Musculoskeletal Flashcards

1
Q

bones composed of?

A
  • Composed of collagen fibers (Ca++,

* Osteoblasts and Osteoclasts

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2
Q

functions of bones

A
  • Provide support for body
  • Protect internal organs
  • Store calcium, phosphorus, other minerals
  • provide movement in conjunction with muscles
  • produce red/white blood cells in bone marrow of long bones
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3
Q

problem with bone leads to?

A

anemia, leukopenia

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4
Q

MS assessment

A
Inspect for deformities (Ie in hip fx is one leg longer than other)
Inspect and palpate any swelling 
Feel for increased temperature 
• Observe for redness 
Palpate for tenderness around joint 
Assess ROM
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5
Q

Pg 1493 has list of lab tests specifically r/t bone disorders that we should be familiar with

A

look

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6
Q

osteoporosis

A

• Skeletal disease: low bone mass, deterioration of bone tissue
• Most common metabolic bone disease
structure and mass change

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7
Q

osteoporosis etiology

A

Etiology/pathophysiology:
•Incompetent bone remodeling (more broken down than rebuilt)
• Primary or secondary (Primary: unsure why, relationship to hormone, just happens with age. Secondary: something is causing it ie steroids. With secondary can identify cause and treat cause. Primary much more common)
• Changes in both cortical and cancellous bone (Affects whole bone, every bone in body. But those that cause more problems are th weight bearing ones)
-changes in bone turnover process result in bone structure changes
Ververy common post menopausal becase lose protective function of estrogen

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8
Q

osteoporosis s/s

A
  • Fractures after minor falls (Sometimes hip fx after a heavy step, putting too much weight on leg, THEN they fall.)
  • Pathologic fractures (spine, femur) (Compression fx of spine, vertebrae themselves squish down with aging.)
  • Spontaneous wedge fractures r/t dec density of spine, inability to manage weight on the spine
  • Kyphosis r/t decreased density of spine and inability to manage the weight
  • Height loss
  • pain
  • vertebral collapse
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9
Q

osteoporosis management/prevention

A
  • Bone resorption inhibitor
  • Hormone replacement therapy (HRT)
  • Calcium supplements (Usually has vitamin D in it: teach pt to read label, buy the one with vit d in it.)
  • Vitamin D
  • Diet: protein, vitamins, minerals
  • Exercise: high-impact (High impact as in weight bearing, not like crazy exercises)
  • complementary/alternative therapy: biofeedback, yoga, massage, reflexology
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10
Q

osteoporosis severity determination

A

Osteoporosis is in degrees: bone density test may show how many standard deviations away from normal. Little loss = osteopenia (very early stages of osteoporosis). More than something like 1 SD = osteoporosis.

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11
Q

noninflammatory arthritis

A

OA
Inf/noninflamm as in the CAUSE, not as in the effect. Both have inflammation, but both don’t have it as the CAUSE.
• Related to overuse/ wear and tear: not equal on both sides. Esp if injury, wear/tear worse on side of injury. So worse in one knee or ONLY in one knee for example. Vs RA: is systemic! So everywhere. Equal.
• Unilateral and not systemic.

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12
Q

inflammatory arthritis

A

Rheumatoid arthritis
Systemic lupus erythematosus
Connective tissue disease that is inflammatory.

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13
Q

autoimmune diseases / tx

A

Some arthritis are autoimmune as in rheumatoid arthritis recognizing something in joint as foreign, causing inflammation from autoimmune response.

  • Defect in immunologic mechanism
  • Possible genetic component (Onset at much younger age for autoimmunes than for like OA.)
  • Characterized by hypersensitivity
  • Tend to be systemic and chronic (bilateral, often times disease itself goes beyond MS system and connective tissue of MS system, since it’s a connective tissue disorder, it’ll cause non MS symptoms as well. But early signs are usually in MS system.)
  • Medications control or reduce immune system response: systemic meds, particularly immunosuppressants
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14
Q

OA, characterizations

A

Ask WHERE the OA is.
-Most common type of arthritis
-Joint pain and loss of function characterized by progressive deterioration and loss of cartilage in the joints
• Decrease in collagen synthesis so wearing down joint and weraing down ability to repair
• Increase in collagen breakdown
-Osteophytes (bone spurs)
-Synovitis (inflammation of the synovium which is lining of the joint itself)
-subluxation (weak joint, partial dislocation)
Get erosion of the bone itself after losing the protective coating.
Tends to be in larger joints: hips, knees, hands, spine. RA starts in very small joints.

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15
Q

OA etiology

A

Multiple factors
• Can be primary idiopathic (Don’t rly know whats causing it.)
Can be secondary to: Congenital joint defects, Trauma, Inflammatory, metabolic disorders

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16
Q

OA Pg 1566 has list of diagnostic tests for OA. Best most simple and low cost test is X RAY. Not a lot of detail, but first stop because it gives enough information.

A

look

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17
Q

nrsg assessment for OA

A

-History
-Physical assessment and clinical manifestations:
• Joint deformity
• Heberden’s nodes, In joint closer to tip
• Bouchard’s nodes, In 2nd joint
• Joint effusions
• Atrophy of skeletal
• Morning stiffness: Happens with OA and RA, but key is with oA, it gets better thru day with movement. RA gets WORSE with movement.
• Pain with overuse of joint: What was their job? OA in hand more commonly with someone who has done fine work with their hands ie sewing

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18
Q

OA nursing management

A
  • Highest priority: pain relief (NSAIDS WOULD be great, but most ppl with OA are older and much higher risk for GIB. Nsaids should be short term only. Tylenol not that good for this because it doesn’t do inflammation, but its safer and appropriate doses.)
  • Heat and cold applications
  • Complementary and alternative therapies: Accupuncture, herbs
  • Exercise, firm mattress, splints: If it’s in the back use mattress, splints for extremities. Don’t completely immobilize joints: need to move the joints. Splints would be temporary.
  • Fall protocol in hospital and at home: Especially if its in a joint like hip or knee.
  • Promotion of independence
  • Weight loss
  • support
  • OA prevention
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19
Q

RA

A
  • Chronic, progressive, systemic inflammatory autoimmune disease affecting primarily the synovial joints
  • Autoantibodies (rheumatoid factors) formed that attack healthy tissue, especially synovium, causing inflammation; development of a pannus
  • cartilage becomes fibrous and calcified (No erosion of cartilage, instead becomes very stiff.)
  • affects synovial tissue of any organ/body system
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20
Q

RA pathology

A

Tissue hypersensitivity leads to inflammation in WHOLE CAPSULE unlike in OA.
Will start to see it in small joints like in the hands.

Get all WBCs and stuff so joint gets very full, inflammation.

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21
Q

RA clinical manifestations

A
  • Remissions and exacerbations
  • Early disease manifestations—joint stiffness, swelling, pain, fatigue, and generalized weakness (Pt will be very tired and weak on top of the other symptoms; key to look for that early because they’ll be weak from the inflammatory response)
  • Systemic Manifestations: Swollen glands (Body responding), dry mouth, pleuritis, anemia, decreased WBCs, vasculitis
  • Late disease manifestations—as the disease worsens, the joints become progressively inflamed and quite painful (joints become practically unusable)
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22
Q

RA pain relief

A

splints for immobilization

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23
Q

RA joint involvement

A

Ulnar deviation: damage to knuckle joints, deviating to one side instead of fingers going straight out.
Also swan neck deformity (subluxation at middle joint, bending wrong way). Classic in RA patients. Rly impt to recognize

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24
Q

RA lab/diagnostics

A
  • Radiologic imaging (Cat, bone scan, x ray, but key is things significant to autoimmune disorders ie the things below)
  • Blood tests include:
    * Rheumatoid factor (This is what goes around causing inflammation. Means it’s a rheumatic disease, and its probably RA.)
    * Antinuclear antibodies (Elevation of ANA is sign of autoimmune)
    * Erythrocyte sedimentation rate (ESR) (Elevated, sign of inflammation. )
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25
Q

RA nrsg management

A
  • Joint mobility, preventing contractures (Joint mobility when nOT having a flare up. Cause if not, they’ll get contractures. But during flare up they should rest, use splints, heat etc)
  • Rest during flare-ups
  • heat applications (paraffin bath)
  • pain medications
  • support, referral (Chronic, irreversible, progressive disease, lifelong. So make sure they have a good support.)
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26
Q

RA medical management

A

• Chronic condition; no cure
• Early intervention
• Can control disease and treat symptoms (They’ll use NSAIDs since they’re younger)
Treatment includes:
• Pharmacologic interventions
• Rest (Flare up), exercises (When not flare up), safeguarding joints
• surgical intervention includes: synovectomy, arthrodesis, and/or reconstructive surgery (Surgery to loosen contracture. Surgeries kinda rare.)

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27
Q

RA systemic complications

A
  • Weight loss, fever, and extreme fatigue (LOW grade fever (not like 101 and up) from inflammation, and slight increase in WBC. Slight increase = inflammatory. Large inc = infection.)
  • Exacerbations
  • Subcutaneous nodules (Subcutaneous nodule. Seen in both diseases, but in RA theyre seen more in other areas while OA is mostly seen in joints. RA kinda more where lymph system is at.)
  • Pulmonary complications
  • Vasculitis (If vasculitis, stiffness and swelling in vessel itself: whatever organ is supplied by vessel is where u will see the problem.)
  • Periungual lesions
  • paresthesias
  • cardiac complications (myo/pericarditis)
  • resp fibrosis

Because there’s connective tissue in all these areas

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28
Q

gouty arthritis etiology/patho

A

Etiology:
• Imbalance in purine metabolism (Causes excessive uric acid, gets stuck in joints)
• Risk factors: heredity, enzyme defect, lead exposure.
• Strong genetic predisposition

Pathophysiology:
Uric acid crystals accumulate in joints
75% of patients affected in great toe (Can go other places in body, but this is most common.)
other joints: elbow, ankle, wrist, finger, knees

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29
Q

gouty arthritis pain:

A

Instead of the uric acid crystals being excreted through the kidneys, they accumulate in the joints. The crystals are needlelike, causing excruciating pain, usually in the joints of the elbows, wrists, fingers, knees, ankles, and toes, with 75% of patients affected in the great toe.

Buildup in distal AND proximal joints at same time, unlike other kinds of arthritis.

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30
Q

gouty arthritis lab/diagnostics

A
  • Elevated blood levels of uric acid (Most impt test: uric acid level.)
  • Presence of an elevated level does not necessarily mean that gout is the cause (!! Ie if they don’t have symptoms but have elevation, may not be gout. Must be elevated at SAME TIME as s/s to be gout.)
  • X-ray examination of the joint
  • Joint aspiration (Don’t do this. So unnecessary. Just check blood, don’t stick this very painful joint. Not common.)
31
Q

gouty arthritis Management and Health Promotion

A

well balanced, low cal, low purine diet: no organ meats, no red meats.
reduce alcohol or none at all.
antigout meds: 2 meds prescribed. one for baseline, one for flare ups.
but ULTIMATELY all about diet.

32
Q

SLE

A

This and RA are the RLY severe ones. Presentation/causes are different. Ie no rheumatoid factor with SLE.
• Chronic, progressive, inflammatory connective tissue disorder that can cause major body organs and systems to fail.
• Characterized by spontaneous remissions and exacerbations.
• Autoimmune complexes tend to be attracted to the glomeruli of the kidneys. (So most pt with lupus also have kidney problems to the point of kidney failure.)
• most SLE pts have some degree of kidney involvement

33
Q

common issue in pts with SLE?

A

Psychosocial issues common in sle and RA : they both know its chronic, progressive, problems with body image, issues with role performance from chronic fatigue, starts in younger patients.

34
Q

SLE clinical manifestations

A

Systemic so problems in all joints, atrophy, fever (slight elevation in temp and WBC but not huge like infection), fatigue, etc
• Skin involvement : butterfly rash
• Polyarthritis
• Muscle atrophy
• Fever and fatigue
• Renal involvement
• Pleural effusions
• Percarditis(Probs most common after kidneys)
• Raynauds phenomenon (Because it affects connective tissue ^ , affects circulation)

35
Q

SLE outcomes/evaluation

A

outcome:
Adaptation, reduction of complications

evaluation:
Patient understands: 
Physiological changes, therapeutic regimen
Coping strategies 
Preventing complications 
Reducing medication side effects
36
Q

SLE interventions

A
  • Reducing injuries
  • Controlling discomfort
  • Rest and activity: Don’t eliminate activity, but rest during exacerbation.
  • Skin integrity: Well lubricated, protect from sun, from cold.
  • Reducing oronasopharyngeal ulcers

Splints for exacerbation, prevent injury, educate on fall risk because of fatigue and weakness, educate on modulating activity, controlling discomfort, etc

37
Q

SLE pt teaching

A
  • improve diet: Want them to have nutrient dense food but be careful with high protein because of kidney involvement.
  • control fluid volume
  • reduce anxiety
  • adhere to med regimen: sometimes they’ll use nsaids or steroids if inflammation rly bad and immunosuppressants and stuff like that.
38
Q

fractures healing cascade

A
  • Hematoma forms at site
  • Clotting factors form fibrin meshwork
    • Granulation tissue replaces clot
    • Cartilage collar and bridge connect bone fragments
  • Callus is calcified
  • Mature bone replaces callus (ossification)
  • Consolidation and remodeling
39
Q

how strong is bone after healing from a fx?

A

After fx, that area of bone is always gonna be weaker. Higher risk for future fx.

40
Q

lab tests for lupus?

A

pg 1583

41
Q

open vs closed fx:

A

Open fracture:
• Tear in soft tissue, bone exposed to outside
• Potential for contamination
• Higher morbidity and mortality
Key: goes thru skin. Higher risk for infection! And ESPECIALLY infection that goes right into the bone! Bone infections take lot longer and lot harder to heal. Can lead to sepsis.

Closed fracture:
No opening
Much lower risk for infection, mortality, morbidity.

42
Q

fx tx

A
  • Fixation and/or union must occur within 6-8 hrs. (Wanna align the bone. Use traction to pull the tight muscles to allow for union.)
  • Cast (watch for swelling, no access to soft tissues).
  • Splint or brace: secured with straps or ba
  • Traction (Useful for fx in extremity to keep the two broken ends unionized, prevent muscle from holding it in misalignment.)
  • External fixation
  • ORIF (hip fx)
  • intramedullary rod
43
Q

make sure of what for cast?

A

Need TWO finger space btwn skin and cast. Teach them to check their CAP REFILL, first thing to do if slow or swelling hold above heart level. If still a problem, go ER to take cast off.

44
Q

complication of fx

A
  • Shock (Much more common in open fx from infection getting in bone: septic shock.)
  • Fat embolism syndrome
  • Venous thromboembolism
  • Infection
  • Ischemic necrosis
  • Fracture blisters, delayed union, nonunion, malunion. (not that common. Would be v early in first 3 days or so in hospital, from the break itself: fluid that gets loose.)
    • Goal to get them to heal united.
45
Q

hip fx patho

A
  • Excessive pressure

* Weakened bone structure

46
Q

hip fx manifestations

A
  • Joint surfaces become rough
  • Pain, swelling, deformity (Pain often higher than where the fx is (in buttock, groin)
  • Discomfort to groin, buttock,
  • Stiffness in morning (One leg longer than other because fx leg has been contractured by muscles. Esp with femoral neck fx.)
  • Increasing pain with activity (Thus difficulty moving because pain)
  • inability to rotate, flex, extend hip
47
Q

Look at pg 1489 r/t hip fx, there’s a pt care plan. Look at cause, s/s, what am I gonna do (this is mostly what am I gonna do)

A

doooo

48
Q

total hip arthroplasty etiology/epidemiology

A

This is for hip REPLACEMENT, NOT for hip FRACTURE.
Usually for wear and tear or damage to joint itself, not for fx. Too much damage to bone cartilage, must be replaced.
Can replace joint surface or just ball, depends on pt needs. All involve replacing the ball (femoral head) tho.
Does not involve a true intermedullary rod, but rod must go down into femur.

• Osteoarthritis 
Rheumatoid arthritis pelvis 
• Trauma-related arthritis 
       • Joint damage 
       • Inflammation
49
Q

THA surgical management

A
  • Removal of femoral head
  • Creation of post-hole in femur for implant
  • Repair and placement of head and stem
  • Artificial joint may need replacement in 15-20 yrs, so always wanna use surgery as last resort if possible or delay much as possible since there is chance they will need a second one after 20 ish yrs if they’re young ish (50). There’s also increased risk for surgery for older pt
50
Q

THA nrsg management/discharge planning

A
Initial assessment:
Hypovolemia, bleeding complications, hypoxemia, neurovascular compromise (Rbc, h/h since ortho surgeries are very bloody. Good neuro/circulation checks particularly in extremity where surgery was: look for paresthesia, *6 p'S : pain, pulses for circulation, paresthesias (nerve impingement), paralysis (wiggle toes), pallor (sign of dec circulation), polar (temperature: low then dec circulation)) 
Hip precautions 
• Prevent hip from dislocating 
Home modifications 

Collab management/health promotion

They’re gonna be dong rehab even at home. Oftentimes PT will check their home for dangers. Tell them precautions: no throw rugs, etc same things for any fall risk pt is super important

Hip replacement is usually ORIF: open pt, do fixation inside, then close pt.

Assess for hypovolemia: decreased CO and other things.

51
Q

complication of THA:

A

Replacing hip makes joint very weak. Chance of dislocation is high and a big problem. Don’t want hip replacement pt to cross leg in any way past midline. So fresh out of surgery they have abduction/wedge pillows strapped to each leg. After couple days, remind them at home to not even cross ankles in bed. Don’t let hips flex greater than 90 degrees either. A high john at home will help them not flex. Teach them to wear slide in shoes or get assistance cause can’t bend down, maybe get a grabber. Hip precautions will be posted on BB as well as OA vs RA.

52
Q

TKR

A

Replace BOTH sides, back and front of knee.
Patients with progressive arthritis, trauma, rare diseases that damage joint
Most common in United States: severe osteoarthritis
• Progressively increasing pain/stiffness

53
Q

diagnostic test for TKR

A

MRI

54
Q

TKR goal

A

Common, but still difficult to recover from. Goal is to resume normal activity.
Recovery takes significant time: bone must grow around this

55
Q

monitor what for tkr

A

Look for hypovolemia here as well since it still ortho, still bloody.

56
Q

TKR medical management

A

• Arthroplasty improves knee motion
-Allows patient to resume normal activities
• Knee joint is resurfaced with prosthetics
-Lower condyles of femur
-top surface of tibia
-back surface of kneecap

57
Q

TKR nrsg management

A

Early mobilization

Continuous passive motion (CPM): This is for nurse to use, not pt for amount of rotation and speed. This is ordered by the surgeon. It’s changed every day for little more movement every day. Goal: 90 degrees. Usually happens in outpatient rehab, not in hospital.

Pain controlled with medication

Hospital stay 3 to 7 days (Usually go next to rehab hospital for PT multiple times a day.)

58
Q

TKR nrsg discharge goals

A

bend knee 90 degrees, walk with crutches or walker

59
Q

• Look at flyer for cane/crutches, answer questions for pt teaching for cane/crutches

A

look

60
Q

most impt thing for TKR

A

Biggest thing is doing rOM of knee so they don’t lose the rOM and not get contracture. If they can do it themselves that’s what we want them to do. Sometimes we can use CPM, while sleeping or in bed to do activity for them. But it a backup, not primary because it can cause problems: theres a large stand, uncofmfortable for pt in back or on buttock or groin area. More importanly, ther’s probs with alignment: if it’s not perfectly aligned in bed with the pt, its gonna misalign pt hips.

61
Q

nrsg management for ortho pt

A
• Neurovascular assessment: systematic
General appearance 
Pulse strength 
Skin turgor 
Capillary refill testing 
Sensory and motor assessment 
Motor strength testing (Done more by PT. order comes from surgeon, but done by PT)

weight bearing status: from non to full weight bearing
Ordered by surgeon, PT done by PT.

62
Q

nrsg management for ortho pt

A
• Mobility 
Assistive devices: 
Crutches 
Wheelchairs 
Walkers 
Canes 
Reachers 
Sitting down
63
Q

complications of MS trauma/surgery

A
Venous thromboembolism 
Fat embolism syndrome 
Complex regional pain 
Pressure ulcers 
Osteomyelitis 
Hardware infection
Compartment Syndrome
64
Q
HOW DO YOU ADDRESS:
Venous thromboembolism 
Fat embolism syndrome 
Complex regional pain 
Pressure ulcers 
Osteomyelitis 
Hardware infection
Compartment Syndrome
A

iono

65
Q

VTE contributing fx, s/s

A

Virchow’s triad:
Stasis, vessel wall injury, hypercoaguability

Symptoms: 
Chest pain 
Shortness of breath 
Decreased sensorium 
Pink frothy sputum 
Tachycardia 
Tachypnea
66
Q

DVT

A
DVT: Blood clot in venous circulatory system 
Prophylaxis: 
• Heparin 
• Antiembolism stockings 
• Sequential compression devices
67
Q

pulm embolism

A

Pulmonary embolism (PE): Blood clot that travels through heart to pulm a.

  • obstructs circulation
  • PE as result of DVT: know how to recognize it. Know it’s a med emergency. Obviously call surgeon, then no activity, give pt meds to break down the clot or at least to decrease the clot from getting worse (same with like dvt treatment)
68
Q

seriuos complication of PE?

A

pneumonia

69
Q

fat embolism, s/s, complication

A
  • Fat globules from long-bone fractures enter circulatory system
  • Can produce multi- organ failure
Symptoms: 
Respiratory failure 
Neurological dysfunction 
Petechial rash
Same s/s as PE BUTTT because it's fat and thick and can get in way, might see other problems in other areas. But classic triad is hypoxia, dyspnea, and tachycardia. So when we know pt has had long bone fx and see this classic triad altogether, we know this pt probably starting to have fat embolism and action needs to be taken right.
70
Q

prevent fat embolism on med surg

A
  • Close monitoring first 4-12 hrs
  • Incentive spirometer
  • Patient assisted out of bed as soon as possible
  • Monitoring for PNA
71
Q

fat embolism tx

A

intubation, mechanical ventilation with PEEP

supportive care

72
Q

complex regional pain syndrome

A
  • Reflex sympathetic dystrophy: Reflexive maladaptation to untreated pain: pain becomes more diffuse over greater area, very very hard to treat.
  • Diffuse persistent pain
  • Vasomotor, trophic, and bony changes and limited mobility after local injury
  • Refer to physical therapy and pain clinic: NEEDS referral to pain management. This is v serious, v dificult to treat. Must be addressed early. This why appropriate pain management is impt.
73
Q

pressure ulcers prevention

A
Preventive measures: 
• Keeping heels off bed 
• Padding bony prominences 
• Repositioning patient every 2h
• Frequent skin assessment 
• Adequate nutrition, hydration
• Keeping skin clean, dry
74
Q

hardware infection, tx

A

• Late complication

Treatment
• Remove hardware
• Impact patient mobility, pain, age
• Neurovascular injury, deformity