and is resected.

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Rotator Cuff Tendonitis (Shoulder Bursitis)

The glenohumeral joint of the shoulder is the most mobile joint in the body. The four rotator cuff muscles—
subscapularis, supraspinatus, infraspinatus, and teres minor—all take broad origin from the scapular body and
insert just lateral to the articular surface of the humeral head. These muscles act to stabilize the joint by
pulling the humeral head into the shallow scapular glenoid fossa. The combined cross-sectional area of the
rotator cuff musculature is equal to that of the deltoid muscle. Because cross-sectional area is directly related
to muscle strength, it is interesting that the amount of shoulder muscle strength expended on joint stability
through the rotator cuff is equal to that of the deltoid, which is responsible for joint mobility.
Rotator cuff tendonitis, or subacromial bursitis, is common to people involved in sports (e.g., swimmers,
throwers) or who have jobs in which the arm is used overhead (e.g., mechanics). As the shoulder abducts away
from the body, the rotator cuff muscles (especially the supraspinatus) contract under the coracoacromial arch.
As the arm is raised, this arch becomes narrower, impinging on and mechanically irritating the tendons of the
rotator cuff muscles. The subacromial bursa, which is a fluid-filled synovial sac, may become inflamed under
these conditions of friction and can contribute to the pain. However, pathologic changes can also affect the
tendon and run the gamut from edematous inflammation to calcific degeneration to tendon thinning and
tearing (Figure 28-24). Painful inflammatory changes may also affect the subacromial bursa. It is difficult to
distinguish which structure is painful, the bursa or the tendon proper. A rotator cuff tear may show weakness
of shoulder external rotation strength. Pain can mask the reliability of strength testing. A shoulder
arthrogram, ultrasound, or MRI scan can diagnose a rotator cuff tear with good dependability.

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Figure 28-24 A, Viewed from the posterior and anterior perspectives, the cowl of rotator cuff muscles takes
broad origin from the scapula and inserts close to the articular margin of the humeral head. The rotator cuff
acts to pull the humeral head into the glenoid fossa as the arm is abducted away from the body. B, Viewed
from its superior surface, the supraspinatus tendon is torn near its humeral insertion. The tear results from
acromion and coracoacromial ligament attrition, when the shoulder is abducted and forward flexed. (A,
Modified from American Academy of Orthopaedic Surgeons. Athletic Training and Sports Medicine. 2nd
ed. Park Ridge, IL: American Academy of Orthopaedic Surgeons; 1991:235; B, Modified from Rowe CR.
The Shoulder. New York, NY: Churchill Livingstone; 1988:142.)

Factors that contribute to rotator cuff pain include overuse, weakness, muscle imbalance, improper
throwing technique, strenuous training techniques, and an unstable glenohumeral joint. Treatment consists of
rest, eccentric rotator cuff strengthening exercises, and anti-inflammatory medication. Surgical decompression
of the coracoacromial arch is indicated if the condition becomes chronic or if it is necessary to repair a torn
rotator cuff tendon.

Plantar Fasciitis (Calcaneal Bursitis)

1077
Plantar fasciitis is a problem common to runners. The plantar fascia is a thick, fibrous structure attached to
the calcaneus that fans distally along the sole of the foot to envelop the metatarsal heads. It increases and
stiffens the longitudinal arch of the foot during the propulsive toe-off phase of gait. When the inflexible
plantar fascia is repeatedly impacted and stretched by running, it is injured at its calcaneal origin, becoming
inflamed and painful. The inflammatory reaction can produce a traction spike of new bone, which on
radiograph is called a heel spur. It is not clear how much of the heel pain can be attributed to the spur. Many
patients who have had foot x-rays for other reasons have evidence of heel spurs but no symptoms of heel pain.
Classically, plantar heel pain is worse when gait is initiated in the morning, after sitting, or at the start of
jogging. Contributory factors include both flat (planus) and high-arched (cavus) feet, toe or sand running,
obesity, and improper shoe wear (e.g., slippers). Nonoperative treatment includes rest, medication, weight loss
if applicable, proper shoe wear, heel padding, or cushioned shoe orthoses. If the condition has been of long
duration, recovery may be slow. Surgical release of the plantar fascia from its calcaneal origin is reserved for
the most recalcitrant cases.

Patellar Overload Syndrome

Anterior knee pain is common to sports participants. The patella is embedded in the quadriceps muscle and
glides through the femoral groove. The patella functions much like a pulley to increase the mechanical
efficiency of the quadriceps in extending the knee joint. When the patella is abnormally loaded or malaligned,
abnormal patellar wear and irritation can produce chondromalacia, or cartilage (chondro-) softening (malacia).
Patellofemoral knee pain is located anteriorly and is aggravated by climbing or descending stairs and hills,
squatting, kneeling, arising from a chair, or after prolonged sitting. These activities all stress the knee extensor
(quadriceps) mechanism. As the quadriceps muscle is inhibited by the discomfort, it may atrophy.
Nonoperative treatment is often effective. Avoidance of aggravating activities and anti-inflammatory
medications and the use of patellar orthotics known as “knee sleeves” are effective treatment adjuncts.
Straight-leg raising and quadriceps-strengthening exercises are important to successful rehabilitation.
Quadriceps exercises over a full arc of motion are to be avoided because they place excessive load on the patella
and exacerbate the condition. The diagnosis of chondromalacia should be reserved for injury to the articular
cartilage observed either by MRI or by arthroscopy.

Exercise Compartment Syndrome (Shin Splints)

Shin splints are leg pain that is intensified during exercise. In recreational runners, the pain is usually localized
to the anterior leg compartment (see Figure 28-22) containing the tibialis anterior extensor digitorum and
extensor hallucis longus muscles. In competitive runners, the pain often emanates from the distal medial leg in
the deep posterior compartment musculature (posterior tibialis, flexor digitorum, and flexor hallucis longus).
Intramuscular pressures increase during contraction, which decreases blood flow. Muscle perfusion therefore
occurs primarily during muscle relaxation. Sustained increases in compartment pressure decrease muscle
perfusion, producing pain, and the cessation of exercise. This phenomenon is known as an exercise
compartment syndrome. When measured, compartment pressures can increase to well over 100 mm Hg with
exercise. In the asymptomatic individual, pressures return to normal levels very rapidly during periods of rest.
In patients with exercise compartment syndromes, interstitial tissue pressures fall off slowly and have a delayed

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return to normal values. Tibia stress fractures, periostitis, nerve entrapment, and fascial muscle hernias have a
similar clinical presentation. The diagnosis of exercise-related compartment syndrome is based on objective
pressure measurements. When conservative treatments (e.g., rest, cushioned shoe orthotics, and changes in
training patterns and running surfaces) fail, the condition can be successfully treated with a surgical fasciotomy
of the involved leg compartment.

Sprains

A sprain is a ligament injury. Ligaments are collagenous structures that originate from and insert on bone.
Ligaments stabilize joints, and they are injured under tensile or stretching loads. Sprains are classified
according to the three grades of damage. Grade I sprains exhibit microscopic ligament damage, which
produces ligament tenderness but no change in joint stability when the joint is subjected to stress. Grade II
sprains show a greater degree of damage, with rupture of entire fascicles of ligament collagen. The ligament is
in macroscopic continuity but is stretched or partially torn and therefore demonstrates joint laxity when
stressed. There is a firm end point on clinical testing. When grossly disrupted with total loss of joint stability,
the ligament injury is classified as a grade III sprain.

Ankle Sprains
The lateral ankle ligaments are the most commonly sprained ligaments in the body. The lateral ankle is
supported by three discrete ligaments: the anterior talofibular, calcaneofibular, and posterior talofibular
ligaments (Figure 28-25). Because the longer fibular malleolus buttresses the ankle from abduction or eversion
stress, the broad deltoid ligament that connects the medial tibial malleolus to the talus is not commonly
injured.

Figure 28-25 A, Extensive medial deltoid ligament of the ankle. B, The lateral ankle is supported by three
discrete ankle ligaments. The most commonly sprained anterior talofibular ligament, the calcaneofibular, and
the posterior talofibular ligaments. The anterior talofibular ligament resists anterior translation of the ankle
(anterior drawer test); the calcaneofibular resists inversion stress (talar tilt). (Modified with permission from
Wilson FC, ed. The Musculoskeletal System: Basic Processes and Disorders. 2nd ed. Philadelphia, PA: JB
Lippincott; 1983.)

When the ankle is subjected to an inversion stress, the anterior talofibular ligament is the first lateral
ligament to be torn. With more severe injury, the calcaneal-fibular ligament will also be disrupted. These two

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ligaments resist anterior talar displacement on the tibia (anterior drawer test, Figure 28-26) and abnormal
inversion talar tilt, respectively.

Figure 28-26 Anterior drawer test. The anterior talofibular ligament resists anterior ankle stress. The anterior
drawer test is positive when this ligament is disrupted and will detect excessive anterior translation of the foot
on the leg. (Reprinted with permission from American Academy of Orthopaedic Surgeons. Athletic Training
and Sports Medicine. 2nd ed. Park Ridge, IL: American Academy of Orthopaedic Surgeons; 1991:414.)

The diagnosis of a lateral ankle ligament sprain and its severity is determined by the extent of ligament
tenderness and by manual and radiographic stress tests. Treatment consists of ice, elevation, compressive
wraps, and early weight bearing. Primary surgical ankle ligament repair is rarely indicated because most ankle
sprains have no residual joint instability and the outcomes of early versus late ankle reconstruction are similar.
Ligaments contain proprioceptive nerve endings that are also injured by a sprain. Recurrent ankle sprains may
be the result of inadequate proprioceptive feedback, and thus, balance board proprioceptor retraining is an
effective component of ankle rehabilitation.

Knee Ligament Sprains

The knee is situated between the two largest bones, the femur and the tibia, and is spanned by the body’s
strongest muscles, the quadriceps and hamstrings. In general terms, the knee is stabilized by four ligaments:
the two collateral ligaments that resist varus and valgus stress and the two cruciate ligaments that primarily
resist AP motion (Figure 28-27).

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Figure 28-27 Knee joint stability depends on the two collateral and cruciate ligaments. The medial collateral
ligament is broad and large and resists varus or abduction stress. The anterior cruciate ligament resists anterior
tibial translation, whereas the posterior cruciate prevents posterior tibial shear. (From Lawrence PF. Essentials
of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

The collateral ligaments are usually damaged by trauma. The anterior cruciate ligament (ACL) can be
injured in isolation in twisting with hyperflexion or hyperextension noncontact modes. The ACL is the only
one of the four ligaments that is intrasynovial. In patients with bloody effusions (hemarthrosis) following knee
injury, 70% have an ACL injury. In those with an acute ACL tear, 50% have a concomitant meniscus tear.
The medial collateral ligament and ACL are frequently injured in combination from a valgus stress (e.g., as
occurs from a blow to the lateral thigh). When a collateral ligament is severely injured, the knee joint capsule
and synovial lining are disrupted. The knee may not contain an effusion because hemorrhage leaks through
the torn capsule.
Collateral ligament damage can be detected by local tenderness, pain, and laxity when the knee is
manually stressed in a mediolateral (varus/valgus) plane. Laxity tests of an injured knee are always judged in
comparison to the normal side. Valgus force on the knee will stress the medial collateral ligament, whereas
varus force will test the integrity of the lateral collateral ligament. Full knee extension places the joint in a
position of maximal geometric stability. Joint laxity in knee extension therefore implies a greater degree of
collateral ligament damage. Subtle differences between the laxity on the normal side and that on the injured
side can best be detected with the knee at 20° of flexion.
The anterior drawer test is used to evaluate cruciate ligament integrity. With the knee flexed 45°, the tibia
is pulled forward like a drawer (Figure 28-28). If there is abnormal anterior tibial translation, the anterior
drawer test suggests that the anteromedial fibers of the ACL are torn. Conversely, abnormal posterior tibial
translation to a posteriorly directed tibial force indicates a posterior cruciate ligament (PCL) injury. Anterior
knee laxity may be better appreciated in the 20° knee-flexed position, which is called the Lachman test. This
suggests injury to the posterolateral fibers of the ACL.

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Figure 28-28 The anterior drawer test is performed with the foot stabilized and the knee flexed 90°. With the
examiner’s thumb placed on the joint line, the tibia is pulled anteriorly. Excessive anterior tibial shift suggests
that the anterior cruciate ligament is incompetent. The contralateral side can be used as a comparative
reference. A similar test performed in 20° of knee flexion is called the Lachman test and is more sensitive in
the evaluation of acute injuries. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2007.)

Isolated medial collateral ligament injuries heal well with immobilization in a hinged cast-brace, which
protects the knee from valgus stress. An ACL injury is disabling to most athletes. With cutting and twisting
movements, the knee will transiently sublux and give way. PCL-deficient knees are associated with patellar
overload and arthritis, because the quadriceps muscle attempts to compensate for increased posterior tibial
displacement. The less stout lateral collateral ligament (LCL) is often injured in conjunction with one of the
two cruciate ligaments. Acute repairs of combination knee ligament injuries should be strong enough to
tolerate early motion to prevent the common postoperative complication of joint stiffness.
The indications for surgical ligament repair and reconstruction are controversial. In general, younger
patients whose activities cause symptoms of instability are candidates for surgery. The ACLs heal poorly and
are generally reconstructed with soft tissue autografts from the patellar tendon, hamstrings tendon, or fascia
lata.

Meniscal Injury

The knee joint is minimally constrained by virtue of its bony geometry. The medial and lateral meniscal
fibrocartilages increase joint surface contact and aid in joint stability. In stance, the menisci transmit 40% to
60% of the weight-bearing load placed across the joint. The menisci also assist with joint lubrication and
hyaline cartilage nutrition. The menisci move anterior to posterior as the knee is flexed. In flexion, the menisci
are trapped between the femoral condyle and the tibial plateau. If a twisting, rotatory motion occurs when the
knee is flexed, the menisci may split longitudinally (Figure 28-29C and D). Meniscal tissue loses hydration
and becomes more brittle with age. Shearing, horizontal cleavage tears not seen on the meniscal surface are

1082
frequently found in older patients (Figure 28-29A).

Figure 28-29 Meniscal tears. A, Degenerative horizontal tear. B, Radial tear. C, Displaced bucket handle tear.
D, Longitudinal tear. (Reprinted with permission from American Academy of Orthopaedic Surgeons.
Athletic Training and Sports Medicine. 2nd ed. Park Ridge, IL: American Academy of Orthopaedic
Surgeons; 1991:365.)

Patients with meniscal pathology may have pain and tenderness localized to the joint line (i.e., the
palpable gap between femur and tibia). There may be recurrent effusion. A history of painful giving way
suggests a tear located in the posterior portion of the meniscus. Symptoms of intermittent joint locking occur
with displaceable and bucket handle tears (Figure 28-29C), in which the torn component of the meniscus
becomes trapped between the condyle and acts as a mechanical block to joint motion.
Clinical examination should check for loss of terminal extension (locking), localized joint line tenderness,
and provocative test for displaceable meniscus (McMurray’s test). McMurray’s test involves flexion of the knee
to 90°, followed by internal rotatory movements of the tibia, and then followed by extension into valgus. The
test is repeated with tibial rotation in the opposite direction followed by extension into varus. The test tries to
trap a displaceable fragment of the meniscus between the articular surfaces of the tibia and femur. The test is
positive if the patient experiences joint line pain and the examiner feels a snap or rub at the joint line.
Longitudinal tears (Figure 28-29D) in the peripheral third of the meniscus will heal when repaired,
because this zone is well vascularized. Total meniscectomy leads to the slow development of tibiofemoral
arthritis. Irreparable and displaceable meniscal tears causing mechanical symptoms are best treated by
arthroscopy and partial excision of the meniscus, leaving the stable, untorn meniscus in situ. Meniscal surgery
is performed arthroscopically because it is less traumatic, more precise, and can be performed on an outpatient
basis.

Acromioclavicular (Shoulder) Separation

In addition to the glenohumeral articulation, the shoulder is composed of three other joints: the
acromioclavicular, sternoclavicular, and scapulothoracic articulations. The acromioclavicular joint rotates
approximately 20° with flexion and extension of the shoulder. It is stabilized in this AP (horizontal) plane by
the acromioclavicular ligaments (see Figure 28-1). In the craniocaudal direction (coronal plane), the joint is
constrained by the stronger coracoclavicular ligaments.
The acromioclavicular joint is injured after a blow or fall onto the point (acromion) of the shoulder. The

1083
scapular acromion is driven caudally, whereas the clavicle remains fixed to the chest. If the acromioclavicular
ligaments alone are torn and the coracoclavicular ligaments stretched, the injury is classified as grade II; the
clavicle is partially displaced (subluxed) from the acromion (see Figure 28-1C). This may not be obvious but
can be determined by stress radiographs taken with weights strapped to the patient’s wrists. The distance
between the clavicle and the coracoid process will be widened on the affected side. When both
acromioclavicular and coracoclavicular ligaments are disrupted (grade III), the joint will be dislocated. The
distal clavicle will be elevated above the acromion, which is obvious to inspection (see Figure 28-1B).
Treatment of a grade III shoulder separation is controversial. Both surgical and nonsurgical methods yield
functional results.

Gamekeeper’s Thumb

The ulnar collateral ligament of the thumb metacarpophalangeal (MCP) joint is a critical structure because it
stabilizes the thumb during grip and index finger pinch. As the thumb is out of the plane of the hand, this
ligament is vulnerable to abduction stress. It is injured in skiers who fall while still gripping their pole or in
ball handling sports (Figure 28-30). Loss of the stabilizing effect of the thumb MCP ulnar collateral ligament
renders pinch weak and painful. To stress test the ligament, the thumb MCP joint is positioned in 35° of
flexion to relax the volar plate and the short thumb flexor. The adductor pollicis aponeurosis may be
interposed between the ligament and the proximal phalanx, and this can prevent ligament healing. Ligament
exploration with repair or reattachment is performed. Good clinical results are also reported with use of a
hand-based adduction splint for 6 weeks.

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Figure 28-30 A, Lateral depiction of a torn collateral ligament metacarpophalangeal joint. B, The ulnar collateral
ligament of the thumb metacarpophalangeal joint is critical to opposable thumb function. Injury to this
ligament (gamekeeper’s thumb) renders the thumb unstable and weakens its contribution to pinch and grip
strength. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams
& Wilkins; 2007.)

Mallet (Baseball) Finger

A sudden blow causing flexion to the tip of an extended finger can cause rupture of the digital extensor
tendon. The finger distal interphalangeal (DIP) joint is in a flexed position, and the patient cannot actively
extend this joint (Figure 28-31). This injury heals well if splinted in full DIP extension for 6 weeks.

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Figure 28-31 Mallet or baseball finger, which results from rupture of the extensor tendon. (Reprinted with
permission from Brinker MR. Review of Orthopaedic Trauma. 2nd ed. Philadelphia, PA: Lippincott Williams
& Wilkins; 2013.)

Boxer’s Fracture

The index and long finger metacarpals have limited mobility and act as rigid posts for the fine precision work
of the hand. In contrast, the ring and little finger metacarpals are more mobile and are important to power
grip because motion is needed for these fingers to surround an object. For a fist to impart maximal kinetic
energy, the more rigid radial side of the fist should strike the object. When the ulnar fist strikes an object, the
little finger metacarpal neck often fractures (boxer’s fracture). With marked amounts of fracture angulation
(>45°), closed reduction and plaster immobilization is the preferred and usually successful treatment.
Occasionally, percutaneous pins may be required to stabilize a very unstable fracture.

Achilles Tendon Rupture

Achilles tendon ruptures occur in the middle-aged athlete who stresses the tendon beyond its tolerance.
Systemic and local steroid injections weaken tendinous tissue and predispose it to rupture. With an Achilles
tendon rupture, the athlete feels a severe pain in the calf. There may be swelling, ecchymosis, and sometimes a
palpable gap between tendon ends. Active plantar flexion of the ankle is weak but present because the tibialis
posterior and long toe flexors are still functional.
The Thompson test (Figure 28-32) verifies whether the gastrocnemius–soleus complex is intact. With the
patient lying prone and the foot hanging free over this end of the stretcher, the examiner squeezes the calf
muscle belly. Normally, the foot plantar flexes. Lack of plantar flexion indicates that the Achilles tendon is
torn. The diagnosis can be easily confirmed by ultrasound.

Figure 28-32 The Thompson test will provoke ankle plantar flexion when the gastrocnemius-soleus Achilles
tendon complex is intact. Absence of this response indicates a tear of the Achilles tendon. (From Lawrence
PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

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 Nonoperative treatment in a long leg cast with the foot in plantar flexion permits excellent tendon healing.
This method is cumbersome. Surgical treatment may be more expeditious for athletes. Both types of
treatment are effective.

Turf Toe

Turf toe is a hyperextension injury to the great toe metatarsophalangeal (MTP) joint (Figure 28-33). The
flexor hallucis brevis tendon is ruptured either at its proximal phalangeal insertion or by a fracture of its
sesamoid bones. The plantar plate may also be torn. The injury occurs during football pile-ups, in which a
player falls on the posterior aspect of a prone player’s foot, hyperextending the great toe. The injured player
experiences exquisite plantar great toe pain exacerbated by passive extension of the MTP joint. The toe-off,
propulsive phase of gait is painful. Treatment consists of rest, taping of the toe in plantar flexion, and the use
of a stiff forefoot, in-shoe orthosis. Untreated turf toe has been implicated as the cause of great toe MTP
arthritis and loss of extension known as hallux rigidus.

Figure 28-33 A turf toe injury occurs from hyperdorsiflexion of the great toe metatarsophalangeal joint and
ruptures the flexor hallucis brevis mechanism through the tendon or its sesamoid bone. (Reprinted with
permission from Rodeo SA, O’Brien S, Warren RF, Barnes R, Wickiewicz TL, Dillingham MF. Turf toe: an
analysis of metatarsophalangeal joint sprains in professional football players. Am J Sports Med. 1990;18:280–
285.)

Myositis Ossificans

Bone deposited in a muscle after a blunt injury is known as traumatic myositis ossificans (Figure 28-34).
When a deep muscle (often the quadriceps) is contused, the muscle closest to bone has the greatest amount of
direct damage. Either a metaplasia of muscle cells or a release of osteogenic material from the underlying bone
causes bone to form within the injured muscle. Early symptoms are deep muscle tenderness and loss of joint
motion. The condition is self-limited and may be decreased by nonsteroidal anti-inflammatory agents. If the

1087
lesion is large or causes mechanical problems, surgical excision is indicated. When a lesion is resected early
(i.e., before 18 months), there is a high rate of recurrence. A systemic form of myositis ossificans occurs in
patients with traumatic paralysis or extensive burns.

Figure 28-34 Myositis ossificans. Bone deposition in the quadriceps muscle after an anterior thigh contusion.
(From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2007.)

PEDIATRIC MUSCULOSKELETAL PROBLEMS

The term orthopedic is derived from the Greek word for straight, orthos, and the word for child, pais. The
diagnosis and treatment of pediatric deformities thus represent the origin of the specialty of orthopedics. This
section deals with common pediatric musculoskeletal disorders.

LOWER LIMB TORSION: IN-TOEING AND OUT-TOEING

The most common childhood “deformities” are actually normal variations of musculoskeletal development.
Flat feet, bowlegs, knock-knees, in-toeing, and out-toeing are commonly seen in young children but are
unusual in adolescence. Because these conditions seem to resolve spontaneously, they must be considered part
of the natural process of skeletal growth and development. The first 2 years of life are a remarkable period of
physical growth. The average child attains almost half of its adult size and stature during these first 2 years.
Body structure also changes radically as the skeletal frame is subjected to the demands of locomotion and
bipedal gait.
The common rotational deformities of in-toeing and out-toeing can be ascribed to one of three lower limb

1088
sites: the femur (anteversion or retroversion), the tibia (internal or external torsion), or the forefoot
(metatarsus adductus). Although rotational variations may run in families, the most common cause is the
intrauterine positioning (Figure 28-35). Certain sleeping or sitting postures may accentuate these conditions
and delay their resolution. Femoral version describes the anatomic relationship of the femoral head and neck
with the femoral shaft. The femoral neck is offset from the shaft in the coronal plane. This relation, called
femoral anteversion, is seen if one looks down the shaft of the femur as one would a gun barrel: the femoral
neck is canted an average of 10° to 15° anterior (Figure 28-36). At birth, femoral anteversion averages about
40°. It decreases to 10° by adulthood, with most of the change occurring in the first 3 years of life (Figure 28-
37).

Figure 28-35 Cramped intrauterine confines often mold the child’s plastic bone structure. Note that in utero
fetal posture forces the tibias to be internally rotated and the forefeet adducted. (From Lawrence PF.
Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

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Figure 28-36 Femoral neck version or torsion as seen from the distal femoral condyles. (Reprinted with
permission from Wilson FC, ed. The Musculoskeletal System: Basic Processes and Disorders. 2nd ed. Philadelphia,
PA: JB Lippincott; 1983.)

Figure 28-37 The average amount of femoral anteversion decreases from about 40° at birth to the normal 10° in
adulthood. The most dramatic change occurs within the first 2 years of life. (Reprinted with permission from
Dunlap K, Shands AR, Hollister LC, et al. A new method for determination of torsion of the femur. J Bone
Joint Surg. 1953;35(2):289–311.)

All rotational deformities are best evaluated with the child placed prone. Femoral anteversion is present
when medial or inward rotation of the femur is in excess of 30° more than external femoral rotation (Figure
28-38). When external (outward) femoral rotation is excessive, femoral retroversion is present.

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Figure 28-38 Clinical evaluation of a patient with in-toeing caused by femoral anteversion. A, Internal femoral
rotation is in greater excess than in part B. B, External femoral rotation. (Reprinted from Staheli L.
Rotational problems of the lower extremities. Orthop Clin North Am. 1987;18:506. Copyright © 1987
Elsevier.)

When the prone child is viewed from above with his or her knee flexed, the angle that the sole of the foot
makes with the thigh (i.e., the thigh–foot angle) allows for assessment of internal versus external tibial torsion
(Figure 28-39A). The normal lateral border of the foot is straight. If it is curved inward or its lateral border is
convex, metatarsus adductus is present (Figure 28-39B). If the foot is flexible and can be passively corrected to
neutral alignment, treatment is probably unnecessary. When the deformity is rigid, corrective serial casting is
beneficial. Metatarsus adductus is often associated with internal tibial torsion. Both result from fetal
positioning, the latter being the most common cause of rotational lower extremity problems (see Figure 28-
35).

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Figure 28-39 A, External tibial torsion is detected by a thigh–foot angle pointed away from the midline. B,
Metatarsus adductus as a cause of in-toeing is noted by a convex lateral foot border. If the foot cannot be
passively corrected to neutral, the deformity is rigid and may require serial casts for correction. (Reprinted
from Staheli L. Rotational problems of the lower extremities. Orthop Clin North Am. 1987;18:506. Copyright
© 1987 Elsevier.)

As the skeleton adapts to growth and bipedal posture, these torsional “deformities” resolve. A slight
amount of in-toeing has been noted in the better athletes. In-toeing is advantageous during cutting maneuvers
because a limb that is internally rotated will be aligned with the intended change of direction and is more
effective in push-off acceleration.

ANGULAR LIMB DEFORMITIES: BOWLEGS AND KNOCK-KNEES

Angular lower limb alignment, bowlegs and knock-knees (genu varum and valgum; see Figure 28-9), are
another common cause for an orthopedic consultation. For most children, these conditions represent the
spectrum of normal development. It is rare for limb malalignment to persist and cause functional or cosmetic
impairment sufficient to require surgical intervention. Normal, nonambulatory infants have physiologic
bowlegs with tibiofemoral angles of 20° or more of varus (bow). At approximately 18 months of age, the angle
corrects as the femur and tibia become collinear. After 3 years of age, the limbs assume the normal adult
alignment of 7° of skeletal valgus (Figure 28-40).

Figure 28-40 Changes in tibiofemoral alignment with growth shows that there is a natural progression from
bowlegs at birth to physiologic knock-knees by the age of 3. (Modified from Kling T. Angular deformities of
the lower limb in children. Orthop Clin North Am. 1987;18:514. Copyright © 1987 Elsevier.)

Pathologic conditions can cause knee bowing, including growth arrest of the medial tibial metaphysis,
chondrodysplastic dwarfism, and vitamin D–resistant (hypophosphatemic or renal) rickets. These systemic
conditions also cause deformities of other bones and joints. If bowlegs persist beyond 2 years of age,
radiographic evaluation may be warranted.

FLAT FEET

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Flat feet are another common skeletal variation. The most common type is the flexible flat foot. The
longitudinal arch of the foot is absent or flat in stance, but reconstitutes when the foot is non–weight bearing.
Most flexible flat feet are asymptomatic and result from ligamentous laxity affecting the many small joints of
the midfoot. A flat foot that is rigid and has little passive motion may be caused by a congenital coalition of
the tarsal bones. A flat foot associated with a tight heel cord may be caused by muscular dystrophy or cerebral
palsy. High-arched feet (pes cavus) with clawed toes are the sequelae of peripheral neuropathies, such as
hereditary motor and sensory neuropathy (formerly known as Charcot-Marie-Tooth disease).

DEVELOPMENTAL DYSPLASIA OF THE HIP

The incidence of developmental dysplasia of the hip, previously referred to as congenital dislocation of the
hip, is 1.5 per 1,000 newborns. One-third of cases are bilateral. The condition shows a familial predisposition
and is associated with intrauterine breech presentations. Girls are affected much more often than boys,
possibly because their ligaments are more sensitive to the relaxing effects of maternal estrogen released in
preparation for birth.
The early diagnosis of developmental dysplasia of the hip allows early treatment. All newborns and infants
must be examined for hip instability. The diagnosis is never obvious, but must be sought by careful
examination. Limited or asymmetrical thigh abduction suggests a hip abnormality (Figure 28-41). The
infant’s thigh is gently grasped by the long finger and thumb. With the hip and knee flexed 90°, the thigh is
abducted, whereas the greater trochanter is gently pressed forward in an anterior direction. A palpable jump or
click during this maneuver—Ortolani’s sign—signifies that the femoral head has been reduced into the
acetabulum and that the hip was dislocated. An opposite, provocation maneuver, in which adduction and
posterior pressure is applied by the thumbs over the femoral head, will lever the hip out of the acetabulum
(Barlow’s sign) if the hip is unstable. These two tests are useful in the first 2 weeks of life when the child’s
ligaments are under the relaxing influence of maternal hormones. Treatment is most successful early in life
and is accomplished by manipulative reduction (Ortolani’s maneuver) and immobilization with the hips in a
stable position of flexion and abduction using a Pavlik harness. If the hip remains dislocated, the acetabular
socket does not develop normally and remains shallow.

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Figure 28-41 Limited hip abduction in congenital hip dislocation. The perineum should be perpendicular to the
table. The limit of true hip joint motion is evidenced by concomitant movement of the perineum.

After 1 month of age, limited hip abduction is the most reliable sign of developmental dysplasia of the hip
(Figure 28-41). Asymmetry of thigh and buttock folds or telescoping of the flexed femur are other signs of
late hip dislocation. When the condition is bilateral, all physical signs that depend on noting asymmetry will
be absent, making diagnosis more difficult. When the child begins walking, a short leg limp is evident when
the hip dislocation is unilateral. A waddling, hyperlordotic gait is apparent if the condition is bilateral.
Treatment after walking age is more difficult. Contracted hip muscles are gradually stretched with traction or
an adductor muscle release. Operative hip reduction is likely needed, and the reduced hip must be maintained
in a cast.
The head of the femur is cartilaginous until almost 9 months of age and is not visible on radiograph.
(Radiographs are therefore of limited early diagnostic value.) Ultrasonography shows cartilage well and is
useful in the first 9 months. Hip joint ultrasound can dynamically evaluate the hip under positional stress.
After the femoral head ossifies, radiograph shows a dislocated hip to be displaced lateral and superior to a
shallow acetabulum.
The management of developmental dysplasia of the hip requires prompt attention by an orthopedic
specialist. When treatment is initiated early and followed closely, the prognosis for normal hip development
and function is good.

LEGG-CALVÉ-PERTHES DISEASE

Legg-Calvé-Perthes is a condition of uncertain etiology that results in osteonecrosis of the femoral head in
children 4 to 8 years of age. Boys are affected eight times more commonly than girls. Hip discomfort may be
referred to the medial knee in the distribution of the obturator nerve. Therefore, pediatric patients
complaining of knee pain should have their hip examined. The hip will display a subtle decrease in range of
motion, especially in abduction and internal rotation. Hip abduction strength is also decreased and may cause
a Trendelenburg limp, in which the child leans the torso over the affected hip.
Legg-Calvé-Perthes disease is self-limited and runs a 2- to 4-year course. Initial radiographs show
minimal findings and may show disuse osteoporosis and hip joint space widening. Later, when the dead bone
is being resorbed and revascularized, new bone is laid down on dead bone, causing the femoral head to appear
dense (sclerotic). During this revascularization stage, radiographic changes are most dramatic. Pathologic
fractures of dead trabeculae may occur with weight-bearing loads, causing a flattening of the femoral head.
The femoral head may appear fragmented and laterally displaced. The metaphysis may be rarefied and
broadened. A child with Legg-Calvé-Perthes disease should be referred to an orthopedic surgeon. Treatment
consists of traction to regain motion followed by bracing or surgical osteotomy to keep the articular portion of
the femoral head within the weight-bearing portion of the acetabulum. This may involve femoral or pelvic
osteotomies.

SLIPPED CAPITAL FEMORAL EPIPHYSIS

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A cause of limping in adolescence is a fracture of the proximal femoral growth plate or slipped capital femoral
epiphysis. A slipped capital femoral epiphysis is more common in boys than girls, is bilateral in approximately
33% of cases, and usually occurs during the prepubescent growth spurt (i.e., 10 to 14 years of age). Two
distinctly different body types are susceptible to the condition. One group consists of obese children with
delayed gonadal development; the other includes very tall children who have grown rapidly.
In addition to a limp, patients may have pain localized to the knee or, less frequently, to the groin. The
affected leg is held externally rotated. Internal hip rotation is limited and painful. An AP and Frog lateral
pelvis radiograph is ordered to compare the painful hip to the other side. It is common for this condition to
affect both hips. On AP radiographs, a line drawn tangential to the superior neck does not intersect the
femoral head epiphysis as it does in a normal hip (Figure 28-42A). Displacement is more apparent on the
lateral radiograph, in which the femoral head appears posteriorly on the femoral neck (Figure 28-42B).
Untreated, this femoral head/neck slippage can continue until growth ceases. To prevent further
displacement, the femoral head is fixed with multiple pins.

Figure 28-42 Slipped capital femoral epiphysis. The slipped capital femoral epiphysis on the left is compared to
the normal hip on the right. A, On anterior–posterior radiograph, a line drawn tangential to the top of the
femoral neck should pass through the normal femoral head (right). In a slipped femoral epiphysis, the line
does not intersect the head but passes above it (left). B, On a lateral radiograph, the head of the femur has
slipped posterior to the femoral neck (left). (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed.

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Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

OSGOOD-SCHLATTER DISEASE

Osgood-Schlatter disease affects the insertion of the patellar tendon onto the tibial tubercle. It is believed to
represent partial avulsion of the tibial tubercle in active children with avascular necrosis of the avulsed portion.
The patient complains of pain over the tibial tubercle aggravated by kneeling, direct pressure, and running.
The area is prominent and tender. Radiographs show irregular areas of bone deposition and resorption in the
tibial tubercle. The condition is usually self-limiting and resolves as the growth plates close. Occasionally, a
painful ununited nodule persists and is treated by excision.

CONGENITAL CLUB FOOT

The etiology of congenital club foot (talipes equinovarus) is unknown. It occurs in approximately 1:1,000
births and is twice as common in males as in females. Club feet are bilateral in 33% of cases. The condition is
characterized by three deformities: the ankle or talus is plantar flexed (equinus), the hindfoot or calcaneus is
inverted into varus, and the navicular bone and forefoot are shifted medially and supinated (metatarsus
adductus; see Figure 28-39B). Untreated, this deformity causes the patient to walk on the lateral border of the
foot, not upon the sole. The posterior muscles of the leg are atrophic and contracted. Neuromuscular
abnormalities must be excluded in children with a club foot. Corrective casts are applied immediately with the
gradual application of force directed to correct each of the three deformities. When a club foot is refractory to
serial cast correction, surgical release of the tight soft tissue structures of the posteromedial foot and ankle is
indicated.

SCOLIOSIS

Scoliosis is a curvature of the spine that is either flexible (correctable) or fixed (structural). A mobile form of
scoliosis may be due to poor posture, the muscle spasm secondary to a prolapsed disk, or as compensation for a
shortened leg. A fixed, structural scoliosis is accompanied by a rotational vertebral deformity that is not
correctable by a change in posture. Scoliosis causes an asymmetry of the rib cage that is most noticeable when
the patient bends forward. In stance, if the trunk is laterally shifted and not centered over the pelvis, the
scoliotic curve is said to be decompensated. Decompensated scoliosis may be associated with a higher
incidence of back pain.
Structural scoliosis can be caused by congenital vertebral deformities, neuromuscular diseases (e.g.,
myelomeningocele, cerebral palsy), or neurofibromatosis. Congenital scoliosis is due to abnormalities of
vertebral formation. It is manifested at a young age and is rapidly progressive. These children frequently have
associated neural tube, genitourinary, and cardiovascular malformations that occur at the same stage of
embryologic development. A comprehensive assessment of these organ systems is mandated in the child in
whom congenital scoliosis is identified. Neuromuscular scoliotic curves usually involve the full length of the
spine. These curves result from paraspinal muscle imbalance produced by diseases such as polio, spinal muscle
atrophy, cerebral palsy, and the muscular dystrophies. The scoliosis of neurofibromatosis is characterized by a
short but severe curve.

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 The most common cause of scoliosis is idiopathic. It causes a painless progressive deformity of the
thoracolumbar spine during adolescence. Girls are affected nine times more frequently than boys. The spinal
deformity begins before puberty but increases most rapidly during the adolescent growth spurt. As the
scoliotic curvature increases, the shape of the vertebrae and the attached ribs change. The vertebral bodies
become wedge shaped, and the ribs prominent on the convex side of the curve. These changes of vertebral
structure explain why the curves become inflexible over time. Aside from cosmetic concerns, severe thoracic
spinal curves can compromise cardiopulmonary function. Some patients with large curves also develop
degenerative spinal joint pain. Curve progression is more likely in young patients with larger curves. The goal
of treatment is to prevent the scoliotic curve from increasing in magnitude. Spinal braces work well in smaller
curves but must be worn until the cessation of growth. Larger curves or scoliosis that occurs with congenital or
neuromuscular conditions that progress rapidly in severity despite bracing are managed with surgical
correction and spinal fusion.

INFECTIOUS DISEASES OF THE MUSCULOSKELETAL SYSTEM

Musculoskeletal infection involves either bone (osteomyelitis), joints (septic arthritis), or soft tissues.
Gram-positive organisms, primarily staphylococci, are usually the causative microbes. Gram-negative
organisms have been increasing as a cause, especially in compromised hosts and in the nosocomial
environment.

OSTEOMYELITIS

Bacteria may infect bone by one of the following four mechanisms:

1. Hematogenous spread from a distant site

2. Contamination from an open fracture
3. After an operative procedure on bone
4. Extension from a contiguous infected foci

Acute Hematogenous Osteomyelitis

Acute osteomyelitis occurs most commonly in children and is due to hematogenous spread from a distant site
of infection. In the 0- to 3-month age-group, the common causative organisms are coliforms from the
maternal birth canal to which the infant is exposed during delivery. Haemophilus influenzae from otitis media
and pharyngeal sources is common until age 3. Staphylococcus aureus, which predominates in skin infections, is
common in all age-groups.

Pathology
In children, metaphyseal capillaries turn back toward the diaphysis at the level of the growth plate, forming a
turbulent area where organisms may be deposited. Because of this peculiarity of intraosseous vascular
anatomy, the metaphyses of long bones are the most common foci of acute hematogenous osteomyelitis.
Metaphyseal vessels cross the epiphyseal plate during a brief period of neonatal development, which permits
epiphyseal infection to occur in infancy.

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 As trapped bacteria multiply and pus forms in metaphyseal tissue, the pressure within the unyielding bone
causes intense pain, forcing the infection through the thin metaphyseal cortex to elevate and spread beneath
the periosteum as a subperiosteal abscess (Figure 28-43). Periosteal stripping stimulates new bone formation
that is seen on radiographs. The infection may envelop the bone or burst through the periosteum into the soft
tissues.

Figure 28-43 Osteomyelitis begins in the bony metaphysis, where hematogenous spread leaves bacteria
entrapped in the end arteriolar system of interosseous blood vessels. With exponential bacterial reproduction,
pressure within the unyielding bone causes pain and forces the infection through the thin metaphyseal cortex
to form a subperiosteal abscess. The epiphyseal plate and periosteum provide a temporary barrier to the
infection. X, infected foci; arrow, path of infection; shaded area, periosteum stripped from bone. (Modified
with permission from Salter RB. Textbook of Disorders and Injuries of the Musculoskeletal System. 3rd ed.
Baltimore, MD: Lippincott Williams & Wilkins; 1999.)

Clinical Presentation
The onset is acute, and progression can be rapid, even life threatening. The child experiences severe pain near
the end of a long bone and guards the limb, unwilling to move it. With septicemia, there may be fever,
increased irritability, or malaise. Soft tissue swelling occurs late and indicates that the infection has spread
beyond the bone. The white blood cell (WBC) count and erythrocyte sedimentation rate are usually elevated.
Radiographic changes occur late and may not provide evidence of infection for 1 week or more. A three-phase
technetium pyrophosphate bone scan can distinguish among soft tissue cellulitis, rheumatic fever, and acute
hematogenous osteomyelitis earlier in its clinical course.

Evaluation and Treatment

Blood cultures should be obtained along with a bone marrow aspirate for cultures and Gram stain. Parenteral
antibiotic treatment should be initiated to cover organisms common to the child’s age-group, and final
antibiotic selection will depend on the results of bacteriologic cultures and sensitivities. If local and systemic

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manifestations of the infection have not improved within 24 hours, open surgical drainage of subperiosteal pus
is indicated, as is bone drilling. Antibiotic therapy should be continued for at least 3 weeks to fully eradicate
the organism. Serial sedimentation rates are useful in monitoring the therapeutic response: elevated rates
should return to normal values as the infection resolves. Late complications of hematogenous osteomyelitis
include the development of persistent or recurrent chronic osteomyelitis, pathologic fractures, and growth
disturbances from epiphyseal plate injury.
Adult osteomyelitis typically occurs after an open fracture or as a complication of surgery. Proper
management of open fractures with aggressive and repeated debridement of devitalized tissue, wound
irrigation, appropriate antibiotic coverage, fracture stabilization, and delayed wound closure serve to decrease
the incidence of posttraumatic infection. A clean operative environment (e.g., room, air, personnel),
nontraumatic tissue handling, adequate hemostasis, and prophylactic antibiotic administration—especially in
implant surgery—are surgical methods that prevent postoperative infections. Effective treatment of an
infected implant requires surgical removal of the implant, debridement, and parenteral antibiotics. S. aureus
remains the leading cause of bone infection in adults. Some infections can result from less virulent organisms
such as Staphylococcus epidermidis. Diabetic foot infections tend to be due to mixed aerobic and anaerobic
bacteria.

Chronic Osteomyelitis

The incomplete eradication of a previous bone infection results in chronic osteomyelitis. Bacteria that have
been protected from leukocytes and antibiotics by a surrounding wall of avascular dead bone (sequestrum)
remain dormant in the dead bone. Many years after the initial infection, the bacteria can suddenly multiply,
form a sinus, and drain, or they can cause an acute recurrence of the osteomyelitis. Infected, sequestered bone
needs to be surgically debrided (saucerized). Soft tissue coverage may be required to enhance local blood
supply and antibiotic delivery. A bone graft or bone transport (distraction osteogenesis) may be necessary if
radical amounts of infected bone have been resected.

SEPTIC ARTHRITIS

Pathology

When bacteria invade a synovial joint, the inflammatory process can cause rapid, severe destruction of the
articular cartilage. In children, septic arthritis occurs as an extension of hematogenous osteomyelitis. The
joints commonly involved are those in which the metaphysis resides within the joint capsule: the hip, elbow,
and shoulder. Because the metaphysis is enclosed in the joint capsule, what begins as osteomyelitis can erupt
through the cortex to involve the joint in the septic process (Figure 28-44). Thus, in children, the causative
organisms of septic arthritis are the same as those involved with osteomyelitis. Staphylococcus predominates in
all age-groups. Gram-negative organisms affect children younger than 3 years. In adults, joint infections occur
via hematogenous spread, after penetrating wounds, and rarely as a manifestation of disseminated gonorrhea.

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Figure 28-44 In children, septic arthritis occurs as a consequence of hematogenous osteomyelitis. The joints
involved are those in which the bony metaphysis resides within a joint capsule, such as the hip. When
osteomyelitis erupts through the metaphyseal cortex, it will infect the joint space. X, infected foci; arrow, path
of infection. (Modified with permission from Salter RB. Textbook of Disorders and Injuries of the Musculoskeletal
System. 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999.)

Evaluation
If a newborn is profoundly ill and unresponsive, the diagnosis of septic arthritis may be difficult to establish.
The major finding on physical examination is restricted, painful joint motion. The joint is also tender to
palpation. Early radiographs and peripheral WBC counts are usually nonspecific. Because treatment delay has
dire consequences, the clinical suspicion of a septic arthritis is enough to warrant emergency joint fluid
aspiration for cell count, culture, and Gram stain. To document that the joint has been entered, an arthrogram
should be performed after aspiration. Joint aspiration through an area of cellulitis is contraindicated, because it
may introduce organisms into the joint.
In the patient with active inflammatory arthritides on suppressive medications, acute septic arthritis can be
mistaken for an acute flare of inflammatory arthritis. Joint aspiration for cell count, crystal evaluation, and
Gram stain and culture should be performed to rule out infection. A WBC count <50,000 is typically
noninfectious, whereas >100,000 is infectious. However, a WBC count in the 50,000 to 100,000 range can be
either inflammatory or infectious. Once an aspirate of the joint is performed, the patient should be treated
with antibiotics pending results of the cell count and Gram stain.

Treatment
To prevent the rapid degradation of articular cartilage by pyogenic toxins, treatment of a septic joint is an
emergency. The most effective treatment is surgical incision of the joint capsule (arthrotomy), drainage,
debridement of infected tissue, and joint irrigation. Intravenous antibiotic therapy is started, and the wound is
loosely closed over a drain. In the knee, arthroscopic drainage, irrigation, and synovectomy have proven

1100
equally effective in the treatment of joint sepsis. The potential complications from septic arthritis include
arthritis, epiphyseal necrosis, pathologic joint dislocation, growth disturbances, leg length discrepancies, and
limb deformity.

INFECTED HAND FLEXOR TENOSYNOVITIS

Improperly treated hand infections can cause severe disability. A flexor tendon sheath infection is especially
serious because it can rapidly destroy the tendon’s gliding mechanisms, create adhesions, and cause severe loss
of joint motion. Tendon sheath infection can even cause tendon necrosis.
The prevailing infecting organism is S. aureus. Pyogenic flexor tenosynovitis is commonly caused by a
penetrating palmar injury but can also occur by means of hematogenous seeding.
Kanavel described the four classic physical signs of infected flexor tendon sheaths as follows:

1. The entire digit is enlarged and swollen (looks like a sausage).

2. The finger is held in a flexed posture.
3. There is tenderness over and limited to the course of the tendon sheath (tender with anterior–posterior
pressure but not medial–lateral pressure).
4. There is exquisite pain with passive digital extension.

Pyogenic hand infections are limb threatening and require emergency care. If treated early with parenteral
high-dose antibiotic therapy, the infectious process may be halted. Failure of symptoms and signs to improve
over 24 to 48 hours warrants surgical drainage with irrigation. Early active range-of-motion exercise is needed
to rehabilitate hand function.

NECROTIZING FASCIITIS

Necrotizing fasciitis (“flesh-eating bacteria”) is a rare but potentially deadly soft tissue infection of the fascia
that occurs most commonly in an immunocompromised host (e.g., diabetics). Its diagnosis may be
complicated by the fact that it can mimic cellulitis or compartment syndrome, and it is rapidly progressive and
usually requires emergent diagnosis and treatment. Typically, necrotizing fasciitis develops after a wound has
occurred, most commonly the foot, but it can begin without a break in the skin.
There are three types of necrotizing fasciitis. Type one is polymicrobial, which is most common in the
immunocompromised person. Type two is the classic group A β-hemolytic Streptococcus with or without S.
aureus and usually seen in previously healthy patients. Type three is caused by marine bacteria.
The early clinical presentation involves swelling, erythema, and pain out of proportion to the appearance
of the limb. These may rapidly progress to bullae, necrosis of skin and underlying soft tissues, and
subcutaneous crepitus. As the infection spreads, signs and symptoms of systemic septic shock may develop.
The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score emphasizes the following abnormal
laboratory values as a diagnostic aid: elevated WBC count, glucose, C-reactive protein, and creatinine and low
sodium and hemoglobin.
Treatment consists of a combination of emergent wide surgical debridement and intravenous antibiotics.
Necrosis of fascia and superficial soft tissues can result in gray, watery, foul-smelling “dishwater” pus, as seen

1101
at the time of debridement. Time to surgical debridement is the most important factor for limb salvage and
survival.
The diagnosis of necrotizing fasciitis should be considered for any individual who has unexplained limb
pain and the above abnormal laboratory values. Because of its fulminant course, loss of limb and life are not
uncommon, and even today mortality rates can approach 25%.

INFLAMMATORY DISEASES OF THE MUSCULOSKELETAL SYSTEM

Arthritis means joint inflammation. The two common forms are osteoarthrosis and rheumatoid arthritis.
The management of arthritis as it affects specific joints is well described in orthopedic and rheumatology
texts. In this section, treatment will be discussed in general terms.

OSTEOARTHROSIS

Osteoarthrosis, also called degenerative joint disease, is the most prevalent form of arthritis affecting adults
and is characterized by the progressive narrowing of articular cartilage, sclerosis in the subchondral regions,
and a hypertrophic response of bone and cartilage (osteophyte formation). In the adult population older than
65 years, there will be radiographic evidence of joint degeneration affecting one or more joints. Its incidence
increases with age and has no sex predilection. The etiology of osteoarthrosis is not clearly understood;
however, mechanical joint stresses are related to its development, and arthrosis results from joint surface
incongruity, malalignment, and joint instability.

Pathology

Articular cartilage has physical properties that tolerate a limited amount of stress per unit surface area. When
these forces are exceeded, the cartilage will show signs of wear. Pathologically, articular cartilage becomes
softened, frayed, and eventually fibrillated. Focal cartilage erosions become widespread and expose the
underlying subchondral bone. This bone becomes sclerotic and stiff as the trabeculae thicken and cysts form.
At the periphery of the joint, spur-like bony outgrowths covered by hyaline cartilage (osteophytes) develop.
Osteophytes are a biologic attempt to decrease joint stress by increasing joint surface area and decreasing
motion.
The radiologic hallmarks of osteoarthrosis are as follows (Figure 28-45):

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Figure 28-45 Osteoarthritis affecting the knee joint. A, The anterior–posterior radiograph shows joint space
narrowing, subchondral sclerosis, and a hypertrophic osteophytic response of the bone at the joint margins. B,
Osteophytes (seen better on this lateral radiograph) decrease joint motion and increase joint surface area, in a
biologic attempt to decrease excessive joint surface stresses. C, The knee ultimately required total joint
replacement. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2007.)

1. Localized joint space narrowing

2. Subchondral bone sclerosis
3. Osteophytes
4. Subchondral cysts

Symptoms of degenerative joint disease begin gradually with joint pain brought on by activity and relieved
by rest. The patient may report a history of joint swelling, stiffness, and the slow, progressive loss of joint
motion. Because the articular cartilage has no nerve supply, the pain of osteoarthritis is believed to originate in
the periarticular structures. Pain and crepitus (a grinding sensation) occur with joint motion, and signs and
symptoms often correlate with the degree and extent of radiographic abnormalities. It must be emphasized
that osteoarthrosis is generally a local disease. Multiple joint involvement suggests a systemic process
(inflammatory arthritis).
While weight-bearing joints (e.g., hip and knee) are most frequently involved, degenerative joint disease
may also occur in the hand or in the great toe at the MTP joint. If present in the hand, it commonly affects
the trapeziometacarpal joint in the thumb, and pain occurs at the base of the thumb with pinching.

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Treatment

Nonsurgical Treatment
The goal of nonsurgical treatment of osteoarthrosis is to relieve pain and maintain strength and function.
Reduction of joint load by means of activity modifications, weight loss, or walking aids (e.g., a cane) may
provide some relief from symptoms. Physical therapy alleviates pain with the use of heat while attempting to
maintain joint motion and muscle strength through exercise. Medications for osteoarthritis may include
nonsteroidal anti-inflammatory drugs, simple analgesics, dietary supplements, or intra-articular injection of
steroids of lubricating agents. Nonsteroidal anti-inflammatory drugs that interfere with the pain-producing
products of inflammation (e.g., prostaglandins, lymphokines, kinins) can reduce pain and swelling. These
drugs can have adverse effects, including rashes, peptic ulceration, and tinnitus. Simple analgesics (e.g.,
acetaminophen) have been shown to be efficacious in the management of musculoskeletal pain; however, the
chronic use of narcotics is to be avoided. Intra-articular steroid injections provide dramatic relief of acute
arthritic symptoms. However, the repeated use of steroids may accelerate joint deterioration by deleterious
effects on the metabolism of the cartilage. The injection of intra-articular lubricating agents (hyaluronic acid)
may provide short-term symptomatic relief of arthritis. There are numerous dietary supplements (e.g.,
glucosamine and chondroitin sulfate) whose benefits in the management of degenerative joint disease have
been claimed but have yet to be substantiated in scientific studies. The role of platelet-enriched plasma on the
course of arthritis is not clear at this time.

Surgical Treatment
The selection of surgical procedures depends on the stage, site, and debility caused by the arthrosis. There are
four categories of bony procedures: osteotomy for joint realignment, partial joint replacement, total joint
replacement, and joint fusion (or arthrodesis). An osteotomy realigns the extremity, corrects deformity, and
shifts weight-bearing forces from worn joint surfaces to healthier cartilage. This procedure should be
considered in younger patients with degenerative arthrosis of the knee. An example would be a valgus-
producing tibial osteotomy for a varus knee with symptomatic medial compartment arthrosis.
Partial joint replacement uses prosthetic components to resurface either the medial, lateral, or
patellofemoral compartments of the knee. These devices are used in the presence of single compartment
disease with intact cruciate ligaments and functional range of motion. Total joint arthroplasty (Figure 28-
45C) involves the replacement of articulating surfaces with low-friction, metal, and high-molecular-weight
polyethylene surfaces. Total joint arthroplasty is an extremely successful procedure that profoundly relieves
pain in more than 90% of cases. Joint replacement is not without complications: prosthetic components wear
out, loosen, become infected, and cause local osteoporosis and periprosthetic fractures. Therefore, joint
replacement is reserved for patients with advanced arthrosis and a relatively sedentary lifestyle.
Joint arthrodesis is an effective procedure that converts painful arthritic joint motion into a painless, stable,
stiff joint. Arthrodesis is a durable procedure that is indicated in young, very active patients with isolated joint
involvement (e.g., great toe, spine, ankle). Large joint arthrodesis is contraindicated in patients with systemic
multiple joint inflammatory arthritis.

RHEUMATOID ARTHRITIS

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Rheumatoid arthritis is an inflammatory disorder of unknown etiology. It is a chronic symmetrical
polyarthritis with a relapsing course that frequently leads to progressive joint destruction, deformity, and
incapacitation. The disease occurs in women more commonly than men (3:1 predominance) and has a genetic
basis with individuals with the HLA-DR4 haplotype having a risk of developing the disease. Regardless of the
inciting factor, the immune system is involved in the disease process; 80% of patients have autoantibodies to
the Fc region of immunoglobulin G (IgG), and the immunoglobulin M (IgM) autoantibody is termed the
rheumatoid factor. Although the presence of the rheumatoid factor is not diagnostic of the disorder (1% to 5%
of normal subjects have it), high titers are associated with severe joint disease, multisystem involvement, and a
poor prognosis.

Pathology

The pathology of rheumatoid arthritis results from synovial inflammation of joints and tendon sheaths. As the
synovial membrane becomes infiltrated by macrophages and lymphocytes, it undergoes hypertrophy and
causes joint swelling and effusions. The byproducts of the inflammatory process injure adjacent bone and
cartilage. Hypertrophic synovial cells proliferate, forming a “pannus,” and damage the articular cartilage.
Recurrent joint swelling stretches the capsule and supportive ligaments, which causes joint instability,
deformity, and further mechanical injury. Adjacent inflammatory processes weaken tendons and cause muscle
imbalance in the complex joint systems of the hand. Joint and tendon subluxation is common in rheumatoid
hands that become weak and deformed (Figure 28-46). The systemic nature of the disease is made evident by
its extra-articular manifestations, which include vasculitis, neuropathy, iritis, lymphadenopathy, splenomegaly,
and polyserositis.

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Figure 28-46 Radiographic evidence of rheumatoid arthritic joint involvement, with soft tissue swelling and
multiple metacarpophalangeal joint palmar dislocations. Disuse osteoporosis is evident. Actual cartilage
destruction causes joint space narrowing, as exemplified at the proximal interphalangeal and wrist joints. Bone
erosions occur at the site of synovial attachments. Osteophytic changes of bone hypertrophy typical of
osteoarthrosis are unusual with rheumatic diseases. (From Lawrence PF. Essentials of Surgical Specialties. 3rd
ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

Just as the pathophysiology of rheumatoid arthritis differs from that of osteoarthrosis, so do the radiologic
features. Soft tissue swelling and periarticular osteoporosis are the early signs of rheumatoid arthritis. Diffuse
cartilage destruction leads to generalized joint space narrowing and bone erosions at the site of synovial
attachments (Figure 28-46). Joint deformity, cystic bone destruction, and joint ankylosis mark end-stage
disease. Hypertrophic osteophytes are rare in rheumatoid arthritis.

Treatment

The treatment of rheumatoid arthritis is directed toward pain relief, suppression of the inflammatory
synovitis, prevention of joint deformities, and early joint reconstruction. In its early stages, the synovitis is
inhibited by drug therapy or managed by surgical removal of the diseased synovium (synovectomy). Splinting
the involved joints in functional positions during acute flare-ups rests the joint, prevents contractures, and
minimizes deformity. Exercises to maintain range of motion and muscle strength—although painful and
frustrating to the patient—are encouraged. With advanced joint destruction, tendon ruptures are repaired, and
excisional or replacement arthroplasty helps to restore mobility and function.
To optimize the patient’s function, it is often necessary to use mechanical aids and adaptive apparatus and
to modify the physical layout of both the home and the workplace. The proper management of rheumatoid
arthritis requires the multidisciplinary teamwork of a rheumatologist, surgeon, physiotherapist, occupational
therapist, and social worker.
More recently, anti–tumor necrosis factor (anti-TNF) preparations have been added to the treatment of
patients with systemic inflammatory arthritis. There are reports of dramatic reduction in pain for some
patients. The effects of long-term use of drugs of this class are not known.

OTHER ARTHRITIDES

Although osteoarthrosis and rheumatoid arthritis are the most common arthritic conditions, there are a
myriad of other arthritic diseases, including infections, gout, chronic juvenile arthritis, the
spondyloarthropathies of ankylosing spondylitis, Reiter’s disease, and psoriatic arthritis. Additionally,
neuropathies, hemophilia, and many other diseases may have arthritic manifestations. Complete medical
histories and review of system are thus crucial in determining the underlying etiology of a patient’s joint pain.
Some arthritides, such as gonococcal arthritis and Lyme disease, are caused by infectious agents. Systemic
gonococcal infection may be associated with petechial and pustular rashes on the palms and soles of the feet,
and joint aspiration and culture reveal typical Gram-negative diplococci. Infection usually involves small
joints, especially of the hands and feet. Treatment with cefuroxime 1 g intravenously daily for 7 days or
penicillin 10 to 20 million units daily for 7 days, if sensitive, usually leads to full recovery, because the

1107
organism does not produce collagenase.
Lyme disease is caused by the spirochete Borrelia burgdorferi. The infective agent is carried by ticks that
live on deer. The clinical course tends to be a migratory polyarthralgia with or without a rash. The symptoms
usually subside after antibiotic treatment with doxycycline 100 mg PO bid or amoxicillin 500 mg PO q6h for
10 days.
With gouty arthritis, microscopic analysis of joint fluid under polarized light reveals splinter-like,
monoclinic, negatively birefringent uric acid crystals, whereas in pseudogout, positively birefringent,
rhomboid-shaped, calcium pyrophosphate dihydrate crystals are apparent. Radiographs of the latter may show
typical articular cartilage or meniscal calcification. Acute flares of crystal-induced arthritis are treated with
high doses of nonsteroidal anti-inflammatory drugs or colchicine. Long-term preventive treatment of gout
involves use of allopurinol to decrease systemic uric acid levels.

BONE NECROSIS

Interruption of the blood supply to bone results in bone cell death (osteonecrosis or avascular necrosis).
Traumatic causes of osteonecrosis have been discussed and involve vascular injury or interruption of the blood
supply to bones. The femoral head, talus, carpal lunate, and scaphoid are prone to avascular necrosis. These
bones are all extensively covered by articular cartilage and have limited soft tissue attachments. Legg-Calvé-
Perthes disease of the femoral head represents a form of avascular necrosis in developing skeleton.
Nontraumatic causes of osteonecrosis involve intraosseous microvascular disturbances that result from either
arterial emboli or impairment of venous outflow. Either of these mechanisms can compromise bone perfusion.
Patients on glucocorticoid therapy (especially those with systemic lupus erythematosus and/or those who
have had a renal transplant) are at higher risk for developing osteonecrosis. The thrombi of
hemoglobinopathies (e.g., sickle cell disease), the nitrogen bubbles of decompression sickness (dysbarism), the
glucocerebroside deposits of Gaucher’s disease, hyperuricemic crystals, fat emboli of alcoholism, and
pancreatitis may cause an occlusive form of bone infarction. Affected bones have a paucity of arterial
anastomoses. The femoral head of the hip is the most frequently affected by avascular necrosis.

PATHOLOGY

Bone is a living tissue that is in a dynamic state of homeostasis involving bone resorption, replacement, and
remodeling. Unlike other tissues, normal bone turnover occurs slowly. Following a loss of blood supply, bone
cell and marrow necrosis occur within 24 hours. Although these changes can be detected microscopically by
the absence of osteocytes from their lacunae, there is often a delay of as much as 5 years between the onset of
symptoms and the appearance of radiologic abnormalities. MRI is the most sensitive method of detecting
early osteonecrosis.
The revascularization process is slow. The living bone surrounding the infarction becomes hypervascular.
The hyperemia of the surrounding bone causes local bone mineral resorption appearing as osteopenia on x-
ray. Dead tissue retains its density and appears white (sclerotic) on x-ray. As vessels invade and try to repair
the necrotic zone, new bone is laid down on the old trabeculae, and dead bone is removed by osteoclasts. This
reparative process weakens the femoral head at the margins of the infarct. With persistent weight-bearing

1108
stress, the necrotic subchondral bone may fracture, leading to severe pain and rapid joint degeneration (Figure
28-47). Initially, the articular cartilage remains intact because it is nourished by synovial fluid. When a
subchondral fracture occurs, the bone support is lost. The articular cartilage becomes separated from the
subchondral bone, and a process similar to osteoarthrosis causes joint destruction.

Figure 28-47 Advanced avascular necrosis of the femoral head in a patient with sarcoidosis who had been treated
with systemic steroids. The femoral head is dense (sclerotic). There is evidence of a subchondral lucency
(arrows) with joint surface flattening, collapse, and marginal osteophyte formation. (From Lawrence PF.
Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

EVALUATION AND TREATMENT

The symptoms of osteonecrosis may not become manifest until a subchondral fracture occurs. Symptoms
begin with painful limited active motion. Two-thirds of patients complain of pain at rest, which can occur at
night. In the elderly, spontaneous osteonecrosis of the femoral condyle occurs with the sudden onset of severe
knee pain not associated with trauma. Many cases show increased bone scan activity over the femoral condyle
adjacent to the necrotic zone.
The prevention of joint loading until natural healing processes are completed on the basis of conservative
treatment. Core decompression, in which a hole is drilled through the dead cancellous bone, may be of
benefit. Intraosseous pressure is decreased as the biopsy tract creates an avenue for revascularization.
Although the inciting agent is vascular, the joint deterioration results from loss of mechanical support for
the articular surface. The management principles for advanced disease are similar to those employed in the
treatment of osteoarthrosis. If the volume of dead bone is large, total joint replacement is a reasonable
treatment option. Unfortunately, avascular necrosis occurs in younger patients, whose high activity levels place
stresses that can exceed the design tolerance of implants.

DEGENERATIVE DISEASES OF THE SPINE

LUMBAR SPINE

Low back pain is the most common musculoskeletal complaint for the 30- to 65-year age-group. Eighty
percent (80%) of adults experience an episode of low back pain severe enough to interfere with normal daily

1109
activities. In the United States, the annual cost of back-related medical payments is estimated at $16 billion.
An additional $50 billion is attributed each year to lost worker productivity.

Anatomy and Physiology

Degenerative joint disease is far more common to the joints of the spine than to the joints of the limbs. The
spine is an articulated column of vertebrae that protects the spinal cord and nerve roots. The neural elements
also can be affected by degenerative spinal pathology. The motion segment of the spine is composed of two
bony vertebrae covered with cartilage end plates and the intervertebral disk. Vertebral motion takes place
through a three-joint complex: the intervertebral disk and two posterior synovial facet joints (Figure 28-48A).
The disk is composed of a central gelatinous nucleus pulposus and an elastic annulus fibrosus (Figure 28-
48B). In flexion–extension and lateral bending, the vertebrae moving through the spatial orientation of the
paired facet joints direct spinal motion. The lumbar vertebral facets are in the sagittal plane and permit flexion
and extension. The thoracic facets are oriented in more of a horizontal plane, allowing lateral bending and
rotatory motion. Degenerative spine disease anatomically affects the two sites of spinal motion—the disk
and/or the facet joints. The ligaments that tether the vertebrae together include the anterior and posterior
longitudinal ligaments attached to the vertebral bodies. The ligamentum flavum connects the laminae with
the interspinous and supraspinous ligaments between the spinous processes (Figure 28-49). The paraspinal
muscles are complex and span two to five vertebral segments. These muscles power spinal motion and help
absorb the stresses of erect bipedal posture.

Figure 28-48 A, The spinal motion segment consists of two vertebral bodies and the intervening disk. Motion
occurs through two paired facet joints and the disk. The vertebrae rock or pivot over the disk in flexion and
lateral bending. B, The disk comprises a central gelatinous nucleus pulposus and its peripheral fibrous
encasement, the annulus fibrosus. (Reprinted with permission from American Academy of Orthopaedic
Surgeons. Athletic Training and Sports Medicine. 2nd ed. Rosemont, IL: American Academy of Orthopaedic
Surgeons; 1991:515.)

1110
Figure 28-49 The ligaments of the spinal column. (Reprinted with permission from Wilson FC, ed. The
Musculoskeletal System: Basic Processes and Disorders. 3rd ed. Philadelphia, PA: JB Lippincott; 1983.)

Etiology of Low Back Pain

Contrary to popular opinion, the vast majority of low back pain is not due to a “slipped disk.” In 80% to 90%
of patients with low back pain, the pain is of unknown etiology and the pathology remains obscure. Fewer
than 10% of patients experience pain in the sciatic nerve (L5–S3) distribution (“sciatica”). Only 1% to 2% of
patients require surgical treatment for a disk herniation. With symptomatic care, 50% improve in 2 weeks and
90% in 3 months.

Pathophysiology

Lumbar Strain (Mechanical Back Pain)

Most cases of back pain result from minor events, not from significant trauma. Many injuries involve
myofascial strains, minor ligament injury, or overuse. Lack of exercise, poor muscle tone, and obesity
contribute to minor postural injuries of the spine. This type of mechanical back pain is common in women
during or after pregnancy. The pain of mechanical strain rarely radiates beyond the knee and remains localized
to the spine and buttocks. More than 80% of these back problems resolve within 6 weeks of onset.

Spondylolysis and Spondylolisthesis

The facet joints of the lumbar spine are oriented in the sagittal plane, which permits flexion and extension
while resisting rotational and lateral bending motion. When the spine is hyperextended, the facet joints are
engaged. If a rotational twisting force is added, the lamina may fracture, either after an acute injury or from
the stress of repetitive microtrauma. The fracture occurs immediately caudal to the superior facet in a region
called the pars interarticularis (Figure 28-50A). This injury, spondylolysis, occurs 10 times more often in
gymnasts than in age-matched controls and may result from back extension during dismount landings.

1111
Figure 28-50 The lumbar facet joints are oriented in the sagittal plane and allow flexion and extension. With
lumbar extension, the facet joints engage; when a significant rotatory force is added, the lamina just inferior to

1112
the facet may fracture. A, If spondylolytic fractures occur bilaterally, the unsupported superior vertebrae may
translate anteriorly, producing spondylolisthesis. B, This fracture is called spondylolysis, which literally means
spine lysis. (Modified from McNab I, McCullough J. Backache. 2nd ed. Baltimore, MD: Lippincott Williams
& Wilkins; 1990.)

If the fracture is bilateral, the superior vertebral body, lacking facet support, may slide forward on the
inferior vertebra. This anterior shift of one vertebra on another is called spondylolisthesis (Figure 28-50B). In
young patients, the condition may be painful and the slippage can progress. Spinal fusion is the standard
treatment for a progressive, painful spondylolisthesis.

Disk Herniation
Disk herniation is the result of extrusion of the nucleus pulposus through the annulus fibrosus. It occurs in
adults 30 to 50 years of age (i.e., during the prime working years). The most frequently involved disks are at
L4–L5 and L5–S1, the most mobile lumbar spinal segments. A ruptured L4–L5 disk will affect the L5 nerve
root, and a ruptured L5–S1 disk affects the S1 root. In adults, the nucleus pulposus loses proteoglycans and
water content, making it less resilient. In the aging process, the annulus fibrosus loses its elasticity, especially
posteriorly, where it is thinnest. The combination of age-related changes and repeated minor trauma can
cause tears in the annulus. If an annular tear is large, it will permit the extrusion of the nucleus pulposus. In
some cases, the herniated disk material causes minimal symptoms. In others, the herniated disk material exerts
direct pressure on the nerve root (Figure 28-51).

Figure 28-51 Magnetic resonance scan of a large L4–L5 herniated disk. The epidural fat plane is obliterated as
the disk exerts extradural pressure on the thecal space. (From Lawrence PF. Essentials of Surgical Specialties.
3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

1113
 Clinically, patients complain of severe pain, often after bending to lift or while twisting with a heavy
object. The pain emanates from the back or buttock and radiates into the leg and foot in a radicular (nerve
root), dermatomal distribution. The pain is accentuated by bending, sitting, and coughing. The supine
straight-leg raising test places traction on the S1 nerve root and, to a lesser degree, the L5 root. This test
reproduces the pain, which should radiate below the knee to be considered positive. Ankle dorsiflexion
accentuates the pain (Lasègue maneuver), whereas ankle plantar flexion should not affect it. The latter test is
helpful to exclude malingerers. Radicular motor weakness, numbness, and reflex diminution provide objective
evidence of nerve root compression (Table 28-4). When a large amount of disk is extruded into the spinal
canal, it may compress more than one nerve root. When multiple nerve roots are involved, the clinical picture
may be confusing because of overlapping patterns of pain and functional losses. Loss of bowel and bladder
continence is a result of a central disk herniation compressing multiple S1–S4 roots. Called the cauda equina
syndrome, this condition is a surgical emergency demanding decompression to prevent permanent
incontinence.

TABLE 28-4 Lumbar Lesions and Associated Radicular Abnormalities

Location Abnormality

L4 Nerve Root

Pain/numbness Medial leg and ankle

Sensory Hypesthesia, medial leg, and ankle

Motor Weak ankle dorsiflexion or weak quadriceps (knee extension)

Reflex Decreased knee jerk

L5 Nerve Root

Pain/numbness Lateral calf and dorsal foot

Sensory Hypesthesia, dorsal foot, great toe

Motor Weak extensor hallux longus

Reflex Usually none; decreased posterior tibial tendon reflex possible (but that reflex present in only 20% of normal
patients)

S1 Nerve Root

Pain/numbness Posterior calf, lateral and plantar foot

Sensory Hypesthesia, lateral foot

Motor Weak toe and ankle flexors, foot evertor

Reflex Decreased ankle jerk

MRI of the lumbosacral spine is the diagnostic test of choice to define the anatomic location of disk
material for patients considered for surgery with unremitting leg pain or progressive neurologic deficit. CT is
less sensitive and specific but may localize pathology. Myelography, the injection of water-soluble dye into the
epidural space, is rarely used unless MRI is not available.

1114
Spinal Stenosis
The spinal facets are synovial joints and are subject to degenerative arthritic changes. As the disks narrow,
there are increased forces on the facet joints. The facet joints narrow and they develop marginal osteophytes.
The development of hypertrophic facet joint osteophytes narrows the space available for existing nerve roots
and may irritate or compress them. The narrowing of the disk may allow the ligamentum flavum to buckle
into the spinal canal. This combination of folds of ligamentum flavum posteriorly and hypertrophic
osteophytes anteriorly can cause encroachment of spinal canal or foraminal contents, causing symptoms of
spinal stenosis.
Spinal stenosis is a pattern of back and leg pain attributed to narrowing of the spinal canal. The pain tends
to begin after being upright or walking for a period of time. It does not tend to diminish unless the patient sits
down or lies down. This feature usually distinguishes it from vascular claudication, where the pain usually
dissipates by standing still for a short period. This pattern of pain is referred to as neurogenic claudication. It
tends to affect people with extensive degenerative disk disease who are usually over 65 years of age.
Surgery for spinal stenosis involves decompression of the spinal cord and roots. Careful preoperative
evaluation is necessary to properly identify the location and extent of pathology. CT and MRI scans of several
spinal levels are needed to define the pathology and extent of neural canal and foraminal compromise. Each
disk space is evaluated for herniation and each facet joint for stenosis of the lateral recess of the spinal canal.

Other Conditions
There are many other causes of back pain. The medical history is extremely helpful in identifying the etiology
of low back disorders. The differential diagnosis includes the following:

1. Disk herniation with nerve root irritation or neurologic deficit

2. Spinal stenosis
3. Vertebral infection
4. Primary or metastatic neoplasms; especially thyroid, lung, breast, renal, and prostate
5. Trauma (see Chapter 9)
6. Rheumatologic conditions (e.g., ankylosing spondylitis, rheumatoid arthritis, Reiter’s disease)
7. Vascular disorders (e.g., aortic aneurysm, aortic dissection)
8. Psychogenic or malingering pain (vague history and bizarre gait with inconsistent physical findings
suggest psychogenic causes)

Treatment

Nonsurgical Treatment
Most cases of back pain are mechanical. Nonsurgical measures that include analgesics, anti-inflammatories,
and stretching and strengthening exercises are often effective. Patient education about the causes and nature
of back pain is important. Instruction in proper postural mechanics and lifting techniques will prevent
reinjury. Patients should be encouraged to take an active interest in and responsibility for their own back care.
Patients with back and referred leg pain may benefit from a short period of rest, analgesic and anti-
inflammatory medications, and heat, followed by an active back exercise program. A brace may provide

1115
symptomatic relief. The brace acts as a proprioceptive device, reminding the patient to lift and bend properly.
The excessive use of bed rest and back braces is to be avoided because both can cause paraspinal muscle
atrophy.
Nonsteroidal anti-inflammatory medications are useful for their analgesic and anti-inflammatory effects.
Narcotic analgesics and antispasmodic agents are used with caution, especially with chronic back pain. Both of
these classes of drugs mask symptoms and may cause chemical dependency.
The two absolute indications for surgical decompression are as follows:

1. When disk herniation causes a progressive neurologic deficit

2. When cauda equina syndrome is suspected with loss of bowel or bladder continence

The majority (>80%) of patients with a symptomatic lumbar disk herniation will improve with
conservative treatment and not require surgery.

Surgical Treatment
Approximately 10% of patients with leg pain do not respond to conservative treatment. If leg pain persists for
more than 2 months of conservative care, surgery may be considered. The results are better if surgery is
performed within 6 months of the onset of symptoms. After 6 months, the patient becomes physically
deconditioned and psychologically dependent. The candidate for surgery should have consistent physical and
radiographic findings. Spinal surgery treats symptoms and does not reverse the degenerative processes of
spinal aging and arthritis. Operations for disk herniations should be precisely defined. In patients with spinal
stenosis, decompression is more extensive. All structures causing nerve root pressure, herniated disks,
osteophytic spurs, and calcified ligaments, are surgically removed from each involved spinal level. The
indications for spinal fusion in this setting are controversial. In patients with spinal instability from
progressive spondylolisthesis or after anatomically extensive decompression, spinal fusion can be an effective
stabilizing and palliative procedure.

CERVICAL SPINE

Degenerative disk disease and disk protrusion also occur in the cervical spine. The erosive synovitis of
rheumatoid arthritis has an affinity for the mobile cervical spine.

Cervical Disk Protrusion

The combined effects of age-related disk degeneration and abnormal stresses can cause cervical disk
herniations. When disk material presses on the posterior longitudinal ligament, symptoms of stiffness and
neck pain may be referred to the scapular region. When the herniated disk material protrudes posterior and
lateral to the posterior longitudinal ligament, it may impinge on a cervical nerve root. Consequently, it may
cause radicular pain, numbness, focal motor weakness, and diminution or loss of upper extremity deep tendon
reflexes (Table 28-5). The most commonly ruptured disks are at the C5–C6 and C6–C7 interspaces, where
cervical flexion–extension motion is the greatest. Likewise, the respective C6 and C7 nerve roots are most
often affected by cervical disk pathology.

1116
 TABLE 28-5 Cervical Lesions and Associated Radicular Abnormalities

Location Abnormality

C5 Nerve Root

Sensory Hypesthesia of the lateral arm

Motor Weak deltoid, biceps

Reflex Decreased biceps reflex

C6 Nerve Root

Sensory Hypesthesia of the lateral forearm and palmar thumb

Motor Weak wrist extension

Reflex Decreased brachioradialis reflex

C7 Nerve Root

Sensory Hypesthesia of the long finger

Motor Weak finger extension, triceps

Reflex Decreased triceps reflex

C8 Nerve Root

Sensory Hypesthesia of the medial forearm and little finger

Motor Weak finger flexion

Reflex None

Myelopathy Diffuse Hypesthesias

Sensory Diffuse weakness, increased muscle tone, rigidity

Motor Hyperreflexia with clonus

Reflex Positive Hoffmann or Babinski sign

Nonoperative treatment involves rest, immobilization with a soft cervical collar, heat, and anti-
inflammatory medication. Traction may help to alleviate nerve root pressure. Indications for surgical
intervention are similar to those in the lumbar spine. Emergency decompressive surgery is indicated if there is
spinal cord involvement (myelopathy) with hyperreflexia, ipsilateral weakness, contralateral numbness, or the
presence of pathologic long tract reflexes (e.g., Babinski or Hoffmann sign).

Cervical Spondylosis

Degenerative disk changes cause disk space narrowing and increases the forces on the facet joints and joints of
Luschka. Osteophytes form at the posterior disk margin, creating a “hard disk.” These bone spurs, called
Luschka’s joints, can encroach on the spinal cord or peripherally on an individual nerve root (Figure 28-52).
The clinical picture is similar to the herniation of the nucleus pulposus (soft disk), except that the onset of
symptoms is more gradual. Treatment for degenerative cervical spondyloarthrosis is similar to that for cervical
disk protrusion. When refractory to conservative treatment modalities, both conditions respond to anterior

1117
cervical diskectomy with a fusion.

Figure 28-52 Osteoarthrotic cervical spondylosis with anterior vertebral body osteophyte formation and disk
space narrowing. Posterior vertebral body osteophytes, also called Luschka (or uncovertebral) joints (arrows),
can cause encroachment on the spinal cord. This is known as a hard disk. (From Lawrence PF. Essentials of
Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

Rheumatoid Arthritis of the Cervical Spine

Rheumatoid arthritis often involves the synovial joints of the cervical spine. Progressive inflammatory
destruction of bone, ligaments, and articular cartilage may cause cervical spine instability or neural
compression.
Rheumatic cervical spine involvement usually assumes one of the following three patterns:

1. Rheumatoid inflammation and swelling of the small synovial joint between the atlas and the odontoid
process can stretch the stabilizing transverse ligament and cause the atlantoaxial joint (C1–C2) to
subluxate with flexion. The two vertebrae no longer move in synchrony, and this causes spinal canal
narrowing and potential cord compromise by the posteriorly displaced dens.
2. Erosive synovitis between the atlas (C1 vertebra) and the occipital condyles causes cranial settling, and
this may result in the protrusion of the odontoid process of the axis (C2) into the foramen magnum.
This phenomenon is termed occipitoatlantoaxial impaction, and it can compress the spinal cord, causing
long tract signs.
3. Finally, facet joint synovitis affecting any cervical vertebrae below the axis can cause segmental instability
known as subaxial subluxation. This instability is demonstrated on lateral radiographs by abnormal
vertebral body tilt or displacement in the AP direction.

The prevalence of cervical instability in patients with polyarticular rheumatoid arthritis is such that

1118
flexion–extension lateral cervical spine radiographs must be obtained for any rheumatoid patient undergoing
intubation for a general anesthetic. Neurologic involvement does not necessarily correlate with the degree of
cervical vertebral subluxation. However, when neurologic impairment is caused by cervical instability, the
treatment of choice is stabilization through surgical spine fusion. Most cases of rheumatoid neck pain,
however, are successfully managed by nonoperative treatment modalities.

METABOLIC ENDOCRINE DISORDERS

Bone is a biphasic material consisting of an inert mineral and an organic matrix. The mineral is composed
of calcium and phosphorus in a hydroxyapatite crystal Ca10(PO4)6(OH)2. The organic matrix (osteoid) is
composed primarily of type I collagen, which has high tensile strength. The mineral phase of bone resists
compressive forces, whereas the organic collagen fiber phase provides reinforcement and resistance to bending
and twisting stress (like the meshed wire in cement). Normal bone is 70% mineral and 30% organic matrix.

OSTEOPOROSIS

Bone strength depends on the amount of bone mineral per unit volume. In osteoporosis, the chemical
composition of the bone is normal, but total bone mineral is more than 2 standard deviations below an age-
matched control. The ratio of bone mineral to organic matrix is normal, but the absolute value of each is
decreased. The bone is therefore weak, less dense, and predisposed to fractures with minimal trauma. The
most common type of osteoporosis is the involutional senile type and is seen in postmenopausal, white
females. The cause is unknown. Other conditions also result in osteoporosis (Table 28-6).

TABLE 28-6 Causes of Osteoporosis

Type Examples

Involutional Postmenopausal age

Nutritional deficiencies Scurvy

Endocrine disorders Hypogonadism

Hyperparathyroidism
Cushing’s disease
Hyperthyroidism

Drug use Corticosteroids

Methotrexate

Disuse Prolonged bed rest

Weightlessness

Inflammatory arthritis Rheumatoid arthritis

Ankylosing spondylitis
Chronic infection (tuberculosis)

Malignant disease Multiple myeloma

Leukemia

Idiopathic

1119
 Osteoporosis is second to arthritis in causes of musculoskeletal morbidity in the elderly. The symptoms
occur when bone mass is so compromised that the skeleton fractures as a result of the mechanical stresses of
everyday life. Compression fractures of vertebral bodies or fractures of the proximal femur (hip; see Figure 28-
18), humerus, and distal radius (Colles; see Figure 28-15) are often the first manifestations of osteoporosis.
These patients should be screened for the medically treatable causes of osteoporosis and a bone mineral
density scan should be obtained to help quantify the severity of their disease. Exercise, dietary calcium, and
vitamin D supplements (and estrogen in early postmenopausal women) can be effective prophylaxis against
the bone loss of osteoporosis. Diphosphonates and calcitonin can be used to treat this condition and have
been shown to increase bone mineral density and decrease fracture rates. Adequate calcium intake during the
growing years as well as a healthy level of physical activity are the current long-term prevention strategies.

OSTEOMALACIA

Osteomalacia is the result of a deficiency in the mineral content of bone. In contrast to osteoporosis, the
amount of bone matrix per unit volume is normal. However, the matrix that is present is incompletely
calcified. Clinically and radiographically, osteoporosis and osteomalacia are similar. Often the distinction is
made by bone biopsy and histomorphometry, an analytic technique that requires ultrathin, nondecalcified,
tetracycline-labeled bone biopsy specimens. In osteomalacia, wide osteoid seams of unmineralized bone are
detected. The ratio of bone mineral to organic bone matrix is decreased because there is a mineral deficiency.
In osteoporosis, the ratio of bone mineral to matrix is normal because the quantity of both is deficient.
Inadequate bone mineralization can result from inadequate dietary vitamin D or calcium intake,
gastrointestinal malabsorption of calcium, problems with the enzymatic conversion of vitamin D, or defective
renal calcium and phosphorus handling (Table 28-7). Correctable defects in the calcium pathway can be
screened by obtaining levels of serum calcium and phosphorus, blood urea nitrogen, and creatinine, which
may detect gastrointestinal, endocrine, or renal causes. In addition to the generalized decrease in bone density
seen radiologically, a band of bone rarefaction, called a Looser zone, is typical of osteomalacia (Figure 28-53).
The Looser zone represents a healing stress fracture and is most often noted in the femoral neck or pubic
rami.

TABLE 28-7 Causes of Osteomalacia

Type Examples

Dietary Vitamin D deficiency (rickets)

Hereditary Hypophosphatemic rickets

Gastrointestinal Biliary disease

Pancreatitis
Celiac sprue
Milk alkali syndrome
Cirrhosis

Drug use Phenytoin

Barbiturates

1120
Chronic renal disease

Figure 28-53 Looser line seen with osteomalacia. The band of rarefaction in the superior pubic ramus and in the
femoral neck (arrows) represents a stress fracture and is due to inadequate bone mineralization. (From
Lawrence PF. Essentials of Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2007.)

The pediatric form of osteomalacia is called rickets and is caused by dietary vitamin D deficiency and lack
of exposure to sunlight. This disease was common during the industrial revolution before the advent of child
labor laws. Today, rickets is seen primarily in a genetic disease called vitamin D–resistant (hypophosphatemic)
rickets, which is transmitted in an autosomal dominant pattern. In growing children, radiographs of
osteomalacia (rickets) demonstrate widened growth plates and cupped metaphyses (Figure 28-54). Soft,
undermineralized long bones may be abnormally bowed.

1121
Figure 28-54 Rickets, the pediatric form of osteomalacia, is noted by diffuse osteopenia and abnormally wide
growth plates. The soft bones may be bowed. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

HYPERPARATHYROIDISM

Hyperparathyroidism causes diffuse bony osteopenia. Parathyroid hormone is involved with the homeostasis
of ionized calcium levels in the blood. In response to low serum calcium or high-serum phosphorus
concentrations, parathyroid hormone increases calcium release from bone, calcium absorption by the
intestines, and calcium reabsorption by the kidney (while decreasing renal absorption of phosphate). These
changes cause a net increase in plasma calcium and a decrease in plasma phosphate levels. Primary
hyperparathyroidism is due to an adenoma or hyperplasia of the parathyroid gland. Secondary
hyperparathyroidism is due to chronic renal insufficiency with decreased phosphate excretion. Radiographs of
hyperparathyroidism show diffuse bony rarefaction but also include disseminated focal osteolytic lesions of
cortical bone called osteitis fibrosis cystica (Figure 28-55).

1122
Figure 28-55 Primary hyperparathyroidism causes increased bone resorption to increase serum calcium levels.
Radiographs of primary hyperparathyroidism show diffuse bone rarefaction. Note the phalangeal cortices
(curved arrow in A) and multiple focal osteolytic lesions of cortical bone (straight arrows in A and B). This
explains why the radiographic picture is described as osteitis fibrosis cystica. (From Lawrence PF. Essentials of
Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

PAGET’S DISEASE

1123
Paget’s disease (osteitis deformans) is a disorder of unknown etiology characterized by excessive bone
resorption and unregulated abundant bone formation. The involved areas of bone are highly vascular and can
cause massive arteriovenous shunting with high-output cardiac failure. In the early (osteolytic) phase of the
disease, bone resorption exceeds deposition. The bone is weak and may fracture and bend. Later, bone
formation predominates (osteosclerotic phase) but is poorly organized. The bones become enlarged and
thickened.
Patients with Paget’s disease complain of bone pain, progressive lower limb bowing, or skull enlargement.
Fractures through pagetic bone are prone to nonunion. Serum alkaline phosphatase levels secreted by bone-
forming osteoblasts can be markedly elevated with Paget’s disease. Microscopically, the bone is irregular, with
a mosaic pattern of mature and immature bone. Radiographs show dense and irregular sclerotic bony
trabeculae (Figure 28-56). Long bone fractures are characteristically transverse and begin as a crack on the
convex or tension side of the deformed bone. In less than 1% of all cases of Paget’s disease, these bone-
forming cells undergo malignant degeneration into osteosarcomas. The majority of cases are asymptomatic
and are discovered incidentally on pelvic radiographs, the pelvis being a frequent site of Paget’s disease. The
medical treatment of Paget’s disease with calcitonin or diphosphonates is reserved for intractable bone pain,
malignant hypercalcemia, cardiac failure, or neural involvement from bony foraminal hypertrophy in the spine.

Figure 28-56 Paget’s disease. The dense irregular sclerotic bony trabeculae signify the excessive, unregulated
formation of bone. The bone is brittle and may fracture pathologically. (From Lawrence PF. Essentials of
Surgical Specialties. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

NEOPLASMS OF BONE

Tumors arising from musculoskeletal tissues are rare. However, bone involvement with metastatic tumor
is common in patients older than 50 years. Primary tumors of breast, prostate, lung, kidney, and thyroid often
metastasize to bone. The sites of tumor metastasis are typically those bones involved with hematopoiesis and
those with a rich blood supply, such as the spine, ribs, skull, pelvis, and long bone metaphyses. Metastases

1124
from breast and prostate may be either osteoblastic (inducing bone formation) or osteolytic (inducing bone
resorption). Metastases from lung, kidney, thyroid, or gastrointestinal tract are usually osteolytic.
The most frequent primary bone tumors and their tissue of origin are listed in Table 28-8. Table 28-9
describes their salient features. The evaluation of primary or secondary bone tumors should be systematic and
multidisciplinary. Before treatment is initiated, the physician must define the tumor according to its histology,
its anatomic relationships to neuromuscular compartments and perivascular spaces, and the likelihood and
mode of its metastatic spread.

TABLE 28-8 Primary Bone Tumors and Their Tissue of Origin

Bone Tumor

Tissue of Origin Benign Malignant

Bone Osteoid osteoma Osteosarcoma

Cartilage Osteochondroma Chondrosarcoma

Enchondroma

Fibrous tissue Fibroma Fibrosarcoma

Marrow elements Eosinophilic granuloma Myeloma

Ewing’s sarcoma

Uncertain Giant cell tumor Aggressive giant cell tumor

TABLE 28-9 Salient Features of Common Bone Tumors

Tumor Main Symptoms Age Common Sites Radiographic Appearance Other

Benign

Osteoid osteoma Pain, often <30 y Femur and tibia Small, radiolucent area <1 cm –
relieved by aspirin surrounded by zone of dense
sclerosis

Osteochondroma Palpable lump; Adolescence Long bone Sessile or pedunculated bone Pain or increase in
may interfere with metaphysis excrescence; cartilage not seen size suggests
tendon function unless calcified malignant change

Enchondroma Swelling or pain Any age Metaphysis of Well-demarcated area of Malignant

(chondroma) with a pathologic tubular bones of radiolucency that may contain transformation is
fracture hands and feet; specks of calcification more common
may be single or with multiple
multiple (Ollier’s cartilage lesions
disease) (osteochondromas
or enchondromas)

Nonossifying Asymptomatic <30 y Cortical Well-demarcated, radiolucent, Ossifies with

fibroma (fibrous unless pathologic metaphysis of the multilocular area adjacent to skeletal
cortical defect) fracture occurs distal femur or cortex maturation
through it tibia

Giant cell tumor Pain and swelling 20–40 y Epiphyseal, Epiphyseal, eccentric Often aggressive;
(osteoclastoma) near joint especially distal expanding; expands to involve should be treated

1125
 femoral, radius, or metaphysis as a malignant
proximal tibial lesion
epiphysis; after
growth plate has
closed

Malignant

Osteosarcoma Tender mass; pain Bimodal; before Metaphyseal; half Irregular, destructive lesion with Slightly more
worse at night 30 y and after 50 y affect distal femur radiodense osteoblastic or common in men
because of and proximal tibia radiolucent osteolytic areas; than women
malignant change periosteal new bone formation
in Paget’s disease juxtaposed to a cortex that is
permeated and destroyed;
neoplastic bone spicules
perpendicular to bone radiating
in a sunburst pattern

Chondrosarcoma Increasing mass; 40–60 y Central sites; Permeative radiolucent lesion Malignant
dull, aching pain pelvic and with calcific densities transformation of
shoulder girdle preexisting
enchondroma or
osteochondroma,
especially if
multiple

Fibrosarcoma Painful, Adolescence and Metaphyseal Poorly defined, destructive, –

destructive lesion young adulthood regions of long radiolucent lesion
bones

Myeloma – 45–65 y Red marrow areas Osteopenia, spinal compression Most common
of the skeleton fractures with minimal trauma primary malignant
bone tumor of
plasma cell origin;
Bence Jones
proteinuria, serum
and urine protein
electrophoresis

Ewing’s sarcoma Enlarging, 10–15 y Diaphysis of Destructive bony lesion; onion May be mistaken
painful, soft tissue femur; ilium, tibia, skin layers of periosteal new for osteomyelitis
mass humerus, fibula, bone formation clinically and
ribs histologically

The most common primary tumor of bone is multiple myeloma. It occurs in late adulthood. Patients may
present with fatigue, bone pain, or, rarely, with a pathologic fracture. Clinical assessment involves general
physical examination, routine blood work (including ESR), and urine for Bence Jones proteins. Protein
electrophoresis should also be carried out. A medical oncologist should be consulted as soon as the diagnosis
of multiple myeloma is suspected.

EVALUATION

The history is of great importance. It should include the patient’s age, medical conditions associated with

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bone tumors (e.g., Paget’s disease, dermatomyositis, prior radiation exposure), systemic symptoms (e.g.,
weight loss, bleeding diathesis, fever), and occupation (which may explain an unusual environmental
exposure). Lifestyle and personal expectations are also important in selecting therapy. The physical
examination should note the color and temperature of overlying tissues, and the size, degree of tenderness,
and mobility of the tumor if it is palpable. A tumor that is confined to bone may have no abnormal physical
findings.
A complete blood count and differential help to exclude infection and hematologic malignancies. Usually,
laboratory studies can detect other organ system involvement and determine the patient’s overall medical
condition. Liver function studies and measurements of uric acid (DNA turnover), alkaline phosphatase,
calcium, and phosphorus are helpful in the evaluation of processes that form or destroy bone. With carcinoma
of the prostate, a prostate-specific antigen level is measured before a rectal examination is undertaken. If
myeloma is suspected, serum protein electrophoresis is obtained.
The plain-film radiograph provides many clues about the behavior of the tumor. It may show a well-
demarcated lesion with a reactive zone of bone formation or undemarcated lesion with bone destruction and
little surrounding bone formation (Figure 28-57). Defining the specific bone and region of involvement
(epiphysis, metaphysis, or diaphysis) aids in diagnosis (see Table 28-9) and staging. Subsequent radiographic
investigation with bone scan, CT, MRI, or other specialized techniques is directed by suspicions generated
from the plain-film radiograph. A bone scan is often an excellent screening test for metastatic disease.
Radioactive, isotopically labeled technetium-99m pyrophosphate is incorporated into regions of active bone
formation or increased vascularity. In multiple myeloma, however, the bone scan is characteristically negative
and shows no increased uptake. CT provides the best definition of cortical bone. It can detect cortical
penetration and intraosseous detail. The CT scan is the preferred method of evaluating the lung for small
pulmonary lesions. With contrast enhancement, a CT scan can define the relation between a tumor and the
surrounding neurovascular structures. MRI is used to evaluate the intramedullary (marrow) extent of a tumor.
The MRI also yields the best definition of soft tissue and neurovascular tumor relationships. Angiography is
used to identify vascular lesions, which can then be embolized to shrink tumor mass and decrease blood loss
before a surgical resection. These special imaging techniques are obtained before biopsy.

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Figure 28-57 Osteogenic sarcoma of the proximal humerus metaphysis showing an aggressive, expanding,
poorly demarcated, bone-forming lesion. (From Lawrence PF. Essentials of Surgical Specialties. 3rd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

A surgical biopsy is performed to obtain tissue for histologic diagnosis. A biopsy may be obtained with
open or closed (needle) techniques and should be performed by the surgical team responsible for definitive
tumor treatment. The biopsy incision is placed so that it can be resected in total and not compromise the
definitive procedure. An open biopsy incision is generally directed in the longitudinal bone axis over the
tumor. To prevent contamination and tumor spread, extensive muscular dissection and neurovascular
structures are avoided, although meticulous hemostasis is maintained. When possible, an intraoperative frozen
section is obtained to ensure that an adequate tissue specimen has been sampled. In closed biopsies, either a
fine-needle aspiration is used to remove cells for cytology or a tissue core is obtained for routine histologic
preparation.

TREATMENT

The treatment of bone tumors depends on the tissue diagnosis, the degree of cell anaplasia, the extent of
spread, the patient’s medical condition, and the sensitivity of the tumor to treatment modalities. These
modalities include surgery, chemotherapy, and radiotherapy.
Benign tumors are cured by local excision. If tumor resection will compromise the structural integrity of
the bone (i.e., femoral neck), bone grafting or implant reinforcement will be necessary. Metastatic lesions may
be palliated with local radiation. When a lesion occupies greater than 50% of a bone’s cortical diameter, a
pathologic fracture is imminent. Prophylactic fixation is preferable with impending pathologic fractures

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because patient morbidity and mortality are higher after fracture.
Generally, malignant bone tumors are resected with wide or radical surgical margins. Adjuvant
chemotherapy and radiation therapy are used to eradicate tumor micrometastases that are assumed to be
present. In some centers, reconstructive techniques using bone and joint allografts alone or in combination
with customized prosthetic joint replacement are used to salvage limbs (limb sparing) and maximize patient
function. Limb salvage techniques should never compromise the eradication of the neoplasm.

GAIT

Normal ambulation is efficient and conserves energy. Abnormal ambulation is inefficient, requires
increased energy expenditure, and usually is a manifestation of neuromuscular pathology. Gait observation and
analysis is thus an essential part of the musculoskeletal examination.
A normal gait cycle (Figure 28-58) extends from the heel strike of one foot to the next heel strike of the
same foot. The normal cycle is divided into the stance phase (60% of the cycle), when the foot is in contact
with the ground, and the swing phase (40% of the cycle), when the foot is off the ground. The stance phase
begins at heel strike, is followed by foot flat, and ends with toe-off. The swing phase is marked by
advancement of the limb to the next heel strike. The stride length is the distance covered during one gait cycle
(heel strike to ipsilateral heel strike). The step length is the distance between the heel strike of one foot and
the heel strike of the contralateral foot. Because the pelvis and trunk as well as the muscles and joints of the
lower limb are involved in gait, abnormalities in these regions may indicate gait abnormalities.

Figure 28-58 The gait cycle. (Modified from Phillips WA. The child with a limp. Orthop Clin North Am.

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1987;18:490. Copyright © 1987 Elsevier.)

An abnormal gait is often called a limp. Most gait abnormalities are detectable during the stance phase,
when body weight is supported by one lower extremity. During stance, pain, muscle weakness, and joint
abnormalities produce their maximal effect. The typical reaction to pain is to quickly unload the affected leg.
Thus, an antalgic (pain-relieving) gait is manifest by a decreased stance phase of the affected limb. The swing
phase of the limb opposite is also decreased, resulting in a shortened step length.
Muscle weakness has significant effects on gait. Quadriceps weakness interferes with the ability to lock the
knee in full extension before heel strike. To compensate, the patient will push the thigh backward with the
hand. Weakness of the foot and ankle dorsiflexors will not allow the controlled placement of the foot after
heel strike to the foot flat position. This results in a foot slap gait as the foot slaps to the ground after heel
strike. Likewise, paralysis of the foot and ankle dorsiflexors caused by peroneal nerve palsy will cause the
patient to bring the knee up higher than normal during the swing phase so the toes clear the ground. This
motion may result in a steppage gate. Other compensatory mechanisms for clearing a dropped foot include
elevating the ipsilateral pelvis (hip-hike gait) or swinging the leg out to the side (circumduction gait). A weak
gluteus maximus, which serves as a hip extensor, causes the trunk to collapse forward during midstance. The
patient will compensate by thrusting the trunk posteriorly in what is called an extensor lurch or gluteus
maximus gait. Weakness of the hip abductor muscles (gluteus medius and minimus) allows the contralateral
pelvis to sink downward during stance. To compensate, the patient’s torso lurches laterally over the weak hip
in what is known as Trendelenburg or gluteus medius gait. Weakness of the calf muscles (gastrocnemius and
soleus) prevents the normal propulsive toe-off push and is manifest as a flat-footed or calcaneal gait.
Joint abnormalities that interfere with the normal range of toe, metatarsophalangeal, ankle, knee, or hip
joint motion also adversely affect gait. For example, an equinus (plantar flexion) ankle contracture causes knee
hyperextension during the stance phase of ambulation.
Armed with knowledge of gait mechanics and a critical eye, the clinician can distinguish many of these
gait patterns when observing a group of people. An abnormal gait pattern may provide the first clue in the
diagnosis of a neuromuscular disease process.

SUGGESTED READINGS

American Academy of Orthopaedic Surgeons. Primary total hip arthroplasty: everything you need to know.
AAOS Instructional Course Lectures; March 2016; Orlando, Florida.
American Academy of Orthopaedic Surgeons. Principles of open fracture management. AAOS Instructional
Course Lectures; March 17, 2017; San Diego, California.
Bronstein R, Schaffer JC. Physical examination of the knee: meniscus, cartilage, and patellofemoral
conditions. J Am Acad Orthop Surg. 2017;25(5):365–374.
Lieberman JR, Heckmann N. Venous thromboembolism prophylaxis in total hip arthroplasty and total knee
arthroplasty patients: from guidelines to practice. J Am Acad Orthop Surg. 2017;25(12):789–798.
Morris BJ, Mir HR. The opioid epidemic: impact on orthopaedic surgery. J Am Acad Orthop Surg.
2015;23(5):267–271.

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 Sample Questions

Questions
Choose the best answer for each question.

1. Which of the following joints are most prone to septic arthritis during childhood?
A. Ankle
B. Knee
C. Hip
D. Wrist
E. Base of thumb

2. Radiographic features of degenerative joint disease include all of the following except one. Which
of the following is the exception?
A. Localized joint space narrowing
B. Marginal erosions
C. Subchondral sclerosis
D. Osteophytes
E. Subchondral cysts

3. Radiographic features of inflammatory joint disease include all of the following except one. Which
of the following is the exception?
A. Generalized joint space loss
B. Periarticular osteopenia
C. Marginal erosions
D. Osteophytes
E. Soft tissue swelling

4. Which of the following bone or portion of bone is LEAST likely to be affected by osteonecrosis?
A. Femoral head
B. Talus
C. Olecranon
D. Lunate
E. Scaphoid

5. The majority of episodes of low back pain resolve over time. What percentage of low back pain
episodes resolve by 3 months following onset?
A. 51%
B. 60%
C. 70%
D. 80%
E. 90%

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Answers and Explanations

1. Answer: C
In children, septic arthritis occurs as an extension of hematogenous osteomyelitis. The joints commonly
involved are those in which the metaphysis resides within the joint capsule: the hip, elbow, and shoulder.
Because the metaphysis is enclosed in the joint capsule, what begins as osteomyelitis can erupt through
the cortex to involve the joint in the septic process. For more information on this topic, please see the
section on Septic Arthritis.

2. Answer: B
Marginal erosions are not a feature of degenerative joint disease. Erosions are typical of inflammatory
joint disease. The radiologic hallmarks of osteoarthrosis are as follows: localized joint space narrowing,
subchondral bone sclerosis, osteophytes, subchondral cysts. For more information on this topic, please
see the section on Osteoarthrosis.

3. Answer: D
Osteophytes are typical of degenerative joint disease. All the other features are typical of inflammatory
joint disease. Soft tissue swelling and periarticular osteoporosis are the early signs of rheumatoid arthritis.
Diffuse cartilage destruction leads to generalized joint space narrowing and bone erosions at the site of
synovial attachments. Joint deformity, cystic bone destruction, and joint ankylosis mark end-stage
disease. Hypertrophic osteophytes are rare in rheumatoid arthritis. For more information on this topic,
please see the section on Rheumatoid Arthritis.

4. Answer: C
The olecranon is not prone to osteonecrosis, whereas the other bones are prone to it. Interruption of the
blood supply to bone results in bone cell death (osteonecrosis or avascular necrosis). Traumatic causes of
osteonecrosis have been discussed and involve vascular injury or interruption of the blood supply to
bones. The femoral head, talus, carpal lunate, and scaphoid are prone to avascular necrosis. These bones
are all extensively covered by articular cartilage and have limited soft tissue attachments. For more
information on this topic, please see the section on Complications of Fracture Healing.

5. Answer: E
The vast majority of episodes of low back pain resolve within 3 months. Contrary to popular opinion, the
vast majority of low back pain is not due to a “slipped disk.” In 80% to 90% of patients with low back
pain, the pain is of unknown etiology and the pathology remains obscure. Fewer than 10% of patients
experience pain in the sciatic nerve (L5–S3) distribution (“sciatica”). Only 1% to 2% of patients require
surgical treatment for a disk herniation. With symptomatic care, 50% improve in 2 weeks and 90% in 3
months. For more information on this topic, please see the section on Etiology of Low Back Pain.

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