Postfracture Period Research Articles

Nontreatment of Hip Fractures in Senile Patients

Five elderly patients with hip fractures were deemed unsuited for surgical repair because of severe organic mental syndromes. All survived the postfracture period without the morbidity of decubitus ulcers and pulmonary complications, or the pain, mental anguish, and expense of hospitalization and surgery. Surgical repair of a hip fracture is not necessarily a mandatory or life-saving procedure. For patients unlikely to walk again, nonoperative management is a reasonable alternative--provided good nursing care is available.

FRACTURE IN THE RAT. CHRONIC MUSCLE GLYCOGEN AND BONE CHANGE.

T HE PHYSIOLOGICAL and surgical literature of the past 30 years has reflected an intense interest in the metabolic reactions that follow the fracture of a major bone. It is now clear that in the presence of such severe injuries the body enters a phase of extensive tissue catabolism. 3-5 The urinary excretion of large amounts of various products of protein breakdown leads to negative nitrogen balance in the well-nourished individual. Decreased glucose tolerance may develop and body fat is rapidly consumed in the early days after the trauma. 5,8,10 This initial breakdown reaction is followed by a prolonged period in which protein containing tissues and fat deposits are restored to their prefracture state. 7 While a considerable body of data has been accumulated to document widespread metabolic change in the postfracture period, there is very little information available concerning the nature and extent of the biochemical reactions of the

Alterations in muscle and liver glycogen secondary to fracture

The glycogen content of selected tissues was measured in a series of rats 5 days after fracture of 1 tibia. Significant decreases in liver and hind limb muscle glycogen were observed. These changes were attributed to the muscular inactivity and increased carbohydrate utilization of the postfracture period.

POSTFRACTURE VASCULAR CHANGES AND HEALING PROCESS.

Introduction Recent investigations have documented the sequence of vascular changes in the postfracture period. Fracture of a long bone leads to acute vasodilation throughout the traumatized limb.6Acute vasodilation is followed by chronic enlargement of the potential vascular space of the limb. With the passage of time, the enlarged vascular space gradually shrinks to prefracture size.5,7,8 While the relationship of these vascular changes to the healing process is unknown, two chief possibilities come to mind. Vascular alterations may be accompanied by metabolic adjustments that may or may not be essential to the fracture healing process. Second, vascular changes, or more specifically, the gradual return of the enlarged vascular bed to prefracture levels, may be related to the consolidation of bony union at the fracture site. It is this latter possibility, a possible relationship of vascular bed recession to bony union, that is the concern of this investigation. The