Fracture Healing and Complications (Early and Delayed)
Weeks to months are required for most fractures to heal. Many fac-tors influence the speed with which fractures heal (Chart 69-3). The reduction of fracture fragments must be accurate and main-tained to ensure healing. The affected bone must have an adequate blood supply. The type of fracture also affects healing time. In gen-eral, fractures of flat bones (pelvis, scapula) heal rapidly. Fractures at the ends of long bones, where the bone is more vascular and can-cellous, heal more quickly than do fractures in areas where the bone is dense and less vascular (midshaft). Weight bearing stimu-lates healing of stabilized fractures of the long bones in the lower extremities.
If fracture healing is disrupted, bone union may be delayed or stopped completely. Factors that can impair fracture healing in-clude inadequate fracture immobilization, inadequate blood sup-ply to the fracture site or adjacent tissue, extensive space between bone fragments, interposition of soft tissue between bone ends, infection, and metabolic problems.
Complications of fractures fall into two categories—early and delayed. Early complications include shock, fat embolism, com-partment syndrome, deep vein thrombosis, thromboembolism (pulmonary embolism), disseminated intravascular coagulopathy, and infection.
Delayed complications include delayed union and nonunion, avascular necrosis of bone, reaction to internal fixa-tion devices, complex regional pain syndrome (formerly called re-flex sympathetic dystrophy), and heterotrophic ossification.
Hypovolemic or traumatic shock resulting from hemorrhage (both visible and nonvisible blood loss) and from loss of extracellular fluid into damaged tissues may occur in fractures of the extremi-ties, thorax, pelvis, or spine. Because the bone is very vascular, large quantities of blood may be lost as a result of trauma, espe-cially in fractures of the femur and pelvis. Treatment of shock consists of restoring blood volume and circulation, relieving the patient’s pain, providing adequate splinting, and protecting the patient from further injury and other complications.
After fracture of long bones or pelvis, multiple fractures, or crush injuries, fat emboli may develop. Fat embolism syndrome occurs most frequently in young adults (typically those 20 to 30 years of age) and elderly adults who experience fractures of the proximal femur. At the time of fracture, fat globules may move into the blood because the marrow pressure is greater than the capillary pressure or because catecholamines elevated by the patient’s stress reaction mobilize fatty acids and promote the development of fat globules in the bloodstream. The fat globules (emboli) occlude the small blood vessels that supply the lungs, brain, kidneys, and other organs. The onset of symptoms is rapid, usually occurring within 24 to 72 hours, but may occur up to a week after injury.
Presenting features include hypoxia, tachypnea, tachycardia, and pyrexia. The respiratory distress response includes tachypnea, dyspnea, crackles, wheezes, precordial chest pain, cough, large amounts of thick white sputum, and tachycardia. Occlusion of a large number of small vessels causes the pulmonary pressure to rise. Edema and hemorrhages in the alveoli impair oxygen trans-port, leading to hypoxia. Arterial blood gas values show the par-tial pressure of oxygen (PaO2) to be less than 60 mm Hg, with an early respiratory alkalosis and later respiratory acidosis. The chest x-ray shows a typical “snowstorm” infiltrate. Eventually, acute pulmonary edema, acute respiratory distress syndrome, and heart failure develop.
Cerebral disturbances (due to hypoxia and the lodging of fat emboli in the brain) are manifested by mental status changes varying from headache, mild agitation, and confusion to delirium and coma.
With systemic embolization, the patient appears pale. Pete-chiae, possibly due to a transient thrombocytopenia, are noted in the buccal membranes and conjunctival sacs, on the hard palate, and over the chest and anterior axillary folds. The pa-tient develops a temperature of more than 39.5°C (about 103°F). Free fat may be found in the urine if emboli reach the kidneys. Kidney failure may develop.
Immediate immobilization of fractures (including early surgical fixation), minimal fracture manipulation, adequate support for fractured bones during turning and positioning, and mainte-nance of fluid and electrolyte balance are measures that may re-duce the incidence of fat emboli. The nurse monitors high-risk patients (adults between 20 and 30 years of age with long bone, pelvic, or multiple fractures or crush injuries, and elderly patients with femur fractures) to identify this problem. Prompt initiation of respiratory support is essential.
The objectives of management are to support the respiratory system, to prevent respiratory and metabolic acidosis, and to cor-rect homeostatic disturbances. Respiratory failure is the most common cause of death. Respiratory support is provided with oxygen given in high concentrations. Controlled-volume ventila-tion with positive end-expiratory pressure may be used to prevent or treat pulmonary edema. Corticosteroids may be administered to treat the inflammatory lung reaction and to control cerebral edema. Vasoactive medications to support cardiovascular function are ad-ministered to prevent hypotension, shock, and interstitial pul-monary edema. Accurate fluid intake and output records facilitate adequate fluid replacement therapy. Morphine may be prescribed for pain and anxiety for the patient who is on a ventilator. In addi-tion, the nurse provides calm reassurance to allay apprehension. The patient’s response to therapy is closely monitored.
Because fat emboli are a major cause of death for patients with fractures, the nurse must recognize early indications of fat em-bolism syndrome and report them promptly to the physician. Respiratory support must be instituted early.
Compartment syndrome is a complication that develops when tis-sue perfusion in the muscles is less than that required for tissue viability. The patient complains of deep, throbbing, unrelenting pain, which is not controlled by opioids. This pain can be caused bya reduction in the size of the muscle compartment because the enclosing muscle fascia is too tight or a cast or dressing is constric-tive, or (2) an increase in muscle compartment contents because of edema or hemorrhage associated with a variety of problems (eg, frac-tures, crush injuries). The forearm and leg muscle compartments are involved most frequently. The pressure within a muscle compart-ment may increase to such an extent as to decrease microcirculation, causing nerve and muscle anoxia and necrosis. Permanent function can be lost if the anoxic situation continues for longer than 6 hours.
Frequent assessment of neurovascular function after fracture is essential. Sensory deficits include paresthesia, unrelenting pain, and hypoesthesia. Paresthesia (burning or tingling sensation) and numbness along the involved nerve are early signs of nerve in-volvement. Motion is evaluated by asking the patient to move fin-gers or toes distal to the potential problem. Motor weakness may occur as a late sign of nerve ischemia. No movement (paralysis) suggests nerve damage.
Peripheral circulation is evaluated by assessing color, temper-ature, capillary refill time, swelling, and pulses. Swelling (edema) reduces tissue perfusion. Cyanotic (blue-tinged) nail beds suggest venous congestion. Pale or dusky and cold fingers or toes and pro-longed capillary refill time suggest diminished arterial perfusion. Edema may obscure the presence of arterial pulsation, and Doppler ultrasonography may be used to verify a pulse. Pulselessness is a sign of arterial occlusion, not of compartment syndrome, because the tissue pressure would need to be above the systolic blood pres-sure for major artery occlusion to occur.
As intracompartment pressure increases, the patient complains of deep, throbbing, unrelenting pain, which is greater than ex-pected and not controlled by opioids. Passive stretching of the mus-cle causes acute pain. With continued nerve ischemia and edema, the patient experiences sensations of hypoesthesia (diminished sen-sitivity to stimulation) and then absence of feeling. Palpation of the muscle, if possible, reveals it to be swollen and hard. The ac-tual tissue pressure can be measured by inserting a tissue pressure-measuring device into the muscle compartment. (Normal pressure is 8 mm Hg or less.) Nerve and muscle tissues deteriorate as compartment pressure increases. Prolonged pressure of more than 30 mm Hg can result in compromised microcirculation. Nerve tissue is more sensitive than muscle to elevated tissue pressures. Paresthesia generally occurs before paralysis.
Prompt management of acute compartment syndrome is essen-tial. The physician needs to be notified immediately if neuro-vascular compromise is suspected. Delay may result in permanent nerve and muscle damage or even necrosis.
Compartment syndrome is managed by elevation of the ex-tremity to the heart level, release of restrictive devices (dressings or cast), or both. If conservative measures do not restore tissue per-fusion and relieve pain within 1 hour, a fasciotomy (surgical de-compression with excision of the fibrous membrane that covers and separates muscles) may be needed to relieve the constrictive muscle fascia. After fasciotomy, the wound is not sutured but instead is left open to permit the muscle tissues to expand; it is covered with moist, sterile saline dressings. The limb is splinted in a functional position and elevated, and prescribed passive ROM exercises are usually performed every 4 to 6 hours. In 3 to 5 days, when the swelling has resolved and tissue perfusion has been restored, the wound is débrided and closed (possibly with skin grafts).
Deep vein thrombosis (DVT), thromboembolism, and pulmo-nary embolus (PE) are associated with reduced skeletal muscle contractions and bed rest. Patients with fractures of the lower ex-tremities and pelvis are at high risk for thromboembolism. Pulmo-nary emboli may cause death several days to weeks after injury..
Disseminated intravascular coagulopathy (DIC) includes a group of bleeding disorders with diverse causes, including mas-sive tissue trauma. Manifestations of DIC include ecchymoses, unexpected bleeding after surgery, and bleeding from the mucous membranes, venipuncture sites, and gastrointestinal and urinary tracts.
All open fractures are considered contaminated. Surgical inter-nal fixation of fractures carries a risk for infection. The nurse must monitor for and teach the patient to monitor for signs of infection, including tenderness, pain, redness, swelling, local warmth, eleva-ted temperature, and purulent drainage. Infections must be treated promptly. Antibiotic therapy must be appropriate and adequate for prevention and treatment of infection.
Delayed union occurs when healing does not occur at a normal rate for the location and type of fracture. Delayed union may be associated with distraction (pulling apart) of bone fragments, sys-temic or local infection, poor nutrition, or comorbidity (eg, dia-betes mellitus; autoimmune disease). Eventually, the fracture heals.
Nonunion results from failure of the ends of a fractured boneto unite. The patient complains of persistent discomfort and ab-normal movement at the fracture site. Factors contributing to union problems include infection at the fracture site, interposi-tion of tissue between the bone ends, inadequate immobilization or manipulation that disrupts callus formation, excessive space between bone fragments (bone gap), limited bone contact, and impaired blood supply resulting in avascular necrosis.
In nonunion, fibrocartilage or fibrous tissue exists between the bone fragments; no bone salts have been deposited. A false joint (pseudarthrosis) often develops at the site of the fracture. Non-union most commonly occurs with fractures of the middle third of the humerus, the lower third of the tibia, and, in elderly people, the neck of the femur.
The physician treats nonunion with internal fixation, bone graft-ing, electrical bone stimulation, or a combination of these thera-pies. Internal fixation stabilizes the bone fragments and ensures bone contact.
Bone grafts provide for osteogenesis, osteoconduction, or osteo-induction. Osteogenesis (bone formation) occurs after transplanta-tion of bone containing osteoblasts. Osteoconduction is provision by the graft of the structural matrix for ingrowth of blood vessels and osteoblasts. Osteoinduction is the stimulation of host stem cells to differentiate into osteoblasts by several growth factors, including bone morphogenic proteins. Bone transplants undergo creeping substitution, a reconstructive process in which the bone transplant is gradually replaced by new bone.
During surgery the bone fragments are trimmed, infection (if present) is removed, and a bone graft is placed in the bony defect. The bone graft may be an autograft (tissue harvested from the donor for the donor, frequently from the iliac crest) or an allograft (tis-sue harvested from a donor other than the person who will receive it). The bone graft fills the bone gap, provides a lattice structure for invasion by bone cells, and actively promotes bone growth. The type of bone selected for grafting depends on function: cortical bone for structural strength, cancellous bone for osteogenesis, and cortico-cancellous bone for strength and rapid incorporation. Bone grafts may be chips, wedges, blocks, bone segments, or demineralized bone matrix. At times, autograft bone, allograft bone, and deminer-alized cortical matrix are combined to optimize graft incorporation and bone healing. Free vascularized bone autografts are grafted with their own blood supply, allowing for primary fracture healing.
After grafting, immobilization and non–weight bearing are required while the bone graft becomes incorporated and the frac-ture or defect heals. Depending on the type of bone grafted, healing may take from 6 to 12 months or longer. Bone grafting problems include wound or graft infection, fracture of the graft, and non-union. Specific autograft problems include a limited quantity of bone available for harvest, increased surgery and anesthesia time, increased blood loss, and donor site pain, hematoma, and infec-tion. Infrequent specific allograft problems include partial accep-tance (lack of host and donor histocompatibility, which retards graft incorporation), graft rejection (rapid and complete resorp-tion of the graft), and transmission of disease (rare).
Osteogenesis in nonunion may be stimulated by electrical im-pulses; the effectiveness is similar to that of bone grafting. Use of electrical impulses is not effective with large bone gaps or synovial pseudarthrosis. The electrical stimulation modifies the tissue en-vironment, making it electronegative, which enhances mineral deposition and bone formation.
In some situations, pins that act as cathodes are inserted per-cutaneously, directly into the fracture site, and electrical impulses are directed to the fracture continuously. Direct current methods cannot be used when infection is present.
Another method for stimulating osteogenesis is noninvasive inductive coupling. Pulsing electromagnetic fields are delivered to the fracture for approximately 10 hours each day by an electro-magnetic coil over the nonunion site (Fig. 69-4). During the elec-trical stimulation treatment period, which takes 3 to 6 months or longer, rigid fracture fixation with adequate support is needed.
The patient with a nonunion has experienced an extended time in fracture treatment and frequently becomes frustrated with pro-longed therapy. The nurse provides emotional support and en-couragement to the patient and encourages compliance with the treatment regimen. The orthopedic surgeon evaluates the pro-gression of bone healing with periodic x-rays.
Nursing care for the patient with a bone graft include pain management, monitoring the patient for signs of infection at the donor and recipient sites, and patient education. The nurse needs to reinforce information concerning the objectives of the bone graft, immobilization, non–weight bearing, wound care, signs of infection, and follow-up care with the orthopedic surgeon.
Nursing care for the patient with electrical bone stimulation focus on patient education that addresses immobilization, weight bearing restrictions, and correct daily use of the stimulator as prescribed.
Avascular necrosis occurs when the bone loses its blood supply and dies. It may occur after a fracture with disruption of the blood sup-ply (especially of the femoral neck). It is also seen with disloca-tions, bone transplantation, prolonged high-dosage corticosteroid therapy, chronic renal disease, sickle cell anemia, and other dis-eases. The devitalized bone may collapse or reabsorb. The patient develops pain and experiences limited movement. X-rays reveal calcium loss and structural collapse. Treatment generally consists of attempts to revitalize the bone with bone grafts, prosthetic replacement, or arthrodesis (joint fusion).
Internal fixation devices may be removed after bony union has taken place. In most patients, however, the device is not re-moved unless it produces symptoms. Pain and decreased func-tion are the prime indications that a problem has developed. Problems may include mechanical failure (inadequate insertionand stabilization); material failure (faulty or damaged device);corrosion of the device, causing local inflammation; allergic response to the metallic alloy used; and osteoporotic remodelling adjacent to the fixation device (in which stress needed for bone strength is transferred to the device, causing a disuse osteoporosis). If the device is removed, the bone needs to be protected from refracture related to osteoporosis, altered bone structure, and trauma. Bone remodeling reestablishes the bone’s structural strength.
Complex regional pain syndrome (CRPS), formerly called reflex sympathetic dystrophy (RSD), is a painful sympathetic nervoussystem problem. It occurs infrequently. When it does occur, it is most often in an upper extremity after trauma and is seen moreoften in women. Clinical manifestations of CRPS include severe burning pain, local edema, hyperesthesia, stiffness, discoloration,vasomotor skin changes (ie, fluctuating warm, red, dry and cold, sweaty, cyanotic), and trophic changes (ie, glossy, shiny skin; increased hair and nail growth). This syndrome is frequently chronic, with extension of symptoms to adjacent areas of the body. Disuse muscle atrophy and bone deossification (osteoporosis) occur with persistence of CRPS. Patients may exhibit ineffective individual coping related to the chronic pain.
Prevention may include elevation of the extremity after injury or surgery and selection of an immobilization device (eg, external fix-ator) that allows for the greatest ROM and functional use of the rest of the extremity. Early effective pain relief is the focus of man-agement. Pain may need to be controlled with analgesics, anes-thetic nerve blocks, or intravenous bisphosphonate pamidronate. NSAIDs, corticosteroids, muscle relaxants, and antidepressants are also used. With pain relief, the patient can participate in ROM exercises and functional use of the affected area. The nurse needs to help the patient cope with CRPS manifestations and explore multiple ways to control pain. The nurse avoids using the involved extremity for blood pressure measurements and venipunctures.
Heterotrophic ossification (myositis ossificans) is the abnormal formation of bone, near bones or in muscle, in response to soft tissue trauma after blunt trauma, fracture, or total joint replace-ment. The muscle is painful, and normal muscular contraction and movement are limited. Early mobilization has been recom-mended. Indomethacin (Indocin) may be used prophylactically if deep muscle contusion has occurred. Usually, the bone lesion resorbs over time, but the abnormal bone eventually may need to be excised if symptoms persist.
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