Although fractures are sometimes described in terms of the external mechanism by which they are created, they may also be thought of simply in terms of the physiologic processes involved.
"TYPICAL" FRACTURES Most fractures are the result of significant trauma to healthy bone. The bony cortex may be disrupted by a variety of forces, including a direct blow, axial loading, angular (bending) forces, torque (twisting) stress, or a combination of these.
PATHOLOGIC FRACTURES Fractures that occur from relatively minor trauma to diseased or otherwise abnormal bone are termed pathologic fractures. This implies that a preexisting pathologic process has weakened the bone and rendered it susceptible to fracture by forces that, under normal circumstances, would not disrupt the cortex. Common examples of such injuries are fractures through metastatic lytic lesions, fractures through benign bone cysts (as in the humerus of Little League pitchers), and—perhaps most common—vertebral compression fractures in patients with advanced osteoporosis. Numerous other disease processes may render patients susceptible to pathologic fracture.
Because these injuries are often not associated with a history of significant trauma, pathologic fractures may go undetected unless there is a preexisting index of suspicion based on the knowledge that such injuries can occur.
STRESS FRACTURES In some cases, bone may undergo a "fatigue" fracture from repetitive forces applied before the bone and its supporting tissues have had adequate time to accommodate to such forces. An example is the insidious occurrence of a metatarsal shaft fracture in unconditioned foot soldiers (the so-called march fracture). The physiologic principle of stress fracture can be easily envisioned by anyone who has "cut" an aluminum finger splint to the desired length by bending it back and forth. The pliable metal—too hard to cut with an ordinary scissors—ultimately gives way in the face of repeated stresses requiring relatively little force.
The processes that render bone susceptible to stress fracture are not generally agreed upon. The important point is that diagnosis depends on a familiarity with the entity, because x-rays are typically negative early in the patient's course. Early diagnosis may be purely clinical, based on the history and physical findings. Days or weeks may pass before the fracture line or new bone formation becomes visible on x-ray, ultimately confirming the suspicions of the physician who, having made the correct presumptive diagnosis, will have treated the patient appropriately from the outset.
SALTER (EPIPHYSEAL) FRACTURES Fractures involving the physis—the cartilaginous epiphyseal plate near the ends of the long bones of growing children—are called Salter fractures after Salter and Harris, the physicians who devised the most popular method of classifying these injuries. 1 The supply of new bone material needed for the elongation of bones during growth is provided by specialized cells within the physis. When growth is completed, the physis is transformed into bone, ultimately fusing with the surrounding bone and disappearing as a distinct entity. By definition, Salter fractures cannot occur in fully grown adults.
Any damage to the epiphyseal plate during a child's growth may destroy part or all of its ability to produce new bone substance, resulting in aborted or deformed growth of the bone thereafter. The potential for growth disturbance from an epiphyseal injury is related to the number of years the child has yet to grow (the older the child, the less time remains for deformity to develop) and to the pattern of the fracture line through the epiphyseal area. Classification of Salter fractures and their clinical implications are discussed later in this chapter.
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