ch 63 musculoskeletal problems Flashcards
is a severe infection of the bone, bone marrow, and surrounding soft tissue. Although Staphylococcus aureus is the most common cause of infection, a variety of pathogens can cause osteomyelitis
Osteomyelitis
indirect or direct entry
infecting microorganisms can invade by (Osteomyelitis)
with infection with 1 microorganism. Indirect injury accounts for only 20% of all cases. It most often affects children younger than 17 years
Indirect entry (hematogenous) is usually associated (Osteomyelitis)
older age, debilitation, hemodialysis, sickle cell disease, and IV drug use. The vertebrae are the most common site of infection in adults.2
Risk factors in adults are (Osteomyelitis)
when an open wound (e.g., penetrating wounds, fractures, surgery) allows microorganisms to enter the body. Osteomyelitis also may be related to a foreign body, such as an implant or an orthopedic prosthetic device (e.g., plate, total joint prosthesis). It may occur in the feet of patients with diabetes or vascular disease–related ulcers or in the hips or sacrum near a pressure injury. More than 1 microorganism is usually involved
Direct entry osteomyelitis most often affects adults. It can occur
The area of dead bone eventually separates from the surrounding living bone, forming
sequestra
part of the periosteum that continues to have a blood supply forms new bone called
involucrum
through the blood. Thus sequestrum may become a reservoir for microorganisms that spread to other sites, including the lungs and brain.
antibiotics or white blood cells (WBCs) have difficulty reaching the sequestrum
to the initial infection or an infection of less than 1 month in duration
Acute osteomyelitis refers
constant bone pain that worsens with activity and is unrelieved by rest; swelling, tenderness, and warmth at the infection site; and restricted movement of the affected part. Systemic manifestations include fever, night sweats, chills, restlessness, nausea, and malaise. Later signs include drainage from cutaneous sinus tracts or the fracture site.
Local manifestations of acute osteomyelitis include constant
to a bone infection that lasts longer than 1 month or an infection that did not respond to initial antibiotic treatment.
Chronic osteomyelitis refers
lessened. Local signs of infection become more common, including constant bone pain and swelling and warmth at the infection site. Over time, granulation tissue turns to scar tissue. The avascular scar tissue is an ideal site for continued microorganism growth because it cannot be penetrated by antibiotics
Systemic manifestations of Chronic osteomyelitis are
septicemia, septic arthritis, pathologic fractures, and amyloidosis.
Long-term, and mostly rare, complications of osteomyelitis include
is the definitive way to identify the causative agent.
-patient’s blood and wound cultures are often positive
Bone or soft tissue biopsy
Increased WBC count and erythrocyte sedimentation rate (ESR) may occur. High C-reactive protein (CRP) may occur with acute infection.
-signs of osteomyelitis usually do not appear on x-rays until 2 to 4 weeks after the initial clinical symptoms.
- CT scan may be more helpful in assessing the extent of infection
-MRI may be more sensitive than CT in detecting bone marrow edema, which is an early sign of osteomyelitis.
-Radionuclide bone scans (technetium-99m) also show abnormalities earlier than x-rays. A WBC scan (indium-111–labeled cells) may help pinpoint the area of infection.2
diagnosis of osteomylitis
edema
early sign of osteomyelitis
Aggressive, prolonged IV antibiotic therapy is the treatment of choice for acute osteomyelitis if bone ischemia has not yet occurred.
acute osteomyelitis Tx choice
Assess patient for dehydration before starting therapy.
* Ensure renal function testing is done before starting therapy, especially in older patients.
* Monitor peak and trough blood levels to achieve therapeutic effect and minimize renal and inner ear toxicity.
* Teach patient to notify HCP if any vision, hearing, or urinary problems develop.
Gentamicin Side effects
(1) surgical removal of the poorly perfused tissue and dead bone and (2) extended use of antibiotics. In adults with chronic osteomyelitis, oral therapy with a fluoroquinolone (e.g., ciprofloxacin [Cipro]) for 6 to 8 weeks may be prescribed instead of IV antibiotics
- Oral antibiotics also may be given for 4 to 8 weeks after acute IV therapy is done to ensure the infection is resolved
Treatment of chronic osteomyelitis includes
A implanted to help combat the infection. After debridement of the dead, infected tissue, a suction irrigation system may be inserted, and the wound closed.
crylic bead chains containing antibiotics may be
may be given as an adjunct therapy in refractory cases of chronic osteomyelitis. It stimulates new blood growth and healing in the infected tissue
Hyperbaric O2
wound coverage over the dead space (cavity) in the bone. Bone grafts may help to restore blood flow
Muscle flaps or skin grafts provide
those who are immunocompromised or have diabetes, orthopedic prosthetic implants, or vascular insufficiency.
Persons at risk for osteomyelitis are
common as the patient often positions the leg in a flexed position to promote comfort.
Flexion contracture of the affected lower extremity is
quickly due to Achilles tendon contracture if the foot is not supported in a neutral position by a splint or boot.
Footdrop can develop
and injure the peroneal nerve.
tight splint or dressing may compress
include hearing deficit, impaired renal function, and neurotoxicity (e.g., limb weakness or numbness, cognitive changes, vision changes, headache, behavioral problems).
possible adverse and toxic reactions associated with prolonged high-dose antibiotic therapy
hives, severe or watery diarrhea, blood in stools, and throat or mouth sores.
Reactions associated with cephalosporins (e.g., cefazolin) include
Tendonitis or tendon rupture (especially the Achilles tendon) can
occur with use of fluoroquinolones (e.g., ciprofloxacin).
Candida albicans and Clostridium difficile in the genitourinary (GU) and gastrointestinal (GI) tracts, especially in immunosuppressed and older adult patients. Teach the patient to report any changes in the oral cavity (e.g., whitish yellow, curdlike lesions) or the GU tract (e.g., perianal itching, discharge).
Lengthy antibiotic therapy can cause an overgrowth of
in which cancer has spread from another site, is a more common problem.
Metastatic bone cancer,
than primary malignant tumors.
Benign bone tumors are more common
osteochondroma, osteoclastoma, and enchondroma
main types of benign bone tumors are
is the most common primary benign bone tumor. It is characterized by an overgrowth of cartilage and bone near the end of the bone at the growth plate
Osteochondroma
the pelvis, scapula, or long bones of the leg.
Osteochondroma most often occur in
a painless, hard, immobile mass; shorter-than-normal height for age; soreness of muscles close to the tumor; one leg or arm longer than the other; and pressure or irritation with exercise. Some may be asymptomatic. Diagnosis is confirmed using x-ray, CT scan, and MRI.
Manifestations Osteochondroma include
is a malignant tumor that develops in bone, muscle, fat, nerve, or cartilage.
sarcoma
osteosarcoma, chondrosarcoma, and Ewing’s sarcoma
The most common types of sarcomas are
childhood and young adulthood. They cause bone destruction and have rapid metastasi
Primary malignant tumors occur most often during
is an extremely aggressive primary bone cancer that rapidly spreads to distant sites. It usually occurs in the pelvis or metaphyseal region of the long bones of extremities, especially in the distal femur, proximal tibia, and proximal humerus
Osteosarcoma
of spread (metastasis) from a primary tumor at another site.
most common type of malignant bone tumor occurs because
breast, colon, prostate, lungs, kidney, and thyroid.5
Common primary sites include
the primary tumor to the bone via the lymph and blood supply
Metastatic cancer cells travel from
the spine, ribs, or pelvis.
Metastatic bone lesions often occur in
is a group of genetic diseases characterized by progressive symmetric wasting of skeletal muscles without evidence of neurologic involvement.
Muscular dystrophy (MD)
is the most common type.
Duchenne MD
are X-linked recessive disorders usually seen only in males
Duchenne and Becker MD (types of Muscular dystrophy)
disorders are caused by a mutation of the dystrophin (DMD) gene.
Duchenne and Becker MD (types of Muscular dystrophy) defined
is a protein that helps keep skeletal muscle fibers intact. Abnormal dystrophin can cause defects in the muscle fiber and muscle fiber degeneration.
Dystrophin
Genetic testing can detect a mutation in the DMD gene and confirm a diagnosis.6
–Other diagnostic studies for MD include muscle serum enzymes (especially creatine kinase), electromyogram (EMG) testing, and muscle fiber biopsy. Classic findings on muscle biopsy include fat and connective tissue deposits, muscle fiber degeneration and necrosis, and a deficiency of dystrophin. An ECG may show abnormalities that suggest cardiomyopathy.
diagnostic studies for MD include
Corticosteroid therapy is part of the standard of care. It may slow disease progression for up to 2 years.
Treatment for Muscular dystrophy
is the first corticosteroid approved to treat Duchene
Deflazacort (Emflaza)
first disease-modifying drug to treat Duchene
Eteplirsen (Exondys 51)
is most often due to a musculoskeletal problem. It may be localized or diffuse.
Low back pain
, patients feel soreness or discomfort when a specific area of the lower back is palpated or pressed.
localized pain
over a larger area and comes from deep tissue.
Diffuse pain occurs
radicular or referred
Low back pain may be
irritation of a nerve root. Radicular pain is not isolated to a single location. Instead, it radiates or moves along a nerve distribution. Sciatica is an example of radicular pain.
Radicular pain is caused by
is felt in the lower back, but the source of the pain is another location (e.g., kidneys, lower abdomen).
Referred pain
second only to headache as the most common pain problem.
Backache is
the leading cause of job-related disability and a major contributor to missed work days
Backache is
(1) bears most of the weight of the body, (2) is the most flexible region of the spinal column, (3) has nerve roots that are at risk for injury or disease, and (4) has a naturally poor biomechanical structure.
Low back pain is common because the lumbar region
lack of muscle tone, excess body weight, stress, poor posture, smoking, pregnancy, prior compression fracture of the spine, spinal problems since birth, and a family history of back pain. Jobs that require repetitive heavy lifting, vibration (such as a jackhammer operator), and extended periods of sitting are associated with low back pain.
Risk factors low back pain include
(1) acute lumbosacral strain, (2) instability of the lumbosacral bony mechanism, (3) osteoarthritis of the lumbosacral vertebrae, (4) degenerative disc disease, and (5) herniation of an intervertebral disc.
causes of low back pain of musculoskeletal origin include
. Lifting and moving patients, excessive bending or leaning forward, and frequent twisting can result in low back pain that causes lost time and productivity and disability.
Health care personnel who perform direct patient care activities are at high risk for developing low back pain
4 weeks or less.
Acute low back pain lasts
by trauma or an activity that produces undue stress (often hyperflexion) on the lower back.
Most acute low back pain is caused
They develop later (usually within 24 hours) because of a gradual increase in pressure on the nerve from an intervertebral disc and/or associated edema. Symptoms may range from muscle ache to shooting or stabbing pain, limited flexibility or ROM, or an inability to stand upright.
sign/ symp of low back pain
. One test is the straight-leg-raising test
-MRI and CT scans are not done unless trauma or systemic disease (e.g., cancer, spinal infection) is suspected.
Few definitive diagnostic abnormalities are present with nerve irritation and muscle strain
” This formal program is usually taught by an HCP, nurse, or physical therapist. It is designed to teach the patient how to minimize back pain and avoid repeat episodes of pain.
“Back School.
shoes with low heels and shock-absorbing shoe inserts for women.
Recommend flat shoes or
excessive lumbar lordosis, placing stress on the lower back.
avoid sleeping in a prone position because it causes
knees and hips flexed prevents pressure on support muscles, ligaments, and lumbosacral joints.
Sleeping in a supine or side-lying position with
NSAIDs and muscle relaxants (e.g., cyclobenzaprine)
-Massage and back manipulation, acupuncture, and the application of cold and hot compresses may help some patients. Severe pain may require a brief course of corticosteroids or opioid analgesics.
drugs therapy treatment
lumbosacral area is unstable, repeated episodes are likely. Obesity, poor posture, poor muscle support, older age, or trauma may weaken the lumbosacral spine, so it is unable to meet the demands placed on it without strain.
causes of lumbosacral area
than 3 months or involves a repeated incapacitating episode.
Chronic low back pain lasts more
(1) degenerative conditions, such as arthritis or disc disease; (2) osteoporosis or other metabolic bone diseases; (3) weakness from the scar tissue of prior injury; (4) chronic strain on lower back muscles from obesity, pregnancy, or stressful postures on the job; and (5) congenital spine problems.
Causes Chronic low back pain include
is a narrowing of the spinal canal, which holds the spinal cord.
Spinal stenosis
of chronic low back pain
stenosis in the lumbar spine is a common cause
stenosis can be acquired or inherited
-common acquired cause is osteoarthritis.
-Arthritic changes (bone spurs, calcification of spinal ligaments, disc degeneration) narrow the space around the spinal canal and nerve roots, eventually leading to compression
causes of spinal stenosis
narrow the space around the spinal canal and nerve roots, eventually leading to compression
Arthritic changes (bone spurs, calcification of spinal ligaments, disc degeneration)
pain, weakness, and numbness.
Inflammation caused by the compression results in
rheumatoid arthritis, spinal tumors, Paget’s disease, and traumatic damage to the vertebral column. Inherited conditions that lead to spinal stenosis include congenital spinal stenosis and scoliosis.
Other acquired conditions that may cause spinal stenosis include
in the lower back and then radiates to the buttock and leg. It is worse with walking or prolonged standing. Numbness, tingling, weakness, and heaviness in the legs and buttocks may be present. History of decreased pain when the patient bends forward or sits is often a sign of spinal stenosis. In most cases, stenosis slowly progresses.
pain associated with lumbar spinal stenosis often starts
Manage the patient’s pain and stiffness with mild analgesics, such as NSAIDs, for daily comfort. Antidepressants (e.g., duloxetine [Cymbalta]) may help with pain management and sleep problems. The antiseizure drug gabapentin (Neurontin) may improve walking and relieve leg symptoms.
Treatment for chronic low back pain (drugs)
Weight reduction, rest periods, local heat or cold application, physical therapy, and exercise and activity throughout the day help keep the muscles and joints mobilized. Cold, damp weather worsens the back pain. Pain can be decreased with rest and local heat application. Complementary and alternative therapies, such as biofeedback, acupuncture, and yoga, may help reduce the pain. “Back School” (discussed on p. 1485) can significantly reduce pain and improve body posture
Treatment for chronic low back pain (nonpharmacological)
, such as epidural corticosteroid injections and implanted devices that deliver pain medication, are options for those with chronic low back pain that does not respond to the usual therapeutic options.
Minimally invasive treatments for chronic low back pain if other treatments not working
the vertebrae and help absorb shock for the spine
Intervertebral discs separate
the deterioration, herniation, or other dysfunction of the intervertebral discs.
Intervertebral disc disease involves
the cervical, thoracic, and lumbar spine.
Disc disorders can affect
loss of fluid in the intervertebral discs with aging.
Degenerative disc disease (DDD) results from
elasticity, flexibility, and shock-absorbing abilities. Unless it is accompanied by pain, DDD is a normal process
discs lose their
the nucleus pulposus (gelatinous center of the disc) starts to dry out and shrink. This change limits the disc’s ability to distribute pressure between vertebrae.
The discs become thinner as
The pressure is then transferred to the annulus fibrosus (strong outside part of the disc), causing progressive destruction. When the disc is damaged, the nucleus pulposus may seep through a torn or stretched annulus. This is called a herniated disc(slipped disc),
When the disc is damaged,
a condition in which a spinal disc bulges outward between the vertebrae
herniated disc(slipped disc),
degeneration with age or repeated stress and trauma to the spine.
herniated disc can result from
the lumbosacral discs, specifically L4-5 and L5-S1.
most common sites of herniation are
C5-6 and C6-7
Disc herniation may also occur at
spinal stenosis, in which narrowing of the spinal canal forces the intervertebral disc to bulge.
Disc herniation may also occur at C5-6 and C6-7. It may be the result of
spinal nerves emerge from the spinal column through an opening (intervertebral foramen) between adjacent vertebrae. Herniated discs can press against these nerves (“pinched nerve”) causing radiculopathy (radiating pain, numbness, tingling, decreased strength and/or range of motion).
causing radiculopathy
(radiating pain, numbness, tingling, decreased strength and/or range of motion).
sign/symp radiculopathy
DDD and the stresses placed on the vertebrae.
- poorly lubricated joints rub against each other, the protective cartilage is damaged and painful bone spurs occur as one of the changes found in OA.
Osteoarthritis (OA) of the spine is associated with
is low back pain
lumbar disc disease, the most common manifestation
Radicular pain that radiates down the buttock and below the knee, along the distribution of the sciatic nerve, generally
indicates disc herniation.
nerve root irritation ( Back or leg pain may be reproduced by raising the leg.)
positive straight-leg-raising test may indicate
(1) severe low back pain, (2) progressive weakness, (3) increased pain, and (4) bowel and bladder incontinence or retention. Saddle anesthesia (loss of or altered sensation of the perineum, buttocks, inner thighs and back of the legs [saddle area]) may be present. Symptoms of cauda equina syndrome may develop suddenly or evolve slowly over time. They may vary in intensity. Cauda equina is a medical emergency that requires surgical decompression to reduce pressure on the nerves and prevent permanent paralysis.14
Multiple lumbar nerve root compressions (cauda equina syndrome) from a herniated disc, tumor, or an epidural abscess may be marked by
into the arms and hands, following the pattern of the involved nerve. Like lumbar disc disease, reflexes may or may not be present. The handgrip is often weak.
cervical disc disease, pain radiates
shoulder pain and dysfunction, the HCP must rule out shoulder disorders as part of the diagnosis.
manifestations of cervical disc disease may include
X-rays are done to detect any structural defects. A myelogram, MRI, or CT scan is helpful in localizing the damaged site. An epidural venogram or diskogram may be needed if other diagnostic studies are inconclusive. An EMG of the extremities can be done to determine the severity of nerve irritation or to rule out other conditions, such as peripheral neuropathy.
diagnostics for know disc disease
the patient is in constant pain and/or has a persistent neurologic deficit.
Surgery for a damaged disc is generally done if
is a minimally invasive outpatient procedure for treatment of back and sciatic pain.
-needle is inserted into the affected disc with x-ray guidance. A wire is then threaded through the needle and into the disc. As the wire is heated, small nerve fibers that have invaded the degenerating disc are destroyed. The heat also partially melts the annulus fibrosus. This causes the body to generate new reinforcing proteins in the fibers of the annulus.
Intradiscal electrothermoplasty (IDET) (surgery damaged disc)
A needle is inserted into the disc similar to IDET. Instead of a heated wire, a special radiofrequency probe is used. The probe generates energy that breaks the molecular bonds of the gel in the nucleus pulposus. Up to 20% of the nucleus is removed. This decompresses the disc and reduces pressure on the disc and surrounding nerve roots. Subsequent pain relief varies.
radiofrequency discal nucleoplasty (coablation nucleoplasty).(surgery damaged disc)
This titanium device fits onto a mount that is placed on vertebrae in the lower back. The X-Stop is used in patients with pain due to lumbar spinal stenosis. The device works by lifting vertebrae off the pinched nerve.
interspinous process decompression system (X-Stop). (surgery damaged disc)
It involves surgical excision of part of the vertebra (referred to as the lamina) to access and remove the protruding disc. Laminectomy is often done as an outpatient procedure. However, a hospital stay of 1 to 3 days is not uncommon.
Laminectomy is a common, traditional surgical procedure for lumbar disc disease.
Microsurgical discectomy is a version of the standard procedure. The HCP uses a microscope to better see the disc and disc space, which helps in removal of the damaged portion. This helps maintain bony stability of the spine.
Discectomy also can be done to decompress the nerve root.
is a safe and effective outpatient surgical procedure. A tube is passed through the retroperitoneal soft tissues to the disc with the aid of fluoroscopy. A laser is then used on the damaged part of the disc. Minimal blood loss occurs because of access through small stab wounds. The procedure decreases rehabilitation time.
Percutaneous discectomy (surgery damaged disc)
to restore movement and eliminate pain
goals of artificial disc replacement surgery are
used in patients with lumbar disc damage associated with DDD. This artificial disc has a high-density core sandwiched between 2 cobalt-chromium endplates. After removing the damaged disc, the device is surgically placed in the spine (usually through a small incision below the umbilicus). The disc restores movement at the level of the implant
Charité disc is (type of artificial lumbar disc used to treat DDD.)
another type of artificial lumbar disc used to treat DDD.
ProDisc-L is
the Prestige cervical disc, Mobi-C disc, and Secure-C artificial cervical disc.
Options for treatment of DDD of the cervical spine include
-if the spine is unstable
-spine is stabilized by creating ankylosis (fusion) of adjacent vertebrae with a bone graft from the patient’s fibula or iliac crest (autograft) or from donated cadaver bone (allograft). Metal fixation with rods, plates, or screws may be placed to give more stability and decrease vertebral motion.the spine is unstable
spinal fusion may be needed if
, place pillows under the patient’s thighs when supine and between the legs when in the side-lying position to provide comfort and ensure alignment.
*****-bed trapeze, if present, since use is contraindicated for spinal surgery patients.
After lumbar fusion (proper to way move around)
After surgery, most patients need opioids, such as morphine IV, for 24 to 48 hours. Patient-controlled analgesia (PCA) allows maintenance of optimal analgesic levels and is the preferred method of continuous pain management. Once the patient receives oral fluids, oral drugs, such as acetaminophen with codeine, hydrocodone, or oxycodone (Percocet), may be used. Diazepam (Valium) may be prescribed for muscle relaxation.
Treatment after spinal surgery
bony projections that develop along bone edges (in joint)
bone spurs (osteophytes)
Immediately report leakage of CSF on the dressing or if the patient reports a severe headache
Because the spinal canal may be entered during surgery, cerebrospinal fluid (CSF) leakage is possible.
clear or slightly yellow drainage on the dressing. It has a high glucose concentration and is positive for glucose when tested with a dipstick.
CSF appears as
nerve damage
Loss of sphincter tone or bladder tone may indicate
(thoracolumbar sacral orthosis [TLSO] or chairback brace)
rigid orthosis
spinal cord edema, such as respiratory distress and a worsening neurologic condition of the upper extremities.
cervical spine surgery, be alert for signs of
many different conditions, including benign (e.g., poor posture) and serious (e.g., herniated cervical disc)
Neck pain may result from
- Degenerative disc disease, including herniation
- Meningitis
- Osteomyelitis
- Osteoporosis
- Poor posture
- Rheumatoid arthritis
- Spondylosis
- Strain or sprain
- Trauma (e.g., fractures, subluxation)
- Tumor
causes of neck pain
hyperflexion and hyperextension injuries. Patients have stiffness and neck pain with possible radicular pain into the arm and hand.
Cervical neck sprains and strains occur from
the head, anterior chest, thoracic spine region, and shoulders. Weakness or paresthesia of the arm and hand suggests cervical nerve root compression from stenosis, DDD, or herniation.
Pain from neck may radiate to
history, physical examination, x-ray, MRI, CT scan, and myelogram. An EMG of the upper extremities may diagnose cervical radiculopathy.
cause of neck pain is diagnosed by
head support using a soft cervical collar, gentle traction, heat and ice applications, massage, rest until symptoms subside, ultrasound, and NSAIDs. Therapeutic neck exercises and acupuncture also may be used for pain relief.19 Most neck pain resolves without surgical intervention.
Conservative treatment for neck pain in patients without an underlying disorder includes
is the platform that supports the weight of the body and absorbs shock when the person ambulates
foot
(1) congenital conditions; (2) structural weakness; (3) traumatic and stress injuries; and (4) systemic conditions, such as diabetes and rheumatoid arthritis.
foot can be affected by
(1) provide support, foot stability, protection, shock absorption, and a foundation for orthotics; (2) increase friction with the walking surface; and (3) treat foot abnormalities.
Footwear is used to
or worsen a great deal of the pain, deformity, and disability from foot disorders.20 Shoes may cause crowding and angulation of the toes and inhibit normal movement of foot muscles.
Poorly fitting shoes cause
They cause compression of an intermetatarsal plantar nerve, resulting in paresthesia and burning. At first, patients with Morton’s neuroma may describe feeling as if a sock is rolled up under their toes. Neuromas usually occur between the third and fourth toes.
Prolonged use of improper footwear can also cause a Morton’s neuroma.
include NSAIDs, ice, physical therapy, footwear changes, stretching, warm soaks, orthotics, ultrasound, and corticosteroid injections. If these methods do not help, surgery may be needed.
treatment for foot
through the toes, or a protective splint may be placed over the end of the foot.
Depending on the type of foot surgery, pins or wires may extend
the foot is usually immobilized by a bulky dressing, short leg cast, slipper (plaster) cast, or a platform shoe that fits over the dressing and has a rigid sole (also known as a bunion shoe).
-elevate foot with heel off bed (prevent edema)
After foot surgery,
ingrown toenails and reduces the risk for infection.
Trimming toenails straight across helps prevent
of poor circulation, atherosclerosis, and decreased sensation in the lower extremities.esp DM
-patient may develop an open wound but not feel it because of altered sensation from peripheral vascular disease or diabetic neuropathy.
older adult is prone to foot problems because
hormones, nutrition, and genetics.
Normal bone metabolism is affected by
, generalized reduction in bone mass and strength may result
dysfunction occurs in hormones, nutrition, and genetics. then
osteomalacia, osteoporosis, and Paget’s disease.
Metabolic bone diseases include
a vitamin D deficiency that causes bone to lose calcium and become soft.
-same disorder as rickets in children, except the epiphyseal growth plates are closed in adults.
Osteomalacia is caused by
the absorption of calcium from the intestine. Insufficient vitamin D intake can interfere with normal bone mineralization. With little or no calcification, bones become soft.
Vitamin D is required for
limited sun exposure (ultraviolet rays needed for vitamin D synthesis), GI malabsorption (post weight loss surgery, celiac disease), chronic diarrhea, and pregnancy. Residents of long-term care settings may have inadequate sun exposure and thus poor synthesis of vitamin D. Persons with dark skin do not synthesize vitamin D as easily as persons with fair skin. Obese persons are at higher risk because of decreased physical activity. Chronic liver, kidneys, and small intestine disease may contribute to vitamin D deficiency. Long-term use of antiseizure drugs (e.g., phenytoin) and phosphate-binding antacids (e.g., Maalox) may decrease calcium and vitamin D absorption.
Causes Insufficient vitamin D include
are bone pain and muscle weakness. The pain is often worse at night and affects the lower back, pelvis, hips, legs, and ribs.23 Muscle weakness and progressive deformity of weight-bearing bones (e.g., spine, extremities) can lead to problems walking and a waddling gait. Fractures are common and indicate delayed bone healing.
Common manifestations of low calcium(insufficient Vit D) aka osteomalacia
decreased serum calcium or phosphorus, decreased serum 25-hydroxyvitamin D, and increased serum alkaline phosphatase. X-rays may show effects of generalized bone demineralization, especially loss of calcium in the bones of the pelvis and associated bone deformity. Looser’s transformation zones (ribbons of decalcification in bone found on x-ray) are diagnostic of osteomalacia. However, significant osteomalacia may exist without x-ray changes.
Laboratory findings include (decrease Vit D aka osteomalacia)
response when vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol) supplements are used. Calcium or phosphorus supplements may be prescribed. Encourage dietary intake of eggs, meat, and oily fish (e.g., salmon, tuna). Milk and breakfast cereals fortified with calcium and vitamin D should be part of the diet.
Tx supplement for Calcium/ osteomalacia and diet
is a chronic, progressive metabolic bone disease marked by low bone mass and deterioration of bone tissue, leading to increased bone fragility
Osteoporosis
it slowly robs the skeleton of its banked resources. Bones eventually become so fragile that they cannot withstand normal mechanical stress.
Osteoporosis is known as the “silent thief” because
(1) women tend to have lower calcium intake than men throughout their lives (men between 15 and 50 years of age consume twice as much calcium as women); (2) women have less bone mass because of their generally smaller frames; (3) bone resorption begins at an earlier age in women and becomes more rapid at menopause; (4) pregnancy and breastfeeding deplete a woman’s skeletal reserve unless calcium intake is adequate; and (5) longevity increases the risk for osteoporosis.
Osteoporosis is more common in women. This is for several reasons:
. If results are normal and the person is at low risk for osteoporosis, another test is not needed for 15 years. Women who are younger than 65 and at high risk (e.g., low body weight, smoker, prior fractures) should have a bone density test earlier.
Current guidelines recommend an initial bone density test in all women over age 65 years
- Advancing age (>65 yr)
- Female gender
- Low body weight
- White or Asian ethnicity
- Cigarette smoking
- Sedentary lifestyle
- Estrogen deficiency in women (surgical or age-related menopause)
- Family history of osteoporosis
- Diet low in calcium or vitamin D deficiency
- Excess use of alcohol (>2 drinks/day)
- Low testosterone in men
- Long-term use of corticosteroids, thyroid replacement, heparin, long-acting sedatives, or antiseizure drugs
Risk Factors for Osteoporosis
age 20
Peak bone mass (maximum bone tissue) is typically achieved before
heredity, nutrition, exercise, and hormone function.
Peak bone mass largely determined by 4 factors:
Bone is continuously being deposited by osteoblasts and resorbed by osteoclasts, a
process called remodeling.
exceeds bone deposition.
In osteoporosis, bone resorption
inflammatory bowel disease, intestinal malabsorption, kidney disease, rheumatoid arthritis, hyperthyroidism, alcohol use disorder, cirrhosis, hypogonadism, and diabetes.
Diseases associated with osteoporosis include
corticosteroids, antiseizure drugs (e.g., divalproex sodium [Depakote], phenytoin), aluminum-containing antacids, heparin, some chemotherapy drugs, and excess thyroid hormones.
-Long-term corticosteroid use is a major contributor to osteoporosis.
Many drugs can interfere with bone metabolism, including
spine, hips, and wrists.
Osteoporosis occurs most often in bones of the
are back pain and spontaneous fractures. The loss of bone mass causes the bone to become mechanically weaker and prone to spontaneous fractures or fractures from minimal trauma. A person who has a vertebral fracture due to osteoporosis has an increased risk for having a second vertebral fracture within 1 year. Over time, vertebral fractures and wedging cause gradual loss of height and a humped thoracic spine (kyphosis, or “dowager’s hump”)
Typical early manifestations of Osteoporosis
peak bone mass and amount of bone loss.
BMD is determined by
measures bone density in the spine, hips, and forearm.
-represent the most common sites of fragility fractures from osteoporosis.
DEXA (considered the gold standard of BMD studies by the World Health Organization)
uses sound waves to measure bone density in the heel, kneecap, or shin.
QUS BMD may be measured by quantitative ultrasound
in bone density over time and assess effectiveness of osteoporosis treatment.
DEXA studies are useful to evaluate changes
of a healthy 30-yr-old adult and reported as T-scores. A T-score of 0 means the BMD is equal to the norm for a healthy young adult.
BMD test results are compared to the ideal or peak bone mineral density
Differences between the BMD and that of the healthy young adult norm are measured in units called standard deviations (SDs). The more standard deviations below 0 (indicated as negative numbers), the lower the BMD and the higher the risk for fracture.
standard deviations (SDs)
A T-score between +1 and –1 is normal. A T-score between –1 and –2.5 indicates osteopenia (bone loss that is more than normal, but not yet at the level for a diagnosis of osteoporosis)
indicates osteopenia (bone loss that is more than normal, but not yet at the level for a diagnosis of osteoporosis)
osteoporosis. The greater the negative number, the more severe the osteoporosis
T-score of –2.5 or lower indicates
-their own age, gender, and/or ethnic group instead of a healthy 30-yr-old person
-compared with someone their own age, gender, and/or ethnic group instead of a healthy 30-yr-old person.
-If the Z-score is –2 or lower, it may suggest that something other than aging is causing abnormal bone loss.
Z-score instead of a T-score. In this case a person is compared with someone
(1) a T-score of less than −2.5, (2) a T-score between −1 and −2.5 with additional risk factors or (3) prior history of a hip or vertebral fracture.
national Osteoporosis Foundation recommends treatment for osteoporosis for postmenopausal women with
patient’s risk for fracture from osteoporosis also can be calculated with the
Fracture Risk Assessment (FRAX) tool
1000 mg/day for women ages 19 to 50 years and men ages 19 to 70 years and 1200 mg/day in women age 51 years or older and men 71 years or older
recommended calcium intake is
milk, yogurt, turnip greens, cottage cheese, ice cream, sardines, and spinach
-If dietary intake of calcium is inadequate, supplemental calcium may be given.
Foods high in calcium include
Calcium carbonate has 40% elemental calcium. It should be taken with meals because stomach acid is needed to dissolve and absorb this supplement. Calcium citrate has about 20% elemental calcium but is less dependent on stomach acid for absorption. It is better absorbed by patients taking a proton pump inhibitor (e.g., esomeprazole [Nexium]) or histamine receptor blocker (e.g., cimetidine) for acid reflux.
amount of elemental calcium varies in calcium preparations.
they have small amounts of elemental calcium.
Calcium lactate and calcium gluconate are not recommended because
postmenopausal women, older men, persons who are homebound or in long-term care settings, and those in northern climates due to decreased sun exposure.
supplemental vitamin D (800 IU) is recommended for
the bisphosphonates alendronate, risedronate, and zoledronic acid, or denosumab.
prevention and treatment of osteoporosis are
is osteonecrosis (bone death) of the jaw. Its cause is unknown. Those with dental disease, cancer, Paget’s disease, or renal disease are most at risk for this complication.
serious, side effect of bisphosphonates
available as a daily or weekly oral tablet. Zoledronic acid (Reclast) is given as a once-yearly or every-other-year IV infusion.
Alendronate (Fosamax) is (biphosphate)
The immediate-release form of risedronate (Actonel) is given daily, weekly, or monthly, based on the dose.
risedronate (Actonel) (biphosphate)
is given as a once-yearly or every-other-year IV infusion.
Zoledronic acid (Reclast) (biphosphate)
Renal function tests and serum calcium must be assessed before administration.
test assessed before biphosphate adminstration
may be given to postmenopausal women with osteoporosis who are at high risk for fractures.
-given as a subcutaneous injection every 6 months.
Denosumab (Prolia) (monoclonal antibody)
It inhibits the action of sclerostin, a regulatory factor in bone metabolism. This increases bone formation and, to a lesser extent, decreases bone resorption. It is given by subcutaneous injection every month for a total of 12 doses.
new monoclonal antibody romosozumab (Evenity).
of the increased risk for heart disease and breast and uterine cancer.
Women no longer routinely use estrogen replacement therapy or estrogen with progesterone after menopause to prevent osteoporosis because
treatment with bisphosphonates may be considered.
If osteopenia is present on bone densitometry in people who are taking corticosteroids,
is a chronic skeletal bone disorder in which excessive bone resorption is followed by replacement of normal marrow by vascular, fibrous connective tissue.
Paget’s disease(osteitis deformans)
new bone is larger, disorganized, and weaker. Areas commonly affected include the pelvis, long bones, spine, ribs, sternum, and skull.
Paget’s disease(osteitis deformans) effect
may be viral or genetic. Up to 40% of all patients with the disease have at least 1 relative with the disorder.
cause Paget’s disease(osteitis deformans)
-patients do not have any symptoms.
-disease may be found incidentally through x-ray or serum chemistry findings of high alkaline phosphatase.
milder forms of Paget’s disease,
Bone pain may develop gradually and progress to severe intractable pain. Other early manifestations include fatigue and progressive development of a waddling gait. Patients report becoming shorter or their heads are becoming larger. Headaches, dementia, vision deficits, and loss of hearing can result from an enlarged, thickened skull. Increased bone volume in the spine can cause spinal cord or nerve root compression.
sign/symp Paget’s disease(osteitis deformans)
Pathologic fracture is the most common complication and may be the first sign of Paget’s disease. Other complications include osteosarcoma, fibrosarcoma, and osteoclastoma (giant cell) tumors
most common complication of Paget’s disease,
Serum alkaline phosphatase is markedly increased in advanced disease, showing high bone turnover.34 X-rays may show curvature of an affected bone. The bone cortex becomes thicker and irregular, especially in weight-bearing bones and the cranium. Bone scans using a radiolabeled bisphosphonate show increased uptake in the affected skeletal areas.
diagnosis of Paget’s disease(osteitis deformans)
usually limited to symptomatic and supportive care, with correction of secondary deformities by surgical intervention or braces. Bisphosphonate drugs (Table 63.13) are used to slow bone resorption. Zoledronic acid may be given specifically to build bone. Calcium and vitamin D can decrease hypocalcemia, a common side effect of drug therapy. Monitor drug effectiveness by regular assessment of serum alkaline phosphatase.
treatment for Paget’s disease,
is an option for patients who cannot tolerate bisphosphonates
Calcitonin
osteoclastic activity, prevents bone resorption, relieves acute symptoms, and lowers serum alkaline phosphatase. This drug is available as a subcutaneous injection.
Human calcitonin inhibits
a longer half-life and greater milligram potency than human calcitonin. Response to calcitonin therapy is not permanent and often ends when therapy stops.
Salmon calcitonin is 1 form. It has
available components for bone formation.
Vitamin D, calcium, and protein are especially important to ensure
