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858 n ASSOCIATED TOPICS IN PHYSICAL MEDICINE & REHABILITATION

Suicide rate is 7.5 times higher than normal population.• Decreased short-term memory, decreased reasoning, slow processing• Depression is a common finding and should be addressed by rehab psychology.•

OUTCOME IN MS

In general, 85% of patients with MS will have a normal life expectancy. However, the • unpredictable outcome of the disease and variable nature of its impairment make predict-ing it difficult.Seldom fatal• 1/3 require ambulatory assistance within 10 years of diagnosis; 2/3 do not.•

Minimal Record of Disability (MRD)

This consists of different types of rating scales that profile the main dysfunctions of MS.• The most common scale used is the Kurtzke Expanded Disability Status Scale (EDSS).• – A 10-level rating scale used in MS examining 8 different neurologic systems.– Rating scale:

0 = normal 4 = severe disability, but still ambulatory without aid 8 = bedbound10 = death

– Areas tested: pyramidal, cerebellar, brainstem, sensory, bowel and bladder, vision, men-tal status, and general

Other outcome scales used in MS include:• – Kurtzke Functional Systems (FS)– Incapacity Status Scale (ISS)– Environmental Status Scale (ESS)

MRD = EDSS, ISS, and EESFIM: Functional Independence Measure—assesses disability and the need for assistance. Does not assess vision (Kurtzke, 1983) (see Figure 8–4).

nOSTEOPOROSIS

Osteoporosis is a disease characterized by bone mass reduction and a deterioration of the bony microarchitecture. It is caused by an imbalance between bone formation and bone resorption, ultimately leading to osteopenia. Living bone is never metabolically at rest, as it is constantly remodeling and reappropriating its bony matrix and mineral stores along lines of mechanical stress. The factors that control bone formation and resorption are not well understood, but in the normal adult skeleton, the 2 processes are coupled so that net bone formation equals net bone resorption (Figure 11–10).

FACTS ABOUT OSTEOPOROSIS

Most common metabolic bone disease• Normal ratio of organic and mineral components but decreased bone tissue density• Differs from osteomalacia, which has normal or increased bone tissue density, but a • reduced mineral content to organic component ratio).

ASSOCIATED TOPICS IN PHYSICAL MEDICINE & REHABILITATION n 859

FIGURE 11–10 Calcium cycle. (From Kaplan FS. Prevention and Management of Osteoporosis.

Clinical Symposia 1995; 47(1) Copyright Ciba-Geigy, with permission.)


First clinical presentation is usually a fracture.• Major underlying cause of long bone fractures in the elderly is osteoporosis.• However, the diagnosis is not dependent on the patient suffering a fracture.•

EPIDEMIOLOGY

There are > 1.2 million fractures/year in the United States related to osteoporosis.• ~ 70% of fractures in people > 45 years old are related to osteoporosis.• 1/3 of females > 65 years old will have vertebral fractures.• ~ 50% of the population > 75 years old is affected, males and females equally.• Hip fracture is a significant cause of morbidity and mortality in Caucasian women aged • 50 years and above, and to a lesser extent Caucasian men of similar age.– 17.5% of these women will sustain a hip fracture compared to 6% of men.– Fractures usually result in temporary disability, but approx. 50% of females with

hip fractures admitted to nursing home, 14% of these patients in nursing home after 1 year.

– Morbidity: 50% of patients with hip fracture require assistance ADLs, 15–25% long-term placement.

– Mortality: 10–20% of patients die due to complications.The National Osteoporosis Foundation (NOF) uses the quality adjusted life year (QALY) • of fractures to determine the impact of osteoporotic fractures on a person’s life (Matkovic, 1996).

RISK FACTORS FOR OSTEOPOROSIS

Increased Risk

Caucasian or Asian• Female• Advanced age• Thin habitus• Smoking• Excess alcohol• Excess caffeine intake• Inactivity/immobilization• Diminished peak bone mass (PBM) at skeletal maturity• History of fracture as adult• Positive family history• Loss of ovarian function/estrogen depletion, testosterone deficiency• Exercise-induced amenorrhea• Low body mass index (BMI), typically < 20•

Decreased Risk

Obesity•

PHYSIOLOGY

Cellular Components of Bone Remodeling

Osteoblasts:• bone forming cells that produce organic matrix which is mineralized to form normal lamellar boneOsteoclasts:• bone resorption cellsOsteocytes: • osteoblasts incorporated in new bone matrix


Skeletal Mass Components

Cortical bone (compact)Dense outer shell of bone• Concentric lamellae, Haversian systems• 80% of skeleton, most in shafts (diaphysis) long bones• Accounts for majority of skeletal mechanical strength.•

Trabecular bone (cancellous, spongy)Found in central medullary canal; encloses marrow space.• Irregular branching plates, circumferential lamellae• 20% of total skeleton, found in vertebrae and flat bones (axial skeleton), ends of long • bonesVertebral bodies 42%, whole vertebrae 25%• More metabolically active than cortical bone.• Preferentially altered in osteoporosis type I•

Minerals, Hormones, VitaminsCalcium phosphate (in the form of hydroxyapatite)• – Major component of bone– Regulated by parathyroid hormone (PTH), calcitonin, and vitamin D; 99% of body’s

calcium is in bone.PTH—regulated by Ca• + concentrationEffects:• – In bone: activates osteoclasts.– In intestine: stimulates formation of vitamin D in kidneys (inactive form of vitamin D

to active form vitamin D), which results in increases Ca+ uptake.– In kidneys: increased phosphate excretion increases calcium reabsorption.Calcitonin• – Synthesized by C cells in thyroid glands.– Decreases serum Ca+ levels by inhibiting osteoclasts and increasing Ca+ incorporation

into bone.Vitamin D (1,25—Dihydroxyvitamin D• 3)– In the intestines: enhances Ca+ and phosphorus absorption.– In the kidneys: increases reabsorption of Ca+, phosphorus.

MAIN DETERMINANTS OF OSTEPOROSIS

The pathogenesis of osteoporosis is multifactorial. Causes include genetic and environmen-tal factors.1. Increased rate of bone loss

• After PBM is achieved, bone loss occurs gradually thereafter, with the most rapid bone loss occurring in early postmenopausal period in females.

• Rate of age related bone loss is approximately 0.25–1.0% per year in males and females.

• Immediate postmenopausal period: 3–5% bone loss per year in females for approxi-mately 5–7 years after onset of menopause

• Lifetime bone loss: 20–30% in males, 45–50% in females• Greatest contributor to bone loss in mature adults is loss of gonadal function.

2. Quality of bone microstructures• Decreased trabecular bone (trabecular perforation)


3. Failure to achieve adequate peak bone mass (PBM) at skeletal maturity• High risk groups include persons, such as female athletes (“female triad”= anorexia,

amenorrhea, osteoporosis), anorexics, persons with decreased mobility, persons with nutritional deficiencies.

CLASSIFICATION

1. Generalized—Affects Different Parts of Whole Skeleton

Primary Osteoporosis (Involutional)–Most CommonBasic etiology is unknown.

Postmenopausal osteoporosis (also known as Type I)• – Typically during the 15–20 years following menopause– Affects females 50–65 years old.– Trabecular > cortical bone loss– Most fractures in spine, hip, and wrist (Colles fracture) ie, axial skeletonSenile- or age-associated osteoporosis (also known as Type II)• – > 70 years old– 2:1 female:male ratio– Trabecular ≈ cortical bone loss– Fractures: hip, spine, pelvis, humerusJuvenile: children and adolescents; self-limited• Idiopathic: premenopausal females, middle-aged males•

Secondary Osteoporosis (Also Known as Type III)—Acquired or Inherited Diseases/Medication-Induced)Diseases:

Hyperparathyroidism• Hyperthyroidism• Cushing’s disease• Hypophosphatasia• Hypogonadism• Hypoestrogenism (anorexia, exercise induced amenorrhea)• Renal disease• Chronic obstructive pulmonary disease (COPD)• Systemic mastocytosis• Rheumatoid arthritis• Diabetes mellitus• Idiopathic hypercalciuria• Gastrointestinal disease (malabsorption syndromes, liver disease, partial gastrectomy)• Alcoholism• Nutrition (vitamin deficiency, calcium deficiency; high sodium, protein, phosphate, and • caffeine intakes)Malignancy (multiple myeloma, lymphoma, leukemia)• Immobility (tetraplegia/paraplegia/hemiplegia, prolonged bedrest)• Loss of ovarian function • → estrogen depletion, testosterone deficiency

Medication-induced:Corticosteroids: most common cause of secondary osteoporosis; predominantly inhibits • bone formation (↓ osteoblasts); mainly trabecular bone loss, leading to compression defor-mities of the vertebrae and pelvisHeparin• Anticonvulsants•


Excess thyrosine• Lithium• Loop diuretics•

2. Localized—Discrete Regions of Reduced Bone Mass

PrimaryTransient regional: rare, migratory; predominantly involves hip; usually self-limited.• Reflex sympathetic dystrophy (RSD, also known as CRPS Type I): radiographic changes • may occur in first 3–4 weeks, showing patchy demineralization of affected area.

SecondaryImmobilization, inflammation, tumors, necrosis•

De� nition from the World Health Organization (WHO)

The diagnosis of osteoporosis is made by measuring a patient’s bone mineral density (BMD) and comparing it to the mean BMD of a young adult reference population. One method called DXA scan (see Diagnosis section) is utilized to quantify BMD and is considered the gold standard for evaluating BMD. Results from a DXA scan are reported as T-scores and Z-scores. Diagnosis of osteopenia or osteoporosis is based on T-scores.1. The mean young adult bone mineral density (BMD) is the expected normal value of a

patient’s peak BMD at about age 20 compared to others of the same sex and ethnicity.2. A T-score is the number of standard deviations (SD) away from the mean of a reference

population. In this situation, the reference would be the young adult population as men-tioned above.

3. Normal Bone Density: defined as T-score is between -1 SD and + 1 SD (-1 SD ≤ normal T-score ≤ +1 SD).

4. Osteopenia: T-score is between –1 and –2.5, including –2.5.5. Osteoporosis: T-score is < –2.5.6. A Z-score represents the number of SDs the patient’s bone density is compared to adults

of the same age and gender.7. Peak Bone Mass (PBM): the highest level of bone mass achieved as a result of normal

growth generally occurs between adolescence and age 30, with variation at specific skel-etal sites.

DIAGNOSIS

History/Physical Exam

Evaluate for presence of risk factors or predisposing medical conditions.The first clinical indication is usually a fracture:

Fracture of proximal femur, distal forearm• – Usually associated with minimal trauma– Pain usually present.Vertebral body fracture• – Usually associated with minimal trauma– May be painful or asymptomatic.

T-score: –2.5 –1 0 1 2.5

Osteoporosis Osteopenia Within Normal Range


Diagnostic Evaluation

Dual x-ray absorpiometry (DXA) scan, CBC, comprehensive metabolic panel including LFTs, serum Ca+, phosphorus, total alkaline phosphatase

Additional Diagnostic Studies:

Ionized Ca• +, ESR, vitamin D, protein electrophoresis, thyroid function tests, parathyroid hormone, follicle stimulating hormone, estradiol, testosterone, serum and urine markers, urine Ca+/creatinine ratioIliac crest bone biopsy with tetracycline labeling (osteoporosis shows thin cortices and • decreased number of trabeculae)Markers of Bone Resorption• Elevated levels of calcium/creatinine ratio in fasting urine, hydroxyproline/creatinine • ratio in fasting urine, collagen cross links (pyridinolines, telopeptides), TRAP (tartrate resistant acid phosphatase)Markers for Bone Formation• Serum osteocalcin y-carboxyglutamic acid (GLA) protein• Serum total and bone specific alkaline phosphatase• Procollagen propeptide•

Indications for Bone Mineral Density Measurement (National Osteoporosis

Foundation)

Women age 65 and older and men age 70 and older, regardless of clinical risk factors• Younger postmenopausal women and men age 50• –70 of concern based on their clinical risk factor profileWomen in the menopausal transition if there is a specific risk factor associated with • increased fracture risk, such as low body weight, prior low-trauma fracture, or high risk medicationAdults who have a fracture after age 50• Adults with a condition (eg, rheumatoid arthritis) or taking a medication (eg,glucocorticoids, • ≥5 mg/day for ≥3 months) associated with low bone mass or bone lossAnyone being considered for pharmacologic therapy for osteoporosis• Anyone being treated for osteoporosis to monitor treatment effect• Anyone not receiving therapy in whom evidence of bone loss would lead to treatment• Postmenopausal women discontinuing estrogen should be considered for bone density • testingEstrogen deficient women at clinical risk for osteoporosis• Individuals with vertebral abnormalities• Individuals receiving, or planning to receive, long-term glucocorticoid (steroid) therapy ≥5 • mg/d of prednisone or an equivalent dose for ≥3 monthsIndividuals with primary hyperparathyroidism• Individuals being monitored to assess the response or efficacy of an approved osteoporo-• sis drug therapy

Other Indications

1. If risk factors present for fractures in perimenopausal and postmenopausal women2. Screen for bone loss in conditions in which osteopenia is a manifestation.3. Following response to treatment4. Testosterone deficient men5. Research—epidemiologic studies, clinical therapy trials


Radiographic Studies

Dual X-Ray Absorptiometry (DXA, Formerly DEXA)Gold standard for bone mineral density measurement testing• Accurate, precise, fast• Low radiation exposure (scan times are shorter than with DPA and radiation dose is • very low).Uses x-ray source instead of an isotope source.• There is suspicion because the radiation source does not decay and the energy stays con-• stant over time.Allows assessment axial or peripheral skeleton or entire skeleton.• Sites measured: spine, hip radius• Proximal femur density measurement useful for predicting hip fractures.• Lumbar spine density measurement useful for monitoring response to therapy.• Spinal osteophytes and aortic calcifications may contribute to false high readings.•

X-RayNot sensitive in assessing bone mass• 30–35% bone mass loss must occur before demineralization can be detected.• Findings:• – Cortical thinning– Trabecular pattern coarsened due to loss of small trabeculaeFindings in the spine:• – Increased radiolucency– Increased prominence of endplates– Increased concavity of endplates if nucleus pulposus has not degenerated (codfish

vertebrae)– Anterior wedging and vertebral body height loss due to vertebral body compression

fractures

Single Photon Absorptiometry (SPA)/Single X-Ray Absorptiometry (SXA)Inexpensive• Low radiation dose• Requires water bath or gel immersion.• Uses I• 125 (SPA, a radioactive isotope) or x-ray source (SXA).Site measured: radius, calcaneus• Limited to bone measurement of peripheral skeleton; unable to measure bone density of • hip or spine.

Dual Photon Absorptiometry (DPA)No water bath or immersion needed.• Uses AGD• 153 source, a radioactive isotope.Less accurate and precise than dual energy x-ray absorptiometry (DXA)• Increased scan time.• Sites measured: proximal femur, lumbar spine•

Quantitative Computed Tomography (QCT)Allows measurement of trabecular bone alone of spine, apart from cortical bone.• High-dose radiation• Expensive• Sites measured: spine, hip radius• Accuracy compromised by increased fat content of bone marrow in elderly.•


This technique is unique that it provides for true 3-D imaging and reports bone density • measurement as true volume density measurements.The advantage of QCT is its ability to isolate an area of interest from surrounding tissue.•

UltrasonographyInexpensive• No radiation• Not as precise as DXA• Sites measured: calcaneus, tibia, patella, fingers•

TREATMENT

Pharmacologic

Medications that preserve or improve bone mass• Medications that decrease bone resorption•

1. Calcium

Mainstay for prevention and treatment of osteoporosis• Optimal calcium requirements recommended by the National Institutes of Health (NIH) • Consensus Panel (Table 11–11).

TABLE 11–11 Calcium Requirements as Recommended by NIH

Age GroupOptimal Intake of

Calcium (mg)

Birth–6 mo 400

6 mo–1 yr 600

1–5 yr 800

6–10 yr 800–1200

11–24 yr 1200–1500

Men: 25–65 yr 1000

Women: 25–50 yr 1000

Postmenopausal women on estrogen: 50–65 yr 1000

Postmenopausal women not on estrogen: 50–65 yr 1500

Men and women: >65 yr 1500

Pregnant and nursing women 1200–1500

Immobilization + excess calcium intake predisposes patient to kidney stones; maintain • urinary calcium excretion < 250 mg/24 h in those without kidney stones.

2. Vitamin D

Increases Ca• + absorption in gut.– Recommended doses:400–800 IU daily•


3. Estrogen

Mechanism of action:• – Suppresses interleukin 6 secretion with inhibition osteoclast recruitment.– Decreases bone resorption.– Increases calcium absorption in the gut.Dosing regimens:• – 0.625 mg/day –1.25 mg/day conjugated estrogen cycled or continuous with progester-

one 2.5–10 mg– Transdermal estradiol: 0.05–0.10 mg weeklyMaintain therapy 10–20 years after onset of postmenopausal symptoms.• Intact uterus: use progesterone to decrease buildup of endometrium.• If patient has had a hysterectomy, she may use estrogen only.• Benefits:• – Preserves bone mass at multiple skeletal sites.– Decreased incidence of fracture:

n ~ 50% risk reduction of spine fracturen ~ 60% incidence reduction of hip/wrist fracture

– Prevents vasomotor symptoms.Side effects:• – Endometrial cancer risk increased if estrogen is given without progesterone.– Breast cancer if prolonged use after menopause– Thromboembolic disease– Cardiac risks/benefits with use of estrogen remain controversialAbsolute contraindications: breast cancer, estrogen dependent neoplasia, thromboembolic • disorder, hypercoagulable states, unexplained vaginal bleeding.Relative contraindications: uterine leiomyomas or cancer, familial hypertriglyceridemia, • migraine, strong family history breast cancer, endometriosis, chronic hepatic dysfunction, gallbladder disease

4. Calcitonin (Derived From Salmon)

Directly inhibits osteoclastic activity.• Benefits:• – Decreases pain in acute compression fractures through stimulation of beta endorphins.– Preserves bone mass.– ~ 36% incidence reduction of spine fracturesRecommended doses:• – Nasal spray (Miacalcin, Fortical®) 1 spray 200 International units/d, alternate nostrils– Parenteral injection subcutaneously or intramuscularly (Calcimar®): prevention 100 IU

QOD, treatment 100 IU QD– Must have adequate concurrent intake of calcium and vitamin D.Side effects: nasal irritation, facial/hand flushing, local skin irritation, nausea; allergic • reaction with injection form

5. Bisphosphonates

Bisphosphonate have been shown to increase bone mass and reduce the incidence of spine fractures. They are taken 1/2 hour before food/drink/meds in morning in an upright posi-tion to avoid esophageal irritation.

Oral side effects: abdominal pain, nausea, dyspepsia, difficulty swallowing, inflammation • esophagus, and risk of ulceration, osteonecrosis of jaw, visual disturbances, musculoskel-etal pain


Intravenous side effects: flu-like symptoms, fever, muscle and joint pain, headache, • osteonecrosis of jaw, visual disturbancesAlendronate (Fosamax)• – Recommended dosing: prevention – 5 mg/day; treatment – 10 mg daily

n ~ 49% risk reduction of spine fracturesn ~ 56% risk reduction of hip fractures

Risedronate (Actonel)• – Dosing prevention and treatment: 5 mg daily or 35 mg weekly or 75 mg twice

monthly– Risk reduction of new spinal fractures up to 65%Ibandronate (Boniva)• – Dosing prevention and treatment: oral – 2.5 mg daily or 150 mg monthly– Intravenous – 3 mg q 3months– Comparable to Fosamax and Actonel in reduction of vertebral fractureZoledronic acid (Reclast)• – Dosing: intravenous – 5 mg yearly; to be infused in no less than 15 minutes– Reduces vertebral fracture by 70% and nonvertebral by 25%.– Reduces hip fracture by 41%.

6. Teriparatide (Forteo)

Injectable form of recombinant human parathyroid hormone• Stimulates new bone formation in spine and hip.• For treatment of osteoporosis in postmenopausal women and men at high risk for • fractureRecommended dosing: 20 mcg SC daily; approved for use up to 24 months.• Side effects: nausea, dizziness, leg cramps, cough•

7. Selective Estrogen Receptor Modulators (SERMs)

For prevention and treatment of osteoporosis in postmenopausal women unable to take • estrogen due to side effects or risk of breast cancerRaloxifene (Evista• ®)– Dosing: 60 mg daily– Side effects: hot flashes, increased risk of DVT

8. Increase Bone Formation (Positive Bone Formers)

These medications are not FDA approved for the treatment of osteoporosis.1. Sodium fluoride: stimulates osteoblast formation; high dosage may increase risk of non-

spinal fracture, bone fragility.2. Anabolic steroids: may have beneficial effect on bone mass but side effects prohibit their

use; side effects: nausea, GI bleeding, joint pain.3. Testosterone: may benefit men with hypogonadism.

MANAGEMENT

Preventative Exercise

Activities involving weight bearing (axial loading) and pull of functioning muscle preserves or increases bone mass. They reduce the risk of osteoporosis by maximizing bone mass in young adults, maintaining bone mass in mature adults and lessening bone loss in postmeno-pausal women.


Activities associated with increase bone mass:Jogging or running• Weight training• Aerobics• Stair climbing• Racquet, field, and court sports• Dancing•

Therapeutic Exercise

The goals are to mitigate bone loss, increase strength and balance, prevent falls, and avoid fractures. Exercise regiments should be tailored to fitness levels and anticipated propensity to fracture or current fractures.

Goals of Therapeutic ExerciseShort term: education of proper posture, body mechanics, increasing strength and aerobic • capacityLong term: prevention of falls and fractures: proper nutrition, strength, aerobic capacity • with adequate spine support, pain management, psychological support

Exercise PrinciplesWeight-bearing exercises improve bone density.• Avoid spine flexion exercises in spinal osteoporosis, which may predispose to vertebral • compression fracture.Posture correction: avoid kyphotic posture.• Pectoral stretching• Strengthening: back extension, isometric exercises to strengthen the abdomen, upper and • lower extremities.Deep breathing exercises• Balance and transfer training• Proper lifting techniques and body mechanics•

TYPES OF FRACTURES

Vertebral Fractures

Evaluation: history/physical exam, x-rays of spine, bone scan• Acute vertebral fractures—may follow minor injury or physical activity.• Most common osteoporotic fractures: vertebrae > hip > wrist• Vertebral compression fracture is most common type of fracture seen in osteoporosis.• – Most common site: lower thoracic, upper lumbar areas– Typically involve anterior part of the vertebral body and result in anterior wedging.– Treatment: restrict flexion based activities and exercises, which load anterior vertebral

body.

Microfractures–TrabeculaePain in the absence of fracture visible on x-ray. May be seen on bone scan.•

Multiple Spine FracturesMultiple collapsed/anteriorly wedged vertebrae • → kyphosis (Dowager’s hump)Loss of height• Abdominal proturbance, GI discomfort• Pulmonary insufficiency• Costal iliac impingement syndrome•


Facet Joint DiseaseMost prominent abnormality at vertebral collapse level with smaller lesions above and • below level

Retropulsed FragmentsCan cause back pain with neurologic symptoms with fragments in the spinal canal.•

Costal Iliac Impingement Syndrome

Lower ribs impinge on iliac crest causing pain.• Increased pain with lateral rotation and bending.•

TreatmentRelief with soft wide belt which sinks into pelvic cavity avoiding rib contact with iliac • crest.Injection of sclerosing material into margins of iliac and lower ribs• Resection of lower ribs•

Limb Fractures

Hip fractures: multifactorial causes with 2 major risk factors: osteoporosis and falls.Muscle forces acting on hip are greater than the mechanical ability of femur to withstand these forces.

Direction of fall is a major risk factor for fracture.• – Falls to the side result in forces greater than muscle strength.– Elderly tend to fall sideways or drop in place.

Wrist fractures: most common fracture in females > 75 years old.

FALLS

Risk Factors for Falling

Impaired vision (decreased vision, poor depth perception)• Cognitive impairment• Balance/gait abnormalities• Weakness (ie, inability to rise form a chair without using one’s arms)• LE disability/foot problems• Peripheral neuropathy• Sedative use• Polypharmacy• Environmental (inadequate lighting, rugs, lack of railings)•

Fall Prevention Program

General conditioning exercises• Improve balance• Assistive devices: canes, walkers, grab bars, tub benches• Adequate shoe-wear, avoid high heels• Modification of meds• Environmental modification: adequate lighting, removal of throw rugs, handrails for • stairs, ramps


TREATMENT OF VERTEBRAL BODY FRACTURES

Management of vertebral body fractures varies with acuity, location of fracture, and pain. Conservative approaches include bracing and physical therapy. Management can also include kyphoplasty or vertebroplasty.

Acute Vertebral Body Fracture

Usually severe, most intense at fracture level• Sharp pain increased with movement and alleviated with bedrest• Severe pain lasting 2–3 weeks with decreased severity for 6–8 weeks• May be asymptomatic.•

Treatment:Bedrest initially less than 1 week, graduating to bedside activities and progressive • ambulationImmobilization of fracture site with soft orthosis (corset). Rigid orthotic avoided to prevent • disuse osteoporosisPhysical modalities: local heat or cold• Analgesics: initially give around the clock, opiates initially, then within 1–2 weeks, transi-• tion to NSAIDs and acetaminophen.Avoid constipation.• Avoid exertional exercises.•

Chronic Vertebral Body Fracture

Pain less intense than in an acute fracture• Mid-thoracic is most common location.• Mechanical deformity, paraspinal muscle spasm• Radiates laterally, associated with exertion•

Treatment:Periods of bedrest 20–30 minutes BID• Analgesics: nonnarcotic agents, Calcitonin• Orthosis• Assess ADLs, use of devices to avoid aggravation of pain.• PT: core muscle strengthening, balance and flexibility, body mechanics• Avoid flexion-based activities • → increase vertebral compression forces.Physical modalities: heat or cold, TENS, acupuncture• Behavioral modifications: biofeedback, hypnosis, counseling•

Kyphoplasty

A minimally invasive procedure to treat painful, progressive vertebral compression frac-tures typically caused by osteoporosis with the goal of re-establishing vertebral body height and reducing pain.

Technique: fluoroscopic guidance is used to place a hollow-bore needle into a vertebral body. A balloon tamp is inserted into needle and inflated to restore bone height. Cement is then injected into vertebral cavity. The needle is then removed; cement hardens in ~ 15 minutes. Pain usually improves within days.

Risks:Risks associated with local or general anesthesia• Infection•


Bleeding/hematoma• Cement extravasation into spinal canal • → SCI or nerve root damageCement embolism to lungs•

Vertebroplasty

A minimally invasive procedure similar to kyphoplasty. However, no balloon tamp is utilized to restore the vertebral body height. Instead, cement is injected directly into the vertebral body at higher pressures. Vertebroplasty is associated with the same risks as kyphoplasty.

BACK SUPPORTS/BRACING

Orthoses

Indications for Using Bracing for Vertebral FracturesPain relief: for acute fractures, spinal immobilization decreases paraspinal muscle spasm • and overuseStabilize spine• Prevent further fracture• Prevent soft tissue shortening• Decrease flexion• Compensate for weak erector spinal muscles•

Contraindications to Back BracingHiatal hernia• Inguinal hernia• Orthopnea secondary to COPD• Obesity• Kyphoscoliosis•

Risks of Prolonged Use of OrthosisWeakening/atrophy of trunk muscles• Reduced spinal mobility• Increased fracture risk due to disuse osteoporosis•

Types of Orthoses (See Also Chapter 6: Prosthetics and Orthotics)1. Nonrigid Brace—Used in Stable Fractures for Pain Management

Abdominal corset (elastic binder)• Decrease pain: increase intra-abdominal pressure placing anteriorly directed force on vertebral bodies; also serves as a reminder to restrict motion

2. Rigid—(TL, TLSO, Jewett, CASH)—Used in Acute TL FracturesThoracolumbar support—assist spine extension via shoulder straps and paraspinal bars; • increases intraabdominal pressureTLSO (thoracolumbosacral orthosis)• – Fixation from pelvis to shoulders– Greatest immobility– Increased noncomplianceJewett brace• – Forces act to extend thoracolumbar regionCASH (cruciform anterior sternal hyperextension)•

Note: Orthotics that cause excessive hyperextension forces on the spine may induce posterior element type fractures in the osteoporotic patient. This therefore should be a consideration in this patient population.


Other: Postural training supports• consist of a brace suspended by loops from the shoulders with small pouches containing weights up to 2 lb. The weights are positioned just below the inferior angle of the scapula to counteract the tendency to bend forward and may be worn for 1-hour twice/day.

nREHABILITATION OF BURN INJURIES

BURNS

General

A burn is the body’s response to a soft tissue insult from an external agent, such as heat, • cold, chemicals, electricity, and radiation.85–90% of burns are caused by heat.• 10–15% of burns are from frostbite, chemical, and electrical damage.• 1.5–2.0 million people sustain burns each year in the U.S.• 60,000–80,000 burn victims need hospitalization.• 5,000 people die each year from burns.• 35,000–50,000 people have temporary or permanent disability secondary to burns.• Burns are:• – #1 cause of accidental deaths in children under 2. The majority of burns in this age

group occur as a result of abuse.– #2 cause of accidental deaths in children under 4– #3 cause of accidental deaths in children under 19

PathophysiologyNormal skin figure (Table 11–12)•

Cellular Response to Burns

Local reactions to burns include:• a) Exposed collagen causes platelet activation.b) Intense vasoconstriction secondary to epinephrine, prostaglandins, serotonin, and

leukotrienes.c) Within a few hours, histamine release causes vasodilatation and increased capillary

permeability, allowing protein and albumin into the extravascular space. This is fol-lowed by fluid extravasation, which causes severe edema.

d) Late capillary permeability secondary to leukotrienes.e) Swelling and rupture of damaged cells.f) Platelet and leukocyte aggregation with clot formation from tissue thromboplastin,

endotoxin, interleukin-1, and Hageman factor.g) Establishment of a hypermetabolic state.

Systemic Response to Burns

Loss of fluid into extravascular compartment resulting in hypovolemia and shock• Hyperventilation with increased oxygen demand• Inhalational injury causing decreased oxygenation and ARDS• Initial decrease followed in several days by a significant increase in cardiac output•

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