• Is a chronic metabolic disease in which bone loss causes decreased density and possible fractures. • It is often referred to as a “silent disease” because the first signs of osteoporosis in most people follows some kind of fracture.

• Osteoporosis and osteopenia (low bone mass) occur when

osteoclastic (bone resorption) is greater than osteoblastic (bone building) activity. • The result is a decreased BMD (Bone Mineral Density)

bone strength and peaks between 25 and 30 yrs of age.

• Before and during the peak years, osteoclastic activity and osteoblastic activity work • After the peak years, bone resorption activity

at the same rate *exceeds bone building activity and bon density decreases.

BMD: • Decreases most rapidly in

postmenopausal women as serum estrogen levels diminish.

• Trabecular or cancelous (spongy) bone is

lsot first followed by Cortical (compact) bone. This results in thin, fragile bone tissue that is at risk for fractures.

Diagnosis of osteoporosis

• are based on BMD testing that provides a T-score for the patient. • Osteopenia is present when the T score is @ -1 and above -2.5 • Osteoporosis is diagnosed in a person who has a T score at or lower than -2.5.

Generalized osteoporosis

• Involves many structures in the Skelton and is further divided into two categoris o Primary and secondary.

o Primary osteoporosis

is more common and occurs in postmenopausal women and in men in their seventh or eight decade of life.

o Even though men do not experience rapid bone loss that postmenopausal women have, they do have

decreasing levesl of testosterone (which builds bone) and altered ability to absorb calcium.  This results in a slower loss of bone mass in men.

• Secondary osteoporosis:

o May result from other medical conditions, such as hyperparathyroidism; long term drug therapy, such as with corticosteroids; or prolonged immobility such as that seen with spinal cord injury

Causes of secondary osteoporosis (Diseases/ Conditions)

 Diabetes mellitus  Hyperthyroidism  Hyperparathyroidism  Cushings syndrome  GH deficiency  Metabolic acidosis  Paget’s disease  RA  Prolonged immobilization  Bone cancer  Cirrhosisi  HIV/Aids  Chronic wairway llimitations

Assessing riskf actors for Primary osteoporosis

 Older age  Parenteral Hx  Low truama fracture Hx after age 50  Body wt (low), thin build  Chronic low Calcium and or Vitamin D intake  Smoking  Alchohol (3x > day)  Sedentary or prolonged immobility

REGIONAL OSTEOPOROSIS

 An example of secondary disease , occurs when a limb is immobilized related to a fracture, injur or paralysis.  Immobility for longer than 8 to 12 weeks can result in this type of osteoporosis

ETIOLOGY and Genetic risks  Primary osteoporosis is caused by a combonation of

genetic lifestyle an environmental factors

 Primary osteorprosis primarly occurs in women afte

menopause as a result of decreased estrogen levels.

ETIOLOGY and Genetic risks

 Body build and weight seems to influence who gets the disease.  Occurs most often in older, lean built Whites.  Weight bearing exercises rduces bone resorption (loss) and stimulates bone formation. - Prolonged immobility - Exces caffeine

 A diet lacking enough calcium and vitamin D stimulates the parathyroid gland to produce parathyroid hormone (PTH).

 PTH triggers the relese of calcium for m bony matrix.  Activated vitamin D is needed for calcium uptake in the body.  Malabsorption of nutrients in the GI tract also contributes to low serum calcium levels.

 Institutionalized or homebound patients who are not exposed to sunlight may be at a higher risk becsue they

do not receive adequate VITAMIN d FOR THE METABOLISM OF CALCIUM.

 People who drink large a mounts of carbonated beverages each day are at high risk fo

calcium loss and subsequent osteopprosis.

 Protein deficiency may also reduce

reduce bone density because 50% of serum calcium is protein bound, protein is needed to use calcium. However extensive protin intake may increase calcium loss in the urine. -protin intake in healthy adult is @ 0.8 grams per kg o f body weight.

alcohol and tobacco use are ofther risk factors for osteoprois. * Alcohol also has direct toxic effect on bone tissue, resulting in decreased bone formation and increased bone resopriotn.

 Osteoporosis also occurs in young adults who participate I n excessive

exercise or wight loss dietary or in hoe how have eating disorders.

ASSESSMENT- OSTEOPOROSIS:

 Complete health history with assessment of risk factors  Those with risk factors for osteoporosis are at increased risk for fractures when falls occur.

ASSESSMENT- OSTEOPOROSIS:

 Assess for fall risk factors including ; - delirium-dementia-immobility-muscular weakness-Hx of falls-Visual or hearing deficits- current drugs  People with osteoprosos are at an increased risk for fractures if a fall occurs.

PHYSICAL ASSESSMENT/ CLINCAL MANIFESTATION

palpate the vertebral column  The classic “dowager’s hump” or kyphosis of the dorsal spine is often present.  This patient may state that they have gotten shorter as much as 2 to 3 inches in the past 20 years.  Take height and weight

Back pain accompanied by tenderness and voluntary restrictions of spinal movement suggest

one or more compression vertebral fractures, the most common type of osteoporotic fracture.  Movement restriction and spinal deformity may result in constipation, abdominal distention, and respiratory compromise in severe cases.

 Because the patient is predisposed to fractures, nutritional therapy, exercise, lifestyle changes, and drug therapy are used to slow bone resorption and form new bone tissue.  Patient education can help prevent osteoporosis or slow the progress.

 These measure help reduce the chance of fractures and their complications.  Drug therapy role has increased over the past decade and helps prevent fractures related to osteoporosis

Interventions:  Drug therapy should begin when the BMD T-score for the hipsi s below :

- 2 with no other risk factors or when the T score is below: -1.5 with one or more risk factors or previous fracture.

Nutritional Therapy:  Teach about adequate amounts of

protein, magnesium, vitamin K and trace minerals that are needed for bone formation.

 Calcium and vitamin D intake should be increased.  Teach patients to avoid excessive alcohol and caffeine consumption.

 Exe rise is important in management of osteoporosis  Walk 30 minutes three to 5 times a week is the single most effective exercise for osteoporosis

 Calcium and vitamin D supplements may be prescribed.

Calcium and vitamin D:

 Intake of calcium alone is not a treatment for osteoporosis but calcium is an important part of a prevention program to promote bone health.  Most cannot or do not have enough calcium in their diet and therefore calcium supplements are needed.

Calcium and vitamin D:

 Insturct patient of any age to take calcium supplements, that also contain activated vitamin D.  (under the supervision of heath care provier)

 Hypercalcemia:  (excessive serum calcium): can cause

serious damage to the urinary system and other boy systems.  Teach patients to drink plenty of fluids to prevent urinary or renal calculi (stones)

 BPs slow bone resorption by binding with crystal elements in bone, especially spongy, trabecular bone tissue.  They are the most common durgs used for osteoporosis but also are approved for pagets diseas and hypercalceima related to cancer.

Estrogen Agonist/ Antagonists:

 Are a class of drugs designed to mimic estrogen in some parts of the body while blocking its effects elsewhere.

 It increases bone mineral density (BMD), reduces bone resorption and reduces incidence of osteoporotic vertebral fractures.

Other agents:  PTH is prepared as

teriparatide under the brand name forteo and is a bone building agent approved for treatemtn of osteoporosis in postmenopausal women with high risk for fractures.

 Teach to self administer Forteo as a

daily sub Q injections.  This drug stimulates new bone formation, thus increasing BMD.  Reduces risk for fractures in the spin, hip and wrist .

 Is a thyroid hormone that inhibits osteoclastic activity, thus decreasing bone loss.  It is used to trat osteoporosis, pagets disease and hypercalcemia associated with cancer, thereby promoting early recovery.  Given subQ or intranasal

 Is a loss of bone related to a vitamin D deficiency

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Notes

Question	Answer
OsteoPorosis	• Is a chronic metabolic disease in which bone loss causes decreased density and possible fractures. • It is often referred to as a “silent disease” because the first signs of osteoporosis in most people follows some kind of fracture.
Bone: • A dynamic tissue that is constantly undergoing changes in a process refered to as	BONE REMODELING.
• Osteoporosis and osteopenia (low bone mass) occur when	osteoclastic (bone resorption) is greater than osteoblastic (bone building) activity. • The result is a decreased BMD (Bone Mineral Density)
• BMD: determines	bone strength and peaks between 25 and 30 yrs of age.
• Before and during the peak years, osteoclastic activity and osteoblastic activity work • After the peak years, bone resorption activity	at the same rate *exceeds bone building activity and bon density decreases.
BMD: • Decreases most rapidly in	postmenopausal women as serum estrogen levels diminish.
• Although estrogen does not build bone, it helps	prevent bone loss.
• Trabecular or cancelous (spongy) bone is	lsot first followed by Cortical (compact) bone. This results in thin, fragile bone tissue that is at risk for fractures.
Diagnosis of osteoporosis	• are based on BMD testing that provides a T-score for the patient. • Osteopenia is present when the T score is @ -1 and above -2.5 • Osteoporosis is diagnosed in a person who has a T score at or lower than -2.5.
Classification of osteoporosis:	• As regional or generalized
Generalized osteoporosis	• Involves many structures in the Skelton and is further divided into two categoris o Primary and secondary.
o Primary osteoporosis	is more common and occurs in postmenopausal women and in men in their seventh or eight decade of life.
o Even though men do not experience rapid bone loss that postmenopausal women have, they do have	decreasing levesl of testosterone (which builds bone) and altered ability to absorb calcium.  This results in a slower loss of bone mass in men.
• Secondary osteoporosis:	o May result from other medical conditions, such as hyperparathyroidism; long term drug therapy, such as with corticosteroids; or prolonged immobility such as that seen with spinal cord injury
Causes of secondary osteoporosis (Diseases/ Conditions)	 Diabetes mellitus  Hyperthyroidism  Hyperparathyroidism  Cushings syndrome  GH deficiency  Metabolic acidosis  Paget’s disease  RA  Prolonged immobilization  Bone cancer  Cirrhosisi  HIV/Aids  Chronic wairway llimitations
Assessing riskf actors for Primary osteoporosis	 Older age  Parenteral Hx  Low truama fracture Hx after age 50  Body wt (low), thin build  Chronic low Calcium and or Vitamin D intake  Smoking  Alchohol (3x > day)  Sedentary or prolonged immobility
REGIONAL OSTEOPOROSIS	 An example of secondary disease , occurs when a limb is immobilized related to a fracture, injur or paralysis.  Immobility for longer than 8 to 12 weeks can result in this type of osteoporosis
ETIOLOGY and Genetic risks  Primary osteoporosis is caused by a combonation of	genetic lifestyle an environmental factors
 Primary osteorprosis primarly occurs in women afte	menopause as a result of decreased estrogen levels.
 Men also develop osteoporosis after age 50 becsue their	testorone levels decrease.
 Testosterone is a major sex hormone that builds	bone tissue.
ETIOLOGY and Genetic risks	 Body build and weight seems to influence who gets the disease.  Occurs most often in older, lean built Whites.  Weight bearing exercises rduces bone resorption (loss) and stimulates bone formation. - Prolonged immobility - Exces caffeine
 A diet lacking enough calcium and vitamin D stimulates the parathyroid gland to produce parathyroid hormone (PTH).	 PTH triggers the relese of calcium for m bony matrix.  Activated vitamin D is needed for calcium uptake in the body.  Malabsorption of nutrients in the GI tract also contributes to low serum calcium levels.
 Institutionalized or homebound patients who are not exposed to sunlight may be at a higher risk becsue they	do not receive adequate VITAMIN d FOR THE METABOLISM OF CALCIUM.
 Calcium loss occurs at a more rapid rate when phosphorus	intake is high
 People who drink large a mounts of carbonated beverages each day are at high risk fo	calcium loss and subsequent osteopprosis.
 Protein deficiency may also reduce	reduce bone density because 50% of serum calcium is protein bound, protein is needed to use calcium. However extensive protin intake may increase calcium loss in the urine. -protin intake in healthy adult is @ 0.8 grams per kg o f body weight.
 Excessive	alcohol and tobacco use are ofther risk factors for osteoprois. * Alcohol also has direct toxic effect on bone tissue, resulting in decreased bone formation and increased bone resopriotn.
 Osteoporosis also occurs in young adults who participate I n excessive	exercise or wight loss dietary or in hoe how have eating disorders.
ASSESSMENT- OSTEOPOROSIS:	 Complete health history with assessment of risk factors  Those with risk factors for osteoporosis are at increased risk for fractures when falls occur.
ASSESSMENT- OSTEOPOROSIS:	 Assess for fall risk factors including ; - delirium-dementia-immobility-muscular weakness-Hx of falls-Visual or hearing deficits- current drugs  People with osteoprosos are at an increased risk for fractures if a fall occurs.
PHYSICAL ASSESSMENT/ CLINCAL MANIFESTATION	palpate the vertebral column  The classic “dowager’s hump” or kyphosis of the dorsal spine is often present.  This patient may state that they have gotten shorter as much as 2 to 3 inches in the past 20 years.  Take height and weight
Back pain accompanied by tenderness and voluntary restrictions of spinal movement suggest	one or more compression vertebral fractures, the most common type of osteoporotic fracture.  Movement restriction and spinal deformity may result in constipation, abdominal distention, and respiratory compromise in severe cases.
Interventions:	 Because the patient is predisposed to fractures, nutritional therapy, exercise, lifestyle changes, and drug therapy are used to slow bone resorption and form new bone tissue.  Patient education can help prevent osteoporosis or slow the progress.
Interventions:	 These measure help reduce the chance of fractures and their complications.  Drug therapy role has increased over the past decade and helps prevent fractures related to osteoporosis
Interventions:  Drug therapy should begin when the BMD T-score for the hipsi s below :	- 2 with no other risk factors or when the T score is below: -1.5 with one or more risk factors or previous fracture.
Nutritional Therapy:  Teach about adequate amounts of	protein, magnesium, vitamin K and trace minerals that are needed for bone formation.
Nutritional Therapy:	 Calcium and vitamin D intake should be increased.  Teach patients to avoid excessive alcohol and caffeine consumption.
Lifestyle changes:	 Exe rise is important in management of osteoporosis  Walk 30 minutes three to 5 times a week is the single most effective exercise for osteoporosis
Drug Therapy:	 Calcium and vitamin D supplements may be prescribed.
Calcium and vitamin D:	 Intake of calcium alone is not a treatment for osteoporosis but calcium is an important part of a prevention program to promote bone health.  Most cannot or do not have enough calcium in their diet and therefore calcium supplements are needed.
Calcium and vitamin D:	 Insturct patient of any age to take calcium supplements, that also contain activated vitamin D.  (under the supervision of heath care provier)
 Hypercalcemia:  (excessive serum calcium): can cause	serious damage to the urinary system and other boy systems.  Teach patients to drink plenty of fluids to prevent urinary or renal calculi (stones)
Biphosphonates:	 BPs slow bone resorption by binding with crystal elements in bone, especially spongy, trabecular bone tissue.  They are the most common durgs used for osteoporosis but also are approved for pagets diseas and hypercalceima related to cancer.
Estrogen Agonist/ Antagonists:	 Are a class of drugs designed to mimic estrogen in some parts of the body while blocking its effects elsewhere.
is currently the only approved drug in this class and is used to prevent and treat osteoporosis in postmenopausal women.	 RALOXIFENE:
 RALOXIFENE:	 It increases bone mineral density (BMD), reduces bone resorption and reduces incidence of osteoporotic vertebral fractures.
Other agents:  PTH is prepared as	teriparatide under the brand name forteo and is a bone building agent approved for treatemtn of osteoporosis in postmenopausal women with high risk for fractures.
 Teach to self administer Forteo as a	daily sub Q injections.  This drug stimulates new bone formation, thus increasing BMD.  Reduces risk for fractures in the spin, hip and wrist .
Calcitonin	 Is a thyroid hormone that inhibits osteoclastic activity, thus decreasing bone loss.  It is used to trat osteoporosis, pagets disease and hypercalcemia associated with cancer, thereby promoting early recovery.  Given subQ or intranasal
OsteoMalacia:	 Is a loss of bone related to a vitamin D deficiency
OsteoMalacia:  It causes	softening of the bone resulting from inadequate depostes of calcium and phosphorus in the bone matrix  Normal remodeling of the bone is disrupted anc calcification does not occur
OsteoMalacia:  It is the adult equivalent of	rickets or vitamin D deficiency in children.
 Vitamin D deficiency is the most important factor In development of	osteomalacia
 In its natural form, vitamin D is activated by the	ultraviolet radiation of the s un and obtained from certain foods as a nutritional supplements.
 In combination with calcium and phosphorus, the vitamin (D) is necessary for	bone formation.
 Malabsorotoion of vitamin D from the small bowel is a common complication of	partial or total gatrectomy and bypass or resection surgery of the small intestine. Diseases of the small bowel, such as Crohns disease, may cause decreased vitamin and mineral absorption.
Health promotion and Maintenance:  Teach patients to increase vitamin D through	dietary intake, sun exposure, and drug supplements
Health promotion and Maintenance	 Instruct the at risk patient about foods high in vitamin D such as milk and food that ha had it added.  Teach patients to choose those products that are fortified with vitamin D.  The at risk patient should also take vitamin D supplements
Assessements: vit D- deficiency	 Age  Ability to be exposed to sunglight and skin pigmentation  Homebound or chronically institutionalized is at greatest risk.
INTERVENTIONS:  The major treatment for osteomalacia is	vitamin in an active form such as ergocalciferol
Osteoporosis	Decreased bone mass Lack of calcium Osteopenia, fractures Low or normal
Ostemalacia	Demineralized bone Lack of vitamin D Pseudofractures, loosers zones, fractures Low or normal
CAUSES OF OSTEOMALACIA Vitamin D Disturbances:	 Inadequate production  Lack of sunglight exposure  Dietary deficiency  Abnormal metabolism  Drug therapy Liver disease  Renal Disease  Inadequate absorption malabsorption syndrome)  Inflammatory bowel disease
CAUSES OF OSTEOMALACIA Kidney disease:	Chronic kidney disease Acute tubular disorders (acidosis, hypophosphatemia)
Familial Metabolic Error	Hypophosphatemia
PAGET’S DISEAE OF THE BONE (or osteitis deformans):  Is a chronic metabolic disorder in which bone is * The result is bone that is structurally	excessively broken down (osteoclastic activity) and reformed (osteoblatic activity) *disorganized, causing bons to be weak with increased riks for bowing of logn bones and fracturs.
 The two types of paget’s disease can occur	1. Familial or 2. Sporadic
Three pathophysiologic phases of the disorder (paget's diseae) have been described	• Active • Mixed • Inactive
• In the first phase (active phase), the osteoblasts (bone forming cells)	react to compensate in forming new bone. • The result is bone that is vascular, structurally weak, and deformed. • Paget’s disease occurs in one bone or multiple sites.
PHYSICAL ASSESSMENT/ CLINICAL MANIFESTATION The most common areas of involvement are the (paget's disease)	the vertebrae, femur, skull, clavicle, humerus and pelvis. • Then the osteoblatic activity exceeds the osteoclastic activity, the inactive phase occurs. The newly formed bone becomes sclerotic and very hard.
PHYSICAL ASSESSMENT/ CLINICAL MANIFESTATION Paget's disease: (assessment) *• Most are	asymptomatic and the disease may become confined to one bone. • could be accidentally discovered @ xray • ask about Hx of fractures, current bone health • most noticeable at night when pt is sitting or resting.
PHYSICAL ASSESSMENT/ CLINICAL MANIFESTATION	• Pt may report redness, warmth at affected sites. • Arthritis often occurs athe the joints of the ffcted bones, resulting from bowing I nlong bones of the leg. • Some can have joint replacements as a result of very painful weight bearing joints.
PHYSICAL ASSESSMENT/ CLINICAL MANIFESTATION • Nerve impingement is common esp in	lumbosacreal areas, presenting as back pain that radieatsalong one or both legs. • Observe posture, stance, gait to identify deformities. • Assess for kyphosis or lordosis
PHYSICAL ASSESSMENT/ CLINICAL MANIFESTATION • Observe	posture, stance, gait to identify deformaties. *kyphosis or lordosis
PAGET’S DISEASE OF THE BONE (KEY FEATURES) Musculoskeletal manifestations:	• Bone and joint pain • Low back and sciatic nerve pain • Bowing of long bones • Loss of normal spinal curvature • Enlarged, thick skull • Pathologic (fractures) • Osteogenic sarcoma (bone cancer)
PAGET’S DISEASE OF THE BONE (KEY FEATURES): Skin Manifestations	• Flushed, warm skin
PAGET’S DISEASE OF THE BONE (KEY FEATURES): Other manifestations:	• Apathy, Lethargy, fatigue • Hyperparathyroidism • Gout • Urinary or renal stones • Heart failure from build overload
The most dreaded complication of paget’s disease is	CANCER. Most commonly OSTEOGENIC SARCOMA
Graves disease: • It affects the femur, humerus, and old fracture sites and has a	grave prognosis becaue of early metastasis to the lung or extensive local invation. • When severe pain is present in a patient with Paget’s disease, bone cancer is suspected.
• Assess the skin for its	its color and temperature, their skin is typically flushed and warm because of the increased blood florw. • Assess their energy level because apathy, lethargy and fatigue are common
• Other less common manifestations are of paget's:	hyperparathyroidism and gout.
Paget's disease: • Secondary hyperparathyroidism leads to an increase in	serum and urinary calcium levels. • In severe case,serum calcium excess results from prolonged immobilization. • Calcium deposts occur in joint space or as stones in the urinary tract. • Kidney stone are common in pts with pagets disease.
Paget's disease: Diagnostic assessment:	• Increases in serum alkaline phasphatas (ALP) and urinary hydroxyproline leves are the primary laboratory findings indicating possible paget’s disease. • Overeactive oseoblasts can cause an altered ALP level.
Diagnostic assessment:	• ALP an be further evaluated byalkaline phospohat isoenzymase isoenzymes. • The isoenzyme testing can further break ALP into three fractions- liver, bone and intestinal.
Diagnostic assessment: (paget's)	• Elevated bone isoenzymes can help in a more definitive diagnosis and serum isoenzyme levels of bone are sued to monitor effectiveness of treatment.
The 24 hour urinary hydroxyproline	• levels reflects bone collagen turnover and • indcaesthe degree of disease seveirityuca • Paget’s disease often causes an elevated uric acid because nucleicacid from overactive bone metabolism increases.
INTERVENTIONS	• Non surgical or surgical management may be necessary to reduce pain and promote mobility • Non surgical used first
OSTEOMYELITIS	• Infection bony tissue can be a severe and difficult to treat problem. • Bone infection can result in chronic recurrence of o Infection o Loss of function o Mobility o Amputation o Even death
OSTEOMYELITIS Pathophysiology	• Bacteria, virus or fungi can cause infection in bone known as osteomyelitis
OSTEOMYELITIS ( Pathophysiology) • Invasion by one or more pathogenic microorganisms stimulates the *• The inflammation produces an increased	* inflammatory response in bone tissue vascular leak and edema, often involving the surrounding soft tissues. • Ischemia of bone tissue follows and results in necroticbone
Pathophysiology	• This area of necrotic bone separates from surrounding bone tissue and sequestrum is formed. • The presence of sequestrum prevents bone healing and causes superimposed infection, often in the form of bone abscess.
Osteomyelitis is categorized as	exogenous:• In which infecous organism enter from outsie the body as in an open fracture or Endogenous: • Where organisms carried by bloodstream from other areas of infection in the body.
• A third catagor is contiguous, in which bone infection results from	skin infection of adjacent tissue. • Osteomyelitis can be further divided into two major types: • Acute and chronic
Infection cycle of osteomyelitis 1. 2. 3.	-PATHOGEN INVASION  TISSUE INFLAMMATION-- (increased vascularity)   EDEMA FORMATION-- (blood vessel thrombosis)-
Infection cycle of osteomyelitis 4. 5. 6.	 DECREASED BLOOD FLOW TO BONE--- --BONE NECROSIS (sequestrum formation)----  BONE ABSCESS---(superimposed infection)-
osteomyelitis - ETIOLOGY	• Each type of bone infection has its own causative factors • Pathogenic microbes favor bone that has a rich blood supply and a marrow cavity
Acute hematogenous infection	• Results from bacteremia, underlyuing disese or nonpenetrating trauma. • UTIs, esp. in older men tend to spread to the lower vertebrae • Long term IV catheters can be primary source of infection
Acute hematogenous infection	• Pts undergoing long term hemodialysis and IV drug abusers are also at risk for osteomyelitis. • Salmonella infection of the FI tract may spread to bone
Acute hematogenous infection	• Poor dental hygien and gum infection can be a causative factor in contiguous osteomyelitis in facial bone. • Regardless of the source of infection, many infections are caused by Staph aureus
CHRONIC OSTEOMYELITIS	• If bone infection is misdiagnosed or inadequately treated, chronic osteomyelitis may develop.
Hematogenous osteomyeltis:	• Is the most common type of osteomyelitis
ASSESSMENT/ COLLABORATIVE CARE:	• Bone pain with or without other manifestation is a common concern of patients with bone infection. • The patient with acute osteomyelitis has o Fever, usually with temperature greater than 101 F (38.3 C).
ASSESSMENT/ COLLABORATIVE CARE:	• Older adults may not have an extreme temperature elevation because of lower core body temperature and compromised immune system that occur with normal ageing.
ACUTE & CHRONIC OSTEOMYELITIS:	ACUTE & CHRONIC OSTEOMYELITIS:
Acute Osteomyelitis	• Fever (above 101 (38.3C) • Swelling around the affected area • Erthma of the affected area • Tenderness of the affected area • Bone pain that is constant, localized and pulsating; intensifies with movements
Chronic Osteomyelitis	• Ulceration of the skin • Sinus tract formation • Localized pain • Drainage from the affected area
INTERVENTIONS:	• Specific treatment protocol depends on the type and number of microbes present in the infected tissue • If other measures fail to resovle infectious process, surgical may be needed.
NONSURGICAL MANAGEMENT	Antibiotics: • To reverse acute osteomyeslitis, start ANTIMICROBIAL (e.g. antibiotic) therapy asap. • Contact precausions are used to prevent the speread of the offending oragnsim to others
NONSURGICAL MANAGEMENT	IV antimicrobial therapy: • Is usually prescribed for several weeks for acute osteomyelitis. • Observe for the actions, side effects and toxicity of these drugs. • Prolonged thereapy for more than 3 months may be needed to eliminate the infections.
Priority: **even when symptoms of osteomyelitis appear to be improved, teach the patiens tand family that	the full course of IV antimicrobials must be completed to ensure that the infection is resolve.**** • drugs also needed to control [pain
SURGICAL MANAGEMENT	• Because bone cannot heal in the presence of necrotic tissue, a • Sequestrectomy may be performed to debride the necrotic bone and allow revascularization of tissue. • The use of bone grafts to repair bone defects is also widely used
Nursing priority: • After surgery to treat ostemyelitis frequently check for signs of • NEUROVASCULAR compromise including	o Pain- that cannot be controlled o Paresis or Paralysis (weakness or inability yto move) o Paresthesia (abnormal, tingling sensation) o Pallor o Pulselessness • If any of these findings occur, report them immediately ot he surgeon.
Scoliosis	• Occurs when the vertebrae rotate and begin to compress • The spinal column begins to move into a lateral cureve • Degree of curvature increases during periods of growth
Scoliosis	• Curvature greater 50 degrees results in unstable spine, • Curvature of greater than 60 degrees in thoracic spine results in compromise of cardiopulmonary function. • Exact cause of scoliosis is not well understood.
Three types of scoliosis can be described:	• Congenital • Neuromuscular • Idiopathic
Scoliosis	*The most common curve pattern in adults is idiopathic scoliosis and the caue is uknown.
Scoliosis	Congenital scoliosis occurs during embryonic development Neuromuscular scoliosis can result from a neuromuscular condition in childhood or adulthood such as cerebral palsy or spinal cord tumors.
Scoliosis	*Untreated scoliosis can lead to back pain, deformity, and cardiopulmonary complications.
ASSESSMENT:	• A lordosis may be also present. • A loss of lumbar curvature or lordosis described as flat back syndrome may also be present
INTERVENTIONS:	• Adults with less than 50 degree of curvature of the spine may be treated with moist heat, pain medication, and exercise.
INTERVENTIONS:	• Those with greater than 50 degrees of curvature may require surgical intervention to prevent shortness of breath and fatigue, osteoarthritis and severe back pain.
INTERVENTIONS:	• Surgical reconstructive procedure consists of surgical fusion and insertion of instrumentation, including plates, screws or rods to stabilize the spine.
INTERVENTIONS: Nursing priority:	• The priority for nursing care after spinal reconstructive surgery is to assess the patients • RESPIRATORY STATUS AND encourage DEEP BREATHING. • Teach patiens how to use the INCENTIVE SPIROMETER to prevent ATELECTASIS
CARE OF PATIENES WITH MSK TRAUMA	CARE OF PATIENES WITH MSK TRAUMA
Fractures: (pathophyiology)	• Is a break or siruption in the continuity of a bone that often affects mobility and sensation
• A fracture is classified by the extent of the break	o Complete break o Incomplete break
• Complete break	o The break is across the entire width of bone, broken into two distinct sections
• Incomplete break	o The fracture does not divide the bone into two portions , only partly
A fracture is described by the extent of associated soft tissue damage as:	• Open (or compound) or • Closed (or simple)
compound fracture	• The skin surface over the broken bone disrupted ina compound fracture, which causes an external wound. • These fracutrees are often graded to deifne the extend of tissue damage.
• Simple fracture:	Does not extend through the skin and therefore has no visible wound.
In addition to being identified by, fractures are described by their cause:	• A pathologic (spontaneous) fracture • Compression fractures
• A pathologic (spontaneous) fracture	o Occurs after minimal trauma to a bone that has been weakened by disease. o An example, a patient with bone cancer or osteoporosis can easily have a pathologic fracture.
• Compression fractures	o Are produced byb a loading force applied to the long axis of cancellousbone
ACUTE COMPARTMENT SYNDROME -• Compartments are areas in the body in which:	muscles, blood vessels, and nerves are contained within a fascia. *• Most compartments are localized in the extremities.
• Fascia is an	inelastic tissue that surrounds groups of muscles, blood vessels and nerves in the body.
Acute compartment syndrome (ACS) *• Is a serious condition in which increased	increased pressure within one or more compartments reduces circulation to the area.
• The most common sites for this problem in patiens with musculoskeletal trauma are the compartments in the	lower leg and forearm.
The physiological changes of increased compartment pressure are sometimes referred to as	• Ischemic edema cycle
ACS: • Capillaries within the muscle dilate, which	raises capillary pressure • Capillaries then become ore permeable because of the releasae of histamine by the ischemic mucle tissue. • As a result plasma proteins leak into the interstitial fluid space and edema occurs
ACS: • Edema increases	pressure on neve endings and causes pain.
ACS: • Blood flow to the area is	reduced and further ischemia results.
ACS: • Sensory deficit or parestheisa generally appears before changes in	vascular or motor signs.
ACS:• The color of the tissue	tissue pales, and pulses begin to weaken but rearly dispear.
ACS: • If the condition is not treated	CYANOSIS, tingling, numbness, paresis, necrosis and severe pain can occur.
The pressure to the compartment can be from an	external or internal source.
examples of external pressure.	• Tight, bulky dressing and casts
source of internal pressure.	• Blood or fluid accumulation in the compartment is a common source of internal pressure.
ACS: • The injury or trauma causing the problem is	above the compartment involve., which decreases bloowd flow to the more distal area of injury
• ACS is not limited to patients with musculoskeletal problems. • It can also occur in those with	severe burns. *• Extensive insect bites or snake bites or massive infiltration of Iv fluids. • In these situations edema increases internal pressure in one or more compartments.
Problems resulting from compartment syndrome include:	• Infection, persistent motor weakness in the affected extremity, contractures • In extreme cases, amputation of the limb is needed.
Motor weakness	• From injured nerves is not reversible, and the patients my require an orthotic device for assistance immobility.
Volkmann’s contractures of the forearm	• Which can begin within 12 housr of the pressure increase, result from shortening of the ischemic muscle and from nerve involvement
Myoglobinuric renal failure	• From muscle breakdown is a potentially fatal complication of compartment syndrome. • It occurs when large or multiple compartments are involved,.
Myoglobinuric renal failure: *• Injured muscle tissue release myoglobulin (muscle protein) inot the circulation, where it can:	clog the renal tubules and cause acute renal failure.
Myoglobinuric renal failure:	• Damaged muscle cells also release potassium, which cannot be excreted because of the renal failure. • The resulting hyperkalemia may cause dysrhythmias and cardiac arrest.
FAT EMBOLISM SYNDROME	• Is another serious complication in which fat globules are released from the yellow bone marrow inot the blood stream within 12 to 48 hours after an injury or other illness. • These globules clog small blood vessels that supply vital orangs
FAT EMBOLISM SYNDROME	• Mostly the lungs and impair organ perfusion. • FES usually results from long bone fractures or fracture repair but occasionally is seen in patiens who have a total joint replacement.
Earliest manifestation of FES is	• Altered mental status o Which is cused by lwo arterial oxygen level • Dyspnea and chest pain may follow.
Earliest manifestation of FES is	o A muscular, measules like rah may appear over the neck, upper arm , or cheset and abdomen. o This rash is a classic manifestation but can be a late sign.
• FES can result	o In respiratory failure or death, often from pulmonary edema o When the lungs are affected, the complication may be misdiagnosed as Pulmonary embolism from a blood clot.
DELAYED UNION	• Is a fracture that has not healed within 6 months of injury • Some fractures never achieve union; that recently (malunion)
DELAYED UNION	• These problems are most common in pateins with tibial fractures, fractures that involve many treatments techniques ( e.g. cast, traction) and pathologic fractures. • If bone does not heal, typically has chronic pain and immobility from deformity
ETIOLOGY & GENETIC RISK • The primary cause of a fracture is trauma from a	motor vehicle crash or fall esp in older pts. • Dirct blow to the bone or indirect force from muscle contractions or pulling forces on bones.
Incidence / prevention ASSESSMENTS:	• Rib fractures are the most common type in the adult • Femorla shaft fractures in young and middle aged. • If the pt is in severe pain, delay the interview untl more comfortable
EMERGENCY CARE of patient with extremity fractures:	. Assess Airway, Breathing, circulation, quick head to Toe assessment • 2. Remove clothing/ • 3. Remove jewelry on affected side • 4. Keep warm and supine • Immobilize extremeity by splinting
TRACTION:	• Is the application of a pulling force to a part of the body to provide reduction, alignment and rest
TRACTION:	• It is also used as a last resort to decrease muscle spasm (thus relieving pain) and to prevent or correct deformity and tissue damae • A patient in traction is often hospitalized.
The two most common types of traction are	SKIN AND SKELETAL TRACTION
Skin traction: *• Involves the use of a	Velcro boot (Bucks traction), belt, or halter which is usually secured around the affected leg.
Skin traction: *• The purpose of skin traction is to decrease	painful muscle spasm that accompany hip fractures.
Skin traction	• The weight is used as a pulling force and is limited to 5 to 10 pounds to prevent injury to the skin.
Skeletal traction:	• Pins, wires, gongs or screws are surgically inserted directly into bone. • These allow the use of longer traction time and heavier weights- usually 15 to 30 pounds. • Skeletal traction aids in bone realignment
Skeletal traction: *• Pin site care is an important part of nursing management to	prevent infection
Priority nursing action: *• When patients are in traction, weighs usually are	*not removed without a prescription.
Priority nursing action: weights	• They should not be lifted manually or allowed to rest on the floor. • Weights should be freely hanging at all times • Inspect the skin at least every 8 hours for signs of irritation or inflammation
weights	• When possible, remove the belt or boot that is used for skin traction every 8 hours to inspect under the device.
Operative procedures: *• Open reduction with internal fixation (ORIF)	*is one of the most common methods of reducing and immobilizing a fracture.
• External fixation with closed reduction is used when	*patients have soft tissue injury (open fracture).
• Because ORIF permits	early mobilization, it is often the preferred surgical method.
• Open reduction,allows the surgeon to :	directly view the fracture site.
• Internal fixation *o Uses	metal pins, screws, rods, plates, or prostheses to immobilize the fracture during healing.
• Internal fixation *o The surgeon makes	one or more incisions to gain access to the broken bones and implants one or more devices into bone tissue after each fracture is reduced.
• Internal fixation: o A cast, boot, or splint is placed to maintain	immobilization during the healing process. *• After the bone achieves union, the metal hardware may be removed, depending on he location and type of fracture.
• An alternative modality for the management of fractures is the :	external fixation apparatus.
External Fixation: *• Is a system in which	pins or wires are inserted through the skin and affected bone and then connected to a rigid external frame.
External Fixation: *• The system may be used for	upper or lower extremity fractures or for fractures of he pelvis, especially when wound management is needed.
External Fixation: • After a fixator is removed, the patient may be placed in a	cast or splint until healing is complete.
External fixation has several advantages:	• Minimal blood loss compared to internal fixation • The device allows early ambulation and exercise of affected body part
External fixation has several advantages:	• The device maintains alignment in closed fractures that will not maintain position in a cst and stabilizes comminted fracters that require gone grafting.
External fixation disadvantages	• An increased risk for pin site infection • Pin site infection can lead to osteomyelitis, which is serious and difficult ot treast. • For pts with an external fixator, pay special attention to the pins sites for sighns of inflammation or infection.
External fixation disadvantages	• In the first 48 to 72 hours , clear fluid drainage or weeping is expected. • Monitor the pin sites at least every 8-12 hours for drainage, color, odor, and severe redness, which indicate inflammation and possible infection.
External fixation disadvantages	• Pt w/ external fixator may have a disturbed body image. • The frame may be large and bulky and he affected area may have massive tissue damage with dressing.
AMPUTATIONS:	AMPUTATIONS:
Types of amputation:	• May be elective or traumatic • Most are elective and are related to complications or peripheral vascular disease and arteriosclerosis
Types of amputation:	• These complications result in ischemia in distal areas of the lower extremity • Diabetes mellitus is often underlying cause • Amputation is considered only after other interventions have not restored circulation to the lower extremity
Traumatic amputations:	• Most often result from accidents and are primary cause of upper extremity amputations.
Levels of amputation:	• Lower Extremity amputations are performed much more frequently than upper extremity amputations. • An intense effort is made to preserve knee joints with below the knee amputation (BKA).
Levels of amputation:	• The higher the level of amputation, the more energy is required for mobility • Less than 10% are UE
Complications of amputation:	• Hemorrhage • Infection • Phantom limp pain • Neuroma • Flexion contractures.
In phantom limp pain: sensation	felt in the amputated part immediately after surgyer and usually diminishes over time.
Priority nursing:	• Recognize the patiesn phantom limp pain as eal and treat it aggressively • A combonation of drug therapy and complementary and alternative therapies is the best approach for pain management.
Neuroma:	• A sensitive tumor consisting of damaged nerves cells forms most often in amputation of the UE but can occur anywhere. (may or may not feel pain)
STRAINS AND SPRAINS *Strain:	• Is an excessive stretching of a muscle or tendon when it is weak or unstable • Strains are sometimes refered to as muscle pulls • Falls, lifting a heavy item and exercise often cause this injury
• Strains are classified according to their severity	o First degree (mild) strain: o Second degree (moderate)strains o Third degree (severe) strain
o First degree (mild) strain:	 Causes mild inflammation but lttle bleeding  swelling, ecchymosis (bruising), and tenderness are usually present
o Second degree (moderate)strains:	 Involve teraring of the muscle or tendon fibers without complete disruption  Muscle function may be impaired
o Third degree (severe) strain	 Involves a ruptured muscle or tendon with separation of muscle from muscle, tendon from muscle, or tendon from bone.  Severe pain and disability result from severe strains
Sprain:	• Is excessive stretching of a ligament • Twisting motions from a fall or sports activity typically cause the injury • Sprains are als oclassfied according to severity • Pain and swelling result from ligament injuries
Treatment for mild (first degree) spains include:	• RICE
Second degree sprains require	• Immobilization such as elastic bandage and an air stirrup ankle brace or splint and partial weight bearing while the tear heals.
For severe ligament damage (third degree sprain):	• Immobilization for 4 t o6 weeks is necessary • Arthroscopic surgery may be done, particularly for chronic joint instability

Created by: sterfe

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