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Medical Background:

Camacho, John Mathew


Esporlas, John Peter Lovingski
Saddi, Karen Bernadette Marie DJ.

IMMOBILIZATION
- Defined as physical restriction or limitation of the body or its limbs. This may result from
any of the following
Neuromusculoskeletal disorders & injuries such as paralysis
Orthopedic Casts, body jackets & splints
Critical Illness requiring bed rest
Medical or caregiver neglect
Prolonged stay in a reduced gravity position such as sitting or recumbency
Etiology

In 1862, the English surgeon John Hilton advocated bed rest as a basic physiologic approach in the
treatment of human illness. Since that time, it has often been used indiscriminately in the treatment
of acute and chronic illnesses.

Mid-1940s- complications of prolonged bed rest have been increasingly recognized and reported

1948, Deitrick et al. (153) showed that prolonged bed rest may cause multiple adverse effects in a
number of organs and systems.

1960s and 1970s, studies on astronauts in microgravity conditions (in which their bodies rest from
the effects of gravity) have shown significant undesirable effects that may override the therapeutic
effects of bed rest in subacute and chronic conditions, impacting complexity and cost of medical
treatment as well as functional outcome.

In the last three decades, new epidemiologic and randomized studies have been conducted, which
in a great preponderance have demonstrated significant benefits of physical activity and exercises
on cardiopulmonary, musculoskeletal, and total body functions.

Studies have indicated that prolonged bed rest and sedentary lifestyles have negative effects on
health and function, magnified in persons with neurologic disease (1) or in the elderly (2). The
principles long advocated by rehabilitation medicine have contributed significantly to the current
philosophy on the use and misuse of immobility.

(1) A patient with motor neuron disease and its accompanying limb weakness or spasticity would
be expected to develop the same musculoskeletal complications but at a faster rate, and is likely to
lose a significant amount of independent functioning.

(2) People who are chronically sick, aged, or disabled are particularly susceptible to the adverse
effects of immobility
Deconditioning, a general term which is defined as reduced functional capacity of
musculoskeletal and other body systems. It should be considered a distinct diagnosis from the
original condition that has led to a curtailment of normal physical functions.

Deconditioning Process

1. Prolonged reduction of muscle repetitive contractions below 50% of maximum alters


muscle protein synthesis and decreases glycogen and ATP storage.
2. Reduction of oxidative enzymes, mitochondrial function, and microvascular circulation,
impacting muscle metabolic activity.
3. Oxygen supply is attenuated, and the extraction of oxygen from blood is diminished, further
negatively affecting VO2max and cardiovascular reserve.
4. Loss of muscle mass leads to reduction of muscle strength and endurance, reducing muscle
blood flow, red blood cell delivery, oxidative enzyme activity, and oxygen utilization in the
muscle precipitating a further loss of musculoskeletal and cardiovascular functional reserve
to low or dangerous levels.
5. In this cascade of events, specific muscle gene activation and expression are altered as well.
6. Physical inactivity causes change in muscle fiber type composition and decreases formation
of oxidative muscle fiber types I and IIa, the main factors in reduction of endurance and
fitness.

DELETERIOUS EFFECTS OF PROLONGED IMMOBILIZATION

Adverse Effects of Immobility and Inactivity


System(s) Effect(s)
Musculoskeletal Muscle weakness, fatigue, and atrophy Muscle
and joint contractures
Muscle stiffness and pain
Osteoporosis
Hypercalcemia
Cardiovascular and pulmonary Redistribution of body fluids
Dehydration
Orthostatic intolerance
Reduction of cardiopulmonary capacity
Reduction of VO2max
Elimination of bronchial secretions Hypostatic
pneumonia
Genitourinary and gastrointestinal Urinary stasis, stones, and urinary infections
Loss of appetite
Constipation
Metabolic and endocrine Glucose intolerance
Electrolyte alterations
Increased parathyroid hormone production
Other hormone alterations
Immune system Impaired wound healing
Reduction in cellular immunity
Resistance to infection reduced
Anti-inflammatory suppression reduced
Cognitive and behavioral Sensory deprivation
Confusion and disorientation
Anxiety and depression, memory
Decrease in intellectual capacity
Impaired balance and coordination
Cellular/genetic Diminished gene expression
Mitochondrial dysfunction

Musculoskeletal System
A. Physiological Impairments
1. Disuse Atrophy
o Hallmark: decrease in the size of muscle fibers and reduction of muscle mass
o Generalized or localized to the immobilized limb(s) and more prominent in the
antigravity muscles.
o In LMNL, atrophy is regional and related to the particular nerve or root.
o Atrophy associated with muscle disease, more pronounced in the proximal muscles.
o Muscle wasting during bed rest:
slow during the first 2 days but becomes rapid thereafter
by 10 days, 50% of eventual muscle weight loss
o Muscle protein synthesis:
reduced to 50% of the baseline level at 14 days of immobilization
gradually tapers off to reach a new steady state
o In a shortened muscle, the number of sarcomeres in series is reduced as a result of
diminished chronic stretch and adaptation of the muscle to a new resting length.
o In an elongated muscle resting position or during musculoskeletal growth increases
the number of sarcomeres in series
o Type I and type IIa muscle fibers is more prominent than type IIb fiber atrophy
during immobility.
o Synthesis of collagen fibers is also reduced, although this reduction is much less
than the reduction in synthesis of muscle proteins
o Sarcopenia is muscle mass loss associated with aging.
o Decline of mitochondrial function and the reduction of protein synthesis are the
main reasons for the onset and progression of disuse atrophy. However, in the later
stages, protein degradation may become more prominent than decrease in pro- tein
synthesis.
2. Loss of Strength
-When a person is exposed to minimal exertions, maximal strength of a muscle can fall
to 25% to 40% of baseline level over a 2- or 3-week period
-During strict bed rest, muscles may lose 10% to 15% of their original strength per
week
-Over 4 weeks, 35% to 50%
-Loss of strength is rapid after the first day of immobilization and reaches its maximum
10 to 14 days later.
- loss of strength associated with disuse atrophy is more prominent in the lower limbs
than in the upper limbs
20% to 44% in knee flexors and extensors
5% in upper limbs.
3. Loss of Endurance
- Unexercised muscle demonstrates a reduction of adenosine triphosphate (ATP) and
glycogen storage sites and rapid depletion of them after resumption of activity.
-Reduction of muscle protein synthesis and oxidative enzyme function, and premature
anaerobic energy production with rapid accumulation of lactic acid, are important
factors leading to fatigability and reduced endurance
B. Functional Impairments of Disused Muscle
1. Mobility and ADL
-In the lower limbs, type I muscle fibers, which active during standing and slow
ambulation, are especially affected with a rapid reduction in endurance.
-Deep layer of vastus intermedius shows the greatest histochemical changes if the
quadriceps muscle is immobilized in an extended position in contrast to the rest of the
muscle
-Such accelerated rate of atrophy and weakness was also noted in hip and back
extensors, hip abductors, and ankle plantar flexors and dorsiflexors, impacting the
ability to walk
2. Muscle Pain and Stiffness
-Back pains are more prominent when trunk movements are limited in a supine
position. It is speculated that localized, prolonged, low- intensity isometric muscle
contractions may cause this pain.
- Limb muscle pain and stiffness occur after generalized immobility or focal limb
immobilization, especially in the presence of limb swelling.
-When immobilized in a shortened position (extensors in a fully extended position or
flexors in a fully flexed position), a muscle can lose 40% of its original number of
sarcomeres, contributing significantly to weakness and muscle stiffness

C. Disuse Weakness, Deconditioning, and Cardiovascular Disease


-Chronic inactivity impairs and reduces maximal oxygen consumption (VO2max),
cardiovascular reserve, and fitness
-Individuals with an inactive lifestyle and low level of fitness are more prone to develop
coronary artery disease (CAD) and have greater odds of suffering myocardial infarction and
death.
-Hypercortisolemia associated with acute trauma, results in muscle catabolism.

STRENGTH
The scientific literature suggests that, with total immobility,
strength gradually decreases by 0.7% to 1.5 % per day to a maximum of a 25% to 40%
decrease in overall strength.
The decrease appears to be greatest after the first week. Furthermore, different muscle
groups show a variable decrease in strength.
The antigravity muscles and larger muscles, particularly those in the lower limbs, lose
strength disproportionally. Interestingly, in as little as 24 hours of immobilization, muscle
fiber atrophy has been demonstrated in animal studies.
Disuse atrophy has also been reported to start in as little as 4 hours of immobilization.
Muscle atrophy is dependent on the degree and the cause of inactivity and disuse. In the
case of lower motor neuron dysfunction with chronic irreversible flaccid paralysis, muscle
bulk is reduced by 90% to 95%.
In upper motor neuron disease with resulting spasticity, muscle bulk decreases by only
30% to 35% because the increased tone actually prevents complete atrophy.
The atrophy involves both Type I and II fibers, but Type I fibers are predominantly involved
in immobilization atrophy.
If recovery does not occur, muscle fibers are replaced by connective tissue. This process
of collagen reorganization may begin after as little as 1 week of immobilization and will
predispose to contracture formation. Positioning also plays an important role.
Muscles, which are immobilized in a shortened position, will also be predisposed to a more
rapid decline.
ENDURANCE
The decrease in strength and concomitant effects of immobilization on the cardiovascular
system results in decreased endurance.
JOINTS

A. Joint Contracture
Anatomical Classification of Contracture
Type Primary Cause Secondary Cause
Arthrogenic Cartilage damage, congenital deformities, Immobility
infection, trauma, degenerative joint disease
Synovial and fibrofatty tissue proliferation (e.g., Immobility
inflammation, effusion)
Capsular fibrosis (e.g., trauma, inflammation) Lack of ROM
Immobilization as primary cause Mechanical position
Soft and Periarticular soft tissue (e.g., trauma, Immobility
dense tissue inflammation)
Skin, subcutaneous tissue (e.g., trauma, burns,
infection, systemic sclerosis)
Tendons and ligaments (e.g., tendinitis, bursitis, Immobility
ligamentous tear, and fibrosis)
Myogenic
a. Intrinsic Traumatic (e.g., bleeding, edema) Immobility
(structural) Inflammatory (e.g., myositis, polymyositis)
Degenerative (e.g., muscular dystrophy) Fibrosis
Ischemic (e.g., diabetes, peripheral vascular Immobility
disease, compartment syndrome)
b. Extrinsic Spasticity (e.g., strokes, multiple sclerosis, spinal Lack of stretch
cord injuries), hypertonicity
Flaccid paralysis (e.g., muscle imbalance) Faulty joint position
Mechanical (e.g., faulty position in bed or chair) Immobility
Immobilization as primary cause Lack of stretch
Mixed Combined arthrogenic, soft-tissue and muscle
contractures noted in a single joint

Immobilization also affects the joints.


The hyaline cartilage in joints receives its nutrition through the influx and efflux of synovial
fluid caused by joint loading and unloading.
During immobilization, this process stops. The hyaline cartilage is then dependent on
simple diffusion to obtain nutrients.
Unfortunately, the needs of the cartilage exceed the capacity of simple diffusion. Although
qualitative data is not available at this time regarding the extent of articular changes in
humans, studies in immobilized animals indicate a decrease in overall thickness of articular
cartilage of 9% after 11 weeks.
Contracture is a loss of range of motion (ROM) in a joint. It may result from several causes,
such as tightness of connective tissue, muscle, and joint capsule, as well as a joint disorder.
However, in an immobilized person, mechanical factors are most important. If
a muscle is chronically maintained in a shortened position, the muscle fibers and connective
tissue adapt to the shortened length, causing contracture on the relaxed side of the joint.
A muscle held in shortened position for only 5 to 7 days will demonstrate shortening of the
muscle belly because of contraction of collagen fibers and decrease in muscle fiber
sarcomeres. If this position continues for 3 weeks or more, the loose connective tissue in
muscles and around joints will gradually change into dense connective tissue, causing
contracture.
Contributing factors, such as edema, hemorrhage, spasticity, paralysis, pain, muscle
imbalance, soft tissue injury, and advanced age, compound and enhance formation of
contractures.
Muscle imbalance is the most important contributing factor.
In the immobile patient, lower limb contractures are most common, usually involving the
hips, knees, and ankles (two-joint muscles).
In the upper limbs, the wrists, shoulders, and elbows are at risk. Similar pathophysiologic
changes may occur in the joints of the spine, especially in the cervical and lumbar regions.
Development of contractures is one of the most severe, yet in most cases preventable,
disabilities that result from immobilization.
Contractures have a major influence on the functional outcome of rehabilitation. Be aware.
Anticipate and take measures to prevent contractures. Prevention is preferable to
treatment, and is much more cost effective
OSTEOPOROSIS
A. Disuse Osteoporosis
o Bone mass will increase with repeated loading and will decrease with the absence of
muscle activity or with the elimination of gravity.
o Certain populations are more susceptible to the effects of muscle inactivity or
reduced weight bearing (eg. aging adult or the person with an SCI)
o Even healthy adults on bed rest lose bone at a rate that exceeds the rate of new bone
formation, leading to osteopenia
o Bone mass begins to decline in the fourth and fifth decades of life, occurring most
rapidly in women in the first 5 to 7 years after menopause.
Estrogen and calcium deficiencies result in higher rates of bone resorption in contrast to the
decrease in bone formation caused by immobility and nonweight bearing
Disuse osteopenia is characterized by a loss of calcium and hydroxyproline from the
cancellous portion of long bone, epiphyses, metaphyses, and cortical bone near the bone
marrow cavity.
o *Immobilization Hypercalcemia and Hypercalciuria
Despite a normal serum calcium level, immobilized patients are markedly hypercalciuric
o Adolescent boys after acute SCI may show a significant hypercalcemia as well
Patients with the end-stage renal disease on maintenance hemodialysis can also develop an
acute hypercalcemia when placed on bed rest even for 3 days
Symptoms of Hypercalcemia: anorexia, abdominal pain, nausea, vomiting, constipation,
confusion, and, ultimately, coma
o For immobilized healthy persons, urinary calcium excretion (hypercalciuria without
hypercalcemia) increases above normal levels on the second and third days of
recumbency.
The stimulus of weight bearing, gravity, and muscle activity on
bone mass maintains the balance between bone formation and resorption. Several
enzymatic factors also play a part.
Prolonged bedrest leads to bone atrophy that involves both organic and inorganic bone
components.
Increased urinary excretion of calcium and hydroxyproline as well as increased excretion of
calcium in stool result in a decrease in total bone mass, especially from the
weight-bearing bones. In contrast to senile osteoporosis that develops from the marrow
outward, immobilization osteoporosis is more marked in the sub-periosteal region.
In addition, disuse osteoporosis is most apparent in cancellous bone at the metaphysis and
epiphysis and later extends to the entire diaphysis.
Up to a 1% loss of vertebral mineral content may occur per week of immobilization. After
12 weeks of bedrest, bone density is reduced by 40% to 45% and by 50% by the 30th week.
Osteoporosis may lead to compression fractures of vertebral bodies and weight-bearing
long bones with minor trauma, as well as predisposing the patient to wrist and hip
fractures. Incidentally, osteoporosis may not be evident initially on plain x-ray films and
may require more specialized techniques such as DEXA for quantification and diagnosis.
Cardiovascular System
A. Hemodynamic Alterations
- resting HR increases by 1 beat/minute every 2 days, leading to immobilization tachycardia
at rest and AbN increases in heart rate on submaximal exercise and workloads.
-after 3 days, heart rate increases 32% above the prebed rest response when resuming
submaximal activity, 62% after 7 days, and 89% after 21 days of recumbency
- Cardiovascular adaptation syndrome (CAS) is the alteration of cardiovascular function
induced by immobility is. If a patient with CAD develops CAS, cardiac ischemia may be
aggravated.

1. Alteration of Body Fluids in Recumbency

- Normally, 20% of total blood volume is contained within the arterial system, 5% in the
capillaries, and 75% in the venous system.
- Immediately upon lying down, 500 mL of blood shifts to the thorax and cardiac output
increases by 24%.
- Estimated myocardial work is increased by approximately 30%
- loss of plasma volume
-after 24 hours is 5%
-after 6 and 14 days, the loss is 10% and 20%
- Hypovolemia, along with circulatory stasis that is due to bed rest, is an important
precipitating factor in thrombogenesis.

2. Orthostatic Intolerance

- When standing up, there is a shift of venous blood from the thorax and upper limbs to the
legs, causing an increase in venous pressure to 80 to 100 mm Hg
- Venous return to the heart is reduced due to diminished venous compliance, an increase in
venous pooling and intravascular volume deple- tion with end result of decreased stroke
volume and cardiac output, and a significant decrease in the systolic blood pres- sure
response on rising.
-Stroke volume may decrease 15% after 2 weeks of bed rest

- Signs and symptoms: tingling, burning in the lower extremities, dizziness, light-headedness,
fainting, vertigo, increased pulse rate (>20 beats/minute), decreased systolic pressure (>20 mm
Hg), and decreased pulse pressure.
3. Accumulation of Deep Vein Thrombosis
Respiratory System
Bedrest causes mechanical restrictive impairment as a result
of decreased overall strength and a reduction of intercostal, diaphragmatic, and abdominal
muscle excursion in supine breathing.
The costovertebral and costochondral joints and the abdominal muscles may become fixed
in an expiratory position, further reducing maximal inspiration. This results in a decrease in
vital and functional respiratory capacities causing regional differences in
ventilation/perfusion ratio, poorly ventilated as well as overly perfused areas, and
arteriovenous shunts.
If increased metabolic demand occurs, hypoxia results. Mucociliary function is also
impaired. Mucus secretions accumulate in the dependent respiratory bronchioli, leading to
atelectasis and hypostatic pneumonia.
Digestive System
Anorexia, gastroesophageal reflux disease (GERD), and constipation are the result of
decreased metabolic demand, endocrine changes, and decreased gastric and intestinal
motility
Metabolic Effects
Marked hypercalcemia may occur several weeks after immobilization with a peak at 2 to 4
weeks.
This is most often seen in young adult men after trauma. It is associated with hypercalcemic
metabolic alkalosis and may lead to renal failure and ectopic calcification. It manifests
clinically as headache, nausea, vomiting, anorexia, abdominal pain, lethargy, constipation,
and weakness.
Other circulating chemicals affected by immobilization
include nitrogen, phosphorus, sulfur, sodium, potassium, magnesium, zinc, and chloride.
Hormonal Disorders
Significant carbohydrate intolerance has been noted as early as the third day of immobility,
and peripheral glucose uptake may decline 50% after 14 days.
Increase in serum parathyroid hormone, which is related to hypercalcemia from immobility.
Triiodothyronine (T3) blood levels are also elevated during immobility.
Serum corticosteroid levels during bed rest are increased, accompanied with increased
excretion of urinary cortisol.
Nervous System
Sensory deprivation
Perceptual impairment can be altered after 7 days of immobility.
Lack of concentration & motivation, depression & reduced psychomotor skills may
drastically affect.
Balance & coordination are also impaired after prolonged immobility, appears to be due to
altered neural control rather than muscle weakness.
Skin
Skin atrophy results from inadequate nutrition.
Pressure ulcers, a dreaded complication of immobility, are better prevented
than treated.
They occur over bony prominences such as the sacrum, ischium, trochanter, and heel.
They result from prolonged pressure causing ischemic necrosis of soft tissue overlying the
bony prominences.
A Stage I pressure ulcer may begin in as little as 2 hours.
Edema, malnutrition, anemia, hypoalbuminemia, and paralysis are contributing factors
Physical Therapy Considerations

Monitor vital signs carefully, especially during mobilization out of bed for the first few
times.
Progressively raise the head of the bed before or during a physical therapy session to allow
blood pressure to regulate.
Consider the use of lower extremity anti-embolism stockings with or without elastic
wrapping for the patient performing initial static sitting activities to minimize pooling of
blood in the lower extremities if hypotension persists more than a few sessions.
Use stretcher chairs (chairs that can position the patient from supine to different degrees of
reclined or upright sitting) if orthostatic hypotension or activity intolerance prevents
standing activity or if the patient may need to quickly return to a supine position.
Time frames for physical therapy goals will likely be longer for the patient who has been on
prolonged bed rest.
Supplement formal physical therapy sessions with independent or family-assisted
therapeutic exercise for a more timely recovery.
Be aware of the psychosocial aspects of prolonged bed rest. Sensory deprivation, boredom,
depression, and a sense of loss of control can occur. These feelings may manifest as
emotional lability or irritability, and caregivers may incorrectly perceive the patient to be
uncooperative.
As much as the patient wants to be off bed rest, the patient will likely be fearful the first
time out of bed, especially if the patient has insight into his or her muscular weakness and
impaired aerobic capacity.
Leave the patient with necessities or commonly used objects (e.g., the call bell, telephone,
reading material, beverages, tissues) within reach to minimize feelings of confinement.
Treatment & Prevention
- Pain management
- Flexibility Exercises to maintain optimal muscle resting length & viscoelastic properties.
- Strengthening Exercises to prevent disuse weakness & deconditioning
o Progressive resistance exercise using isotonic
- Exercise for endurance & fitness; Aerobic exercises
- ROM exercises (active or passive) with terminal stretch
- Early mobilization & ambulation (weight-bearing)
- LMWHs 5000 units twice a day & warfarin for DVT, ambulation on 2nd or 3rd day if the
partial thromboplastin time is within the therapeutic range.
- Regular pulmonary toileting and deep breathing and coughing exercises and maintain
adequate hydration.
HIP FRACTURE
Anatomy
- Intertrochanteric fractures occur in the region between the greater and lesser trochanters
of the proximal femur, occasionally extending into the subtrochanteric region.
- These extracapsular fractures occur in cancellous bone with an abundant blood supply. As a
result, nonunion and osteonecrosis are less problematic than in femoral neck fractures.
- Deforming muscle forces will usually produce shortening, external rotation, and varus
position at the fracture.
Abductors tend to displace the greater trochanter laterally & proximally
Iliopsoas displaces the lesser trochanter medially & proximally
Hip Flexors, Extensors and abductors pulls the distal fragment proximally.
INTERTROCHANTERIC FRACTURE
- The most common hip fracture
- The ratio of women to men ranges from 2:1 to 8:1, likely because of the post- menopausal
metabolic changes in bone.
- The common presentation of hip fracture may be seen: hip pain with an externally rotated
and shortened limb

Risk Factors for Intertrochanteric fracture


- Advancing age
- Increase number of comorbidities
- Increased dependency in ADLs
- History of Osteoporosis
- Loss of muscle strength, flexibility & balance
- Neurological disorders
Epidemiology
- 75 85 years with women accounting for 77.2% of intracapsular hip fractures
- High rate of fracture is directly connected to having osteoporosis.
- Women>Men
Etiology
- Fx risks depend on; genetic profile, peak bone mass, and strength of bone achieved in ones
lifetime and the subsequent rate of bone loss and osteoporosis (primary cause).
- In healthy adults they may be an outcome of any repeated, strenuous activities. (jumping,
running, working out).
Mechanism of Injury
- Intertrochanteric fractures in younger individuals are usually the result of a high-energy
injury such as a motor vehicle accident or fall from a height.
- Ninety percent of intertrochanteric fractures in the elderly result from a simple fall
- Most fractures result from a direct impact to the greater trochanteric area

BOYD & GRIFFIN INTERTROCHANTERIC FRACTURE

Type I A single fracture along the intertrochanteric line, stable


and easily reducible

Type II Major fracture line along the intertrochanteric line with


comminution in the coronal plane

Type III Fracture at the level of the lesser trochanter with variable
comminution and extension into the subtrochanteric
region (reverse obliquity)

Type IV Fracture extending into the proximal femoral shaft in at


least two planes

Diagnostic Procedures
- Hip radiography & CT scan
Acute sign & symptoms
- Pain in groin or hip region
- Pain with active or passive motion of hip
- Pain with lower-extremity weight bearing
- Lower extremities appears to be shorter
OSTEOPOROSIS
- Porous bone
- Decrease in bone mass density
- Most common in adult women
2 types:
- Primary osteoporosis chronic illness, aging process, idiopathic, postmenopausal
- *Senile osteoporosis age-related osteoporosis, bone loss that normally accompanies aging
- Secondary osteoporosis various endocrine and metabolic disorders (Hyperthyroidism,
hyperparathyroidism, hypogonadism, DM type 1) other disorders that contribute to
accelerated bone loss, CHF, RA, malabsorption syndromes, CRD, malignancies, alcoholism.
Etiology

- Osteoporosis depend on; estrogen depletion; calcium, vitamin D, and testosterone


deficiency; smoking; advanced age; positive family history; diminished peak bone mass;
diminished physical activity; and history of previous fractures are important.
Sign and symptoms:
- Back pain
- Bone fractures
- Decrease in height
- Kyphosis
- Dowagers hump
- Decrease activity tolerance
- Early satiety
Risk factors:

- Increasing age
- family history
- smoking
- glucocorticoid therapy
Diagnostic Procedures

- DEXA Scan for checking the Bone Mass Density


- Radiography
- CT scan

Physical Therapy Intervention


- Weight-bearing exercises
- Aerobic exercises
Drugs

- Calcium: 1,200 mg/day


- Vitamin D for absorption of calcium & mineralization of bone
o Calcitriol
o Cholecalciferol (vitamin D3)
o Ergocalciferol (vitamin D2)