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.
Related Topics
Privacy Policy, Terms and Conditions, DMCA Policy and Compliant
Copyright © 2018-2024 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.