Week 3 Flashcards

(152 cards)

1
Q

Degenerative Disc Disease

A

Back pain is one of the most common health problems in Australia with most people experiencing back pain, specifically lower back pain, at some stage during their life.

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1
Q

Upper Back Pain

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Upper back pain is a discomfort felt from the neck to the thoracic region, often resistant to injury. Risks include sedentary lifestyle, obesity, stress, smoking, pregnancy, prior injuries, and frequent heavy lifting. Causes include herniation of discs, ligament injuries, muscle overuse, osteoarthritis, and kyphosis.

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2
Q

Lower Back Pain [MOST COMMON]

A

Lumbar pain, a common issue due to its high-risk nerve roots and flexibility, can be caused by factors like lumbar sprain, instability, osteoarthritis, degenerative disc disease, or herniation.

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3
Q

Acute Back Pain

A

Back pain lasting less than 4 weeks, primarily caused by spinal stress, typically begins within 24 hours due to increased pressure on the nerve by the intervertebral disc or muscle spasm.

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4
Q

Chronic (persistent) Back Pain

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Back pain lasting over 3 months or repeated incapacitating events, worsening progressively, difficult to identify cause, may be due to previous injury, chronic strain, muscles, congenital abnormalities, or degenerative disorders.

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5
Q

Degenerative Disc Disease (DDD)

A

Normally, intervertebral discs separate the vertebrae of the spine. They provide shock absorption, allow range of movement, and protect our joints.
DDD occurs as a result of the normal aging process combined with the deterioration and herniation of the intervertebral discs. DDD can involve either the cervical, thoracic, and/or lumbar spinal regions.

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6
Q

Causes (DDD)

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A structural degeneration of the area will eventually lead to DDD

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7
Q

Risk Factors (DDD)

A
  • Advancing age → this is the greatest risk
  • Family history / genetics
  • Excessive strain → frequent heavy lifting, repetitive movement
  • Sedentary lifestyle, prolonged sitting, poor posture
  • Smoking
  • Obesity
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8
Q

(DDD)- Diagnosis is made with a combination of the following list:

A
  1. Past medical / surgical history
  2. Clinical Presentation
  3. Imaging
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9
Q

(DDD)- Complications

A
  • Chronic debilitating pain
  • Incontinence
  • Limb weakness
  • Altered limb sensation
  • Herniated disc/s
  • Osteoarthritis
  • Bone spurs
  • Reduced mobility
  • Spinal canal / cord compression
  • Spinal stenosis
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10
Q

Treatment- DDD

A
  • supportive care
  • surgery (last option)
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11
Q

PATHOPHYSIOLOGY-DDD

A

The nucleus pulposus, the gel-like center of the disc, shrinks, limiting its ability to absorb and distribute pressure loads. This pressure is transferred to the annulus, deteriorating the structure. This results in a herniated disc, which places pressure on nearby nerves, leading to clinical manifestations like radiculopathy and altered limb sensation. press against these nerves (pinched nerve) and clinical manifestations occur such as radiculopathy, altered limb sensation, etc.

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12
Q

Herniated Disc

A

Is a condition that occurs when the spinal intervertebral disc bulges out between the vertebrae. Commonly seen between L4 - L5, L5 - S1, C5 - C6, C6 - C7. This below image demonstrates the different types of disc degeneration.

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13
Q

Back pain can be classified as:

A
  1. Localised → pain occurs when area is palpated
  2. Diffuse → pain is spread over a large area, generated from deep tissue
  3. Radicular → irritation of the nerve root, often caused by a herniated disc, eg) sciatica
  4. Referred → pain occurs in one area but originates in another, eg) referred pain from kidneys, abdomen, bladder, ovaries, etc
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14
Q

CLINICAL MANIFESTATIONS- DDD

A
  • Radiculopathy
  • Spinal instability
  • Altered lower limb sensation
  • Decreased lower limb motor function
  • Loss of spinal flexibility
  • Bone spurs
  • Muscle spasms / tension
  • Spinal deformity
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15
Q

What is Osteoporosis?

A

Osteoporosis is a type of metabolic bone disease which is characterised by abnormal bone structure including:
○ Decreased bone density
○ Loss of structural integrity of trabecular (spongy) bone
○ Cortical (compact) bone becomes weaker, thinner, and more porous

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16
Q

What risk factors exist that increase your chances of developing Osteoporosis?

A
  • Genetics → predisposed to low bone mass
  • Advancing age → > 65 years especially with the addition of any endocrine disorders or malignancies, hormonal changes (i.e. in oestrogen, calcitonin, and testosterone) which inhibit bone loss normally
  • Gender → increased risk for women (i.e. 1 in 2 women develop osteoporosis as opposed to 1 in 3 men)
  • Nutritional status → poor intake of calcium and essential vitamins such as Vitamin D, excessive sodium, low magnesium, high caffeine intake: all contribute to a decreased nutrient concentration necessary for bone remodelling
  • Physical exercise → bones need a level of ‘stress’ for bone maintenance
  • Decreased sun exposure → further contributing to Vitamin D loss / deficiency
  • Lifestyle choices → caffeine intake, smoking, excessive alcohol consumption all reduce osteogenesis in bone remodelling
  • Medications → corticosteroids, heparin, thyroid hormone therapy, aluminium containing antacids all affect calcium absorption and its metabolism
  • Comorbidities → obesity, anorexia nervosa, hyperthyroidism, kidney failure all affect calcium absorption and metabolism
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17
Q

What are the different types of Osteoporosis?

A
  1. Generalised → osteoporosis involving major portions of the axial skeleton
  2. Regional → osteoporosis involving one segment of the appendicular skeleton
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18
Q

Diseases associated with Osteoporosis

A

○ Inflammatory Bowel Disease (IBD)
○ Intestinal malabsorption
○ Kidney disease
○ Rheumatoid arthritis
○ Diabetes Mellitus
○ Cirrhosis of the liver (particularly if secondary to alcoholism)
○ Hyperthyroidism
○ Hypogonadism

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19
Q

Diagnosis- Osteoporosis

A

Osteoporosis is a progressive disease and diagnosis can be made on:
* Past medical history
* Clinical presentation and recently experienced clinical manifestations
* Investigations

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20
Q

Investigations- Osteoporosis

A

Osteoporosis can be undetected on routine radiographs until 25-40% demineralisation occurs, causing radiolucency to bones. Diagnostic tests include dual-energy x-ray absorptiometry (DEXA) scan, pathology/laboratory results, other x-rays, and bone mineral density (BMD) to determine fracture risk. Reductions in T-score double the fracture risk.

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21
Q

Complications arising from Osteoporosis

A
  • Disability
    • Pathological fractures
      ○ Especially in the thoracic and
      lumbar spine, neck,
      intertrochanteric region of the
      femur and wrists
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22
Q

Can we prevent Osteoporosis?

A
  • Lifestyle modification
    ○ Balanced diet across the
    lifespan including high calcium,
    vitamin D, use of calcium
    supplements that contain
    Vitamin C
    ○ Regular weight-bearing exercises
    to improve bone mineral density
    (BMD)
    ○ Avoid excessive alcohol intake
    ○ Smoking cessation
    ○ Adequate sun exposure
    ○ Medical advice regarding
    medications and management
    of comorbidities
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23
Q

Treatmen- osteoporosis

A

The aim of treatment is outlined below, including some nursing considerations:
1. Slow down the rate of calcium and bone loss
2. Prevent further deterioration

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24
PATHOPHYSIOLOGY- osteoporosis
Here are some useful definitions to support your understanding of the pathophysiology to follow: 1. Bone Remodelling is formation and resorption 2. Bone Formation is completed by osteoblasts ○ Osteoblasts are bone building cells ○ Number of cells are controlled by hormone levels, cytokines, and other chemical messengers 3. Bone Resorption is completed by osteoclasts ○ Osteoclasts destroy bone cells
25
CLINICAL MANIFESTATIONS- osteoporosis
Most common clinical manifestations include: * Joint and bone pain * Bone deformities * Fractures * Kyphosis * Diminished height * Low energy, fatigue Rare clinical manifestations include: * Fat embolism* * Pulmonary embolism * Pneumonia * Haemorrhage
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Arthritis
Arthritis is an inflammatory joint disease that affects more than 15% of the population. Arthritis rates increase with age and majority of diagnoses are in women over 75 years of age.
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RISK FACTORS- Arthritis
Non-modifiable 1. Advanced age 2. Stressful environment, low socioeconomic areas 3. Genetics → family history of arthritic diseases increases your chances 4. Existing endocrine disorders → electrolyte and hormonal imbalances, particularly chronic, decrease bone / joint stability Modifiable 1. Occupation → load-bearing, heavy-lifting jobs increases your chances 2. Obesity 3. Smoking 4. Excessive alcohol intake 5. Poor diet 6. Sedentary lifestyle
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TYPES OF ARTHRITIS CAUSES
Infectious Cause ○ Invasion of the joint by bacteria, mycoplasma, viruses, fungi, protozoa which causes inflammation ○ Invasion is introduced through ○ An example of this 'infective arthritis' is called septic arthritis (see later in this module) Non-Infectious Cause ○ Under this banner there are two causes of developing arthritis without an infectious cause 1. Inappropriate immune response → rheumatoid arthritis, psoriatic arthritis 2. Deposition of urate crystals in the synovial fluid → gout
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Osteoarthritis (OA) Overview
A chronic, slow, and progressive, non-inflammatory disorder of a synovial joint → cartilage destruction and joint degeneration.
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Classifications of Osteoarthritis
* Primary / secondary * Localised / generalised * Early / moderate / advanced * Stages of OA
31
Causes- OA
OA is usually caused by a known event or condition: * Post-inflammation disorders ○ Rheumatoid arthritis (can actually cause OA) ○ Septic joint * Trauma ○ Fracture / dislocation of a joint ○ Ligament / meniscus injury ○ Cumulative occupation or recreational trauma * Mechanical stress ○ Repeated mechanical activity on the same joint * Inflammation ○ Release of enzymes in response to local inflammation can affect cartilage integrity * Anatomical or Bony disorders ○ Hip dysplasia, avascular necrosis, Paget's disease * Metabolic disorders ○ Calcium crystal deposition (gout), acromegaly, Wilson's disease * Menopause ○ Due to oestrogen reduction
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Risk Factors- OA
Aside from the risk factors listed in the Arthritis Overview, the following list provides more information that links directly to OA: * Obesity puts increased stress on joints such as the hip and knee contributing to OA, as well as limited exercise * Previous joint damage to trauma * Anatomical deformity like malalignment of joints * Genetic predisposition like congenital hip dysplasia, biochemical abnormalities in collagen and bone formation which damages the structure of cartilage
33
Pathophysiology of OA
OA is a complex condition characterized by articular cartilage degradation, bone stiffening, and synovial inflammation. The collagen matrix becomes disorganized, and proteoglycan content is lost. The pathophysiology follows a formula: Risk Factor → Cause → Joint changes occur → Clinical Manifestations. Symptoms include progressive cartilage loss, dull, yellow, granular, soft, less elastic cartilage, fissuring, osteophytosis, synovitis, and thickening of joint capsules due to contact between exposed surfaces.
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Clinical Manifestations- OA
* Pain * Joint stiffness * Crepitus with movement * Asymmetry of joints * Joint effusions * Joint deformity * Functional impairment
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Rheumatoid Arthritis (RA) Overview
A chronic systemic, autoimmune disease where there is inflammation of the connective tissue in synovial joints. * Affects multiple joints, but usually bilaterally eg) if your left hand is effected, likely your right hand will be too * Characterised by periods of remission with exacerbations * Prevalence increases with age and is more common in women * Worse in colder climates * Most commonly affects the fingers, wrists, elbows, feet, ankles, and knees * Can also affect other tissues in the body such as lungs, heart, and eyes
36
Classifications of RA
RA can be classified according to: * Number of joints involved * Serology inflammatory markers, specifically C-Reactive Protein (CRP) and erythrocyte sedimentation rate (ESR) * Duration of symptoms
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Causes- RA
While the main cause is unknown, it is likely linked with genetics and environmental triggers interactive with inflammatory mediators. Such as, a positive family history for RA means you would be likely to develop RA, another example is long-term smoking is seen to be linked to developing RA.
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Risk Factors- RA
* Advancing age → affects more people in their 60's and above * Smoking * Gender → affects more females than males * History of live births * Obesity * Stress * Genetics * Infection * Surgery
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Pathophysiology- RA
Affects the synovial membrane first, before spreading to articular cartilage, fibrous joint capsule, and surrounding ligaments and tendons.
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Inflammatory Phase- RA
* There is an initial immune response to an antigen which triggers the formation of abnormal immunoglobulin G (IgG) * Autoantibodies called rheumatoid factor (RF) develop which combine with IgG to form immune complexes * Inflammatory response initiates phagocytes (specifically neutrophils, macrophages) to ingest these immune complexes * A release of enzymes from this reaction causes cartilage breakdown and thickening of synovial lining * T-helper cells (lymphocytes) are activated which produces more RF * Synovium continues digesting nearby cartilage which further stimulates the inflammatory response
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Secondary Phase- RA
As a result of this ongoing cycle of the inflammatory response: * Synovial membrane thickens which increases the pressure on surrounding vessels, compromising blood supply and increases cell metabolism * Hypoxaemia and metabolic acidosis result which stimulates the release of enzymes from synovial cells into surrounding tissue * Tissues breakdown, articular cartilage erodes, ligaments / tendons are inflamed * Haemorrhage and coagulation of the synovial membrane, fibrin deposits on synovial membrane and in synovial fluid * This results in granulation and scar tissue formation where the clinical manifestations of immobilisation and joint stiffness are seen
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Initial Clinical Manifestations- RA
* Fever * Fatigue * Malaise * Rash * Anorexia * Weight loss * Generalised aching and stiffness * Spleen enlargement * Lymphadenopathy
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Subsequent clinical manifestations- RA
* Joint pain and tenderness → caused by pressure in the joint, this type of pain increases with movement * Joint stiffness → especially following activity * Joints become warm-to-touch * Joints swell and even deform (see images below) * Loss of dexterity → difficulty grasping objects * Disability * Fever, malaise, anorexia continue * Elevated serum leukocyte levels * Elevated serum fibrinogen levels
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Complications- RA
RA increases the risk of developing: * Osteoporosis (OA) * Rheumatoid nodules * Dry eyes / mouth * Infections * Carpal Tunnel Syndrome * Lung Diseases * Cardiac Diseases such as premature heart disease
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Gout Overview
Gout is a complex, recurring, inflammatory arthritis. * A metabolic disorder characterised by an acute exacerbation with long periods of remission and can progress to chronic gout * Disruption of the body's control of uric acid production or excretion ○ Resulting in high levels of serum uric acid * Severity can range from infrequent, mild episodes to multiple severe exacerbations (> 12 per year) * Affects men more than women, with a peak affected age between 40 - 60 years for men, but later years for women
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Primary Classification of Gout
○ 90% of Gout cases ○ Hereditary origin ○ Dysfunction of purine metabolism causing overproduction or retention of uric acid
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Secondary Classification of Gout
Gout develops as a result of other risks factors
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Acute Classification of Gout
○ Sudden onset of symptoms usually in the peripheral joints ○ Symptoms usually occur at night, peaking within several hours and resolving in 2 - 10 days (regardless of being treated or untreated) ○ 1 - 4 joints involved § Exacerbation of great toe is most common, up to 50% of cases → the great toe is prone to chronic strains due to walking § Other joints involved are wrists, fingers, elbows, knees, ankles, mid-tarsals, olecranon bursae
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Chronic Classification of Gout
○ Multiple joints involved ○ Visible deposits of sodium urate crystals called tophi (see image below) § Can be found in synovium, subchondral bone, olecranon bursae, vertebrae, along tendons, skin, and cartilage § The ear helix is the most common area for tophi to be noted
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Gout is caused by defects in uric acid metabolism attributed to one or more of the following:
1. Increase in uric acid production → enough to crystallise 2. Decrease in uric acid excretion 3. Increase in consumption of food / drinks containing high levels of purine eg) seafood, shellfish, alcohol, sugary drinks
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Risk Factors- Gout
* Medications * Obesity * Systemic infection * Trauma → Surgery or Injury * Anorexia Nervosa → prolonged starvation * Post-menopausal women * Comorbidities * Excessive alcohol consumption → increases production of keto acids → inhibits uric acid excretion * Diet → high consumption in purine-rich foods can trigger an exacerbation of gout → eg) seafood, shellfish, spinach, beef, pork, lentils * Exposure to lead
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What is Purine?
○ Purines are natural chemical compounds found in food and produced in the body. ○ Examples include adenine and guanine ○ Used for the production of ATP and nucleic acids ○ Uric acid is the major end produce of purine metabolism → excreted by the kidneys (see image below) ○ Urate is filtered at the glomerulus → reabsorbed or excreted in urine
53
Those with a history of gout will have either:
1. Accelerated purine synthesis OR 2. Breakdown or poor uric acid secretion in the kidneys
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Pathophysiology is closely related to the causes:
* One or more of the aforementioned causes in conjunction with increased urate reabsorption OR sluggish urate excretion by the kidneys means monosodium urate crystals are deposited in renal interstitial tissues * These crystals impair urine flow, these crystals can also accumulate in connective tissues eg) ear lobes, kidneys, heart, joints, synovial membranes and cause an inflammatory response * Neutrophils die and release additional crystals, further damaging the tissue and further inflammation occurs as a result * The exact pathophysiological process of how crystals are deposited in joints and how it then causes gout is unknown, there are however known aggravating mechanisms for crystal deposition
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Aggravating Mechanisms for Crystal Deposition
○ Low body temperature → build up of monosodium urate peripherally as low body temperature reduces solubility of monosodium urate ○ Decreased albumin or glycosaminoglycan levels → decrease urate solubility ○ Changes in ion concentration → enhance urate solubility ○ Changes to pH → enhance urate solubility ○ Trauma → promotes urate crystal precipitation (MOST aggravating mechanism of this list)
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Stages of Crystal Deposition
1. Asymptomatic hyperuricaemia → serum urate is elevated but arthritic symptoms, tophi, and renal complications are not present 2. Acute gouty arthritis → exacerbation of symptoms with elevated serum urate concentration, occurs with sudden or sustained increase in urate levels, can also occur with medications, alcohol, or trauma 3. Tophaceous gout → chronic stage § Occurs as early as 3 years post initial gout episode, or as late as 40 years § Progressive inability to excrete uric acid § Tophi appear in cartilage, synovial membranes, tendons, and soft tissue
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Gout Clinical Manifestations- Acute
* Joint changes ○ Dusky / erythematous appearance ○ Sudden swelling ○ Excruciating pain ○ Hot-to-touch ○ Decreased range of movement * Difficulty weight-bearing * Systemic signs of inflammation ○ Low-grade fever ○ Lymphadenopathy → enlarged, swollen lymph nodes ○ Elevated inflammatory markers (CRP)
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Gout clinical manifestions- chronic
* Lingering joint discomfort * Limited range of movement * Slowly progressive disability * Chronic joint inflammation * Cartilage destruction → OA * Joint deformity
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Gout Complications
* Kidney dysfunction ○ Acute Kidney Injury (AKI) ○ Kidney stones ○ Pyelonephritis * Tophi = grotesque deformities, usually painless, but can lead to additional complications: ○ Large clumps may perforate through the overlying skin causing wound infections ○ Progressive stiffness and movement limitations ○ Persistent aching
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Septic Arthritis Overview
Septic arthritis is an infectious arthritis caused by the invasion of a bacteria into the joint cavity. * Bacteria travels throughout the body in the bloodstream and deposits in any joint cavity ○ This process is referred to as haematogenous seeding * Usually monoarthritic (affecting one joint only) * Large joints most commonly affected → eg) knees (50% of cases), elbows, hips, shoulders * Considered a medical emergency due to the high risk of serious complications
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Causes- Septic Arthritis
* Active infection elsewhere in the body → bacteraemia (bacteria in the bloodstream) ○ eg) Cellulitis, urinary tract infection (UTI), Upper or Lower respiratory tract infection (URTI, LRTI), osteomyelitis, Sexually Transmitted Infection (STI) * Trauma * Surgical incisions and procedures ○ Arthrocentesis, joint injections * IV drug use
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Risk Factors- Septic Arthritis
* Immunocompromise * Recent Infection ○ Cellulitis, skin ulcers, bacteraemia * Medications ○ Corticosteroids, immunosuppressants * Pre-existing joint disease, especially RA * Previous joint replacement or prosthesis * Comorbidities ○ Cardiovascular disease ○ Diabetes Mellitus ○ Cancer ○ HIV ○ Chronic renal failure * Advancing age * IV drug use
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Which Bacteria Cause Septic Arthritis?
○ Staphylococcus aureus (most common: 50% of cases, especially if the line of infection came from IV drug use) ○ Streptococcus haemolyticus ○ Neisseria gonorrhoeae (especially if the line of infection came from an STI) ○ Salmonella
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pathophysiology of septic arthritis
Bacterial colonisation and rapid proliferation in joints can be caused by factors such as vascularized synovial membranes, low fluid conditions, and increased colonization. This leads to joint infection, triggering an acute inflammatory response, with cytokines and interleukins released into joint fluid.
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Clinical Manifestations- Septic Arthritis
* Single joint with severe pain, worse with movement * Poor range of movement * Effusion * Symptoms of inflammation → erythematous and swollen joint, hot-to-touch * Symptoms of infection → fevers, rigors, lethargy, myalgia, tachycardia, weight loss
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Complications- Septic Arthritis
Septic arthritis can cause irreversible cartilage destruction within 8 hours. If left untreated, septic arthritis can progress from a localised infection → septicaemia → sepsis → death (10 - 20% mortality rate). Complications can include: * Unstable vital signs * Increased or uncontrolled pain * Avascular necrosis (see image below) * OA * Osteomyelitis (see image below) * Bony erosion * Fibrous ankylosis (see image below) * Permanent joint dysfunction
66
Psoriatic Arthritis (PsA) Overview
A chronic, immune-mediated inflammatory joint disorder * 1 in 5 affected will have a history of psoriasis ○ Part of a group of joint disorders called seronegative spondyloarthropathy ○ Interrelated multisystem inflammatory disorders which are negative for RA * Can be an oligoarthritis → a chronic, inflammatory arthritis of unknown origin affective <5 joints, with an onset that occurs <6 years of age and lasts for approximately 6 weeks
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What is Psoriasis?
Psoriasis is also a chronic autoimmune disorder characterised by the rapid build up of skin cells that form patches of scaly, itchy, dry skin. ○ These patches will be red or silvery ○ Found mostly on the knees, elbows, torso, and the scalp ○ Some common triggers for psoriasis developing are infections, stress, and cold weather ○ Often considered mild in most sufferers → can range from mild symptoms to rapid and destructive symptoms ○ Typically affects large joints, mostly of the lower extremities, fingers / toes, back / pelvis ○ Affects men and women equally
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Types of PsA
* Symmetric ○ Similar to RA, affecting joints bilaterally at the same time ○ About 50% of PsA patients have this type * Asymmetric ○ Usually more mild in symptoms ○ Affects one side of the body at a time ○ About 30% of PsA patients have this type * Distal ○ Inflammation and stiffness to the ends of the fingers and toes, including nails ○ Causes nail pitting (see image below), white spots, lifting from the nail bed * Spondylitic ○ Pain and stiffness of the spine and neck ○ Affects men more than women * Arthritis Mutilans ○ Most severe form of PsA ○ Deformities of the small joints ○ About 5% of PsA patients have this type
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Causes of PsA
While the main cause is unknown, there is a strong genetic link combined with immune and environmental factors eg) trauma and frequent / certain bacterial infections.
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Risk Factors of PsA
* Having psoriasis * Obesity * Trauma * Smoking * Infections * Stress * Extreme weather
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Pathophysiology of PsA
The pathophysiology of PsA is not fully understood yet. It is, however, a chronic, complex, multifaceted, inflammatory immune-mediated disease characterised by musculoskeletal inflammation. There is an interplay with genetic predisposition, triggering environmental factors and activation of innate and adaptive immune systems.
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Clinical Manifestations of PsA
PsA usually has an insidious, gradual onset which begins with generalised, systemic clinical manifestations: * Joint inflammation → swollen, stiff, painful, erythema, joints are hot-to-touch ○ Interestingly, these symptoms are the worst in the morning * Skin changes → from psoriasis, skin can develop plaques * Ridging and pitting of the nails * Lower back pain * Onycholysis → separation of the nail * Dactylitis → inflammation and swelling of full digits / fingers * Enthesitis → inflammation and pain of point where tendon joins to bone eg) heel
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PsA-Associated Comorbidities
○ Psoriasis ○ Systemic Lupus Erythematosus (SLE), commonly shortened to "Lupus" ○ Crohn's Disease and ulcerative colitis ○ Coronary heart disease ○ Depression ○ Atherosclerosi
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Inflammatory Arthritis
Is a group of diseases that results in joint inflammation, swelling, stiffness, decreased range of movement with potentially disabling clinical manifestations. ○ Less common than osteoarthritis ○ Symptoms worsen with age ○ Can affect a single joint or multiple joints simultaneously ○ Multiple types of inflammatory arthritis, each with a different cause § Wear and tear § Infections § Underlying diseases that might cause: overactive immune response OR a deposit of urate crystals in the synovial fluid
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NURSING ASSESSMENTS of PsA
For patients with musculoskeletal conditions, Primary Assessment, Secondary Assessment and Vital Signs can be completed as part of an admission, start of your shift and/or as clinically indicated. It is a great idea to adopt a 'head-to-toe' approach, see Module 1. Clinical Concepts for more information and the relevant additional readings for further information regarding nursing assessments. * There may be limited variation in the vital signs due to these MSK disorders, regardless of what the patient has presented with, we are particularly looking out for any changes that may be related or indicate a worsening condition. For example: ○ Temperature, changes to blood pressure or heart rate - this could indicate infection as a cause of the symptoms ○ Heart rate or blood pressure increases could indicate pain
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Focused Musculoskeletal System Assessment
* Inspection - general build, muscle configuration and symmetry of joints. Any swelling, nodules, masses, deformity and bilateral discrepancies. * Palpation - with care. Assessing for skin temperature, tenderness, swelling and crepitation. * Motion - Range of movement - passive or active * Strength - flexion and extension, comparing bilaterally. * Measurement - assessing discrepancies in length and/or circumference * Other - posture and gait, use of mobility aids, * Sensation - evaluate dermatomes and reflexes * Some examples include: ○ Straight leg raising test [SUPINE] § If the patient is unable to perform a straight leg raise when lying supine, this may indicate a positive result for degenerative disc disease due to nerve root irritation. ○ Leg raise test [SITTING] § Patient sitting on edge of bed or a chair, without feet touching the floor. Ask the patient to raise one leg at a time, flex their foot at 90° If there is any back pain or leg pain with this action, likely degenerative disc diseas
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Focused Neurovascular System Assessment
* Pain assessment * Falls Risk assessment (*) * Pressure injury risk assessment (*) * Integumentary assessment * Dermatome assessment ○ Assessing for any paraesthesia ○ There are different ways to perform this test too, check your local hospital policy on how best to approach each patient
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NURSING MANAGEMENT of PsA- Non-pharmacological Management
○ Reposition patient ○ Distraction techniques (from the pain) ○ Heat / ice packs (see local hospital policy regarding both products) ○ Assistance with Activities of Daily Living (ADLs) as directed by patient and physiotherapists ○ Where able, encourage light physical activity, use of assistive devices like canes or walkers to improve stability
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NURSING MANAGEMENT of PsA- Initiate pain management plan
○ Nurses are the patient advocates for the joint and bone pain associated with MSK conditions, which is sometimes the only thing that hospitalises our patients. It is important to work with the right interprofessional team (i.e. Pain Management Team) when planning pharmacological pain relief options
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NURSING MANAGEMENT of PsA- Education
○ Explanation of condition and management plan, as inpatient and outpatient ○ Dietary advice: e.g. increase fibre content in diet, increase water consumption - especially for those on opioid analgesics; increase in dietary calcium for patients with osteoporosis, avoiding purines for those with gouty arthritis. ○ Symptoms management ○ Medication Education ○ Lifestyle changes: e.g. weight loss, smoking cessation, minimise alcohol consumption ○ Pain management strategies ○ Promoting knowledge, especially regarding their lifestyle modifications and other modifiable risk factors is important ○ Due to some of the higher risk treatment options, it is our responsibility as nurses to ensure our patient's have the most up-to-date information about the risks involved so they can make informed decisions about their own health
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NURSING MANAGEMENT of PsA- Support
Holistic needs of the patient, including psychosocial, emotional, physical and social
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NURSING MANAGEMENT of PsA- Falls Prevention
○ Practical implications of preventing fractures is limiting the risk of falls when the patient is admitted to hospital ○ Ensure they are within full view of the nursing station, or have a proximity mat, there are many falls prevention strategies ○ It is a good idea to check your ward and your organisations policy on bedside rails
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Musculoskeletal Injuries - Fractures
A fracture is a break in the continuity of a bone and occurs when the force exerted on the bone exceeds what the bone can absorb. * Incidence varies according to individual bones, age, gender ○ With the highest occurrence in young males and the elderly * Severity depends on location and fracture subtype * The average person will experience two fractures in their lifetime * In medical notes, a fracture is often written as '#' eg) Left Femur # * Known in the community as a 'broken bone'
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CLASSIFICATIONS / TYPES OF FRACTURES
The aim of a classification system, particularly for fractures, is to help clinicians: * Organise knowledge * Handover knowledge * Guide treatment * Estimate prognosis * Enhance education / communication to patients and interprofessional team * Improve consistency for all clinicians Fractures can be classified by their: * Location eg) femur fracture * Displacement of fracture lines * Appearance of the limb eg) dinner fork deformity * Which part of the bone is fractured eg) distal leg fracture * Fracture pattern eg) anatomical alignment of bone fragments * Severity of overall injury eg) stable vs unstable
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Main Fracture Categories:
○ Displaced § Bone breaks in two or more parts and shifts so that the ends do not align anymore ○ Non-displaced § Bone breaks either part or all of the way through but does not move and maintains proper alignment ○ Open § Bone breaks through the skin § Bone may recede / remain visible through the skin § Increased risk of deep bone infection ○ Closed § No break / puncture wound through the skin
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Hip Fractures
A hip fracture is a break occurring at the upper third (proximal) of the femur, which extends 5 cm below the lesser trochanter. Commonly referred to as a 'fractured NOF' or #NOF where NOF stands for 'Neck of Femur'. It is estimated that by the age of 90, 33% of all women and 17% of all men will have sustained a #NOF with a large proportion related to osteoporosis and falls. The patient who has sustained a #NOF will frequently have one or more comorbidities (cardiovascular, pulmonary, renal and/or endocrine) potentially exacerbated by age-related factors including weak quadricep muscles, general frailty, medications, and conditions that produce decreased cerebral arterial perfusion.
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HIP FRACTURE CLASSIFICATION
1. Extracapsular → of the trochanteric region 2. Intracapsular → of the NOF ○ This classification has an increased risk of complications due to potential damage to the vascular system that supplies blood to the head and neck of femur ○ If blood supply is compromised, avascular necrosis, or non-union of the femoral head may occur
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HIP FRACTURE COMPLICATIONS
* Up to 25% of patients experiencing at least one episode during the initial stages post-fracture * Delirium can occur due to: ○ Shock ○ Intense pain ○ Hypovolaemia, either from blood loss and/or dehydration ○ Medication ○ Secondary infections * Delirium will lead to decreased function post-fracture and increased mortality / morbidity * To prevent the occurrence of delirium, nurses can use the: ○ Interprofessional Team / holistic approach ○ Adequate pain management § Analgesia § Multi-modal approach § Nerve block ○ Nutritional support ○ Correct electrolyte imbalances ○ Rehydration ○ Minimise delay in treating the fracture ○ Early delirium recognition and escalation using organisational risk assessment checklists
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CAUSES of FRACTURES
* Trauma * Overuse * Pathological where there are underlying diseases processes
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RISK FACTORS of FRACTURES
* Age-related factors ○ Younger population = sustain more trauma-related injuries ○ Older population = muscle deterioration, general frailty * Comorbidities ○ Conditions that produce decreased cerebral arterial perfusion, osteoporosis, diabetes mellitus, rheumatoid arthritis, coeliac disease, inflammatory bowel disease * Lifestyle ○ Smoking, excessive alcohol, obesity all contribute to increasing risk of fractures * Medications ○ Steroids * Family history
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COMPLICATIONS of FRACTURES
Direct * Osteomyelitis → infection in the bone * Delayed, non-union, or malunion of the fracture * Permanent disability → loss of strength, compromised range of movement, uneven limbs * Avascular necrosis Indirect * Soft tissue injury → scarring, infection * Adverse reaction to internal fixation devices * Complex Regional Pain Syndrome (CRPS) * Compartment Syndrome * Rhabdomyolysis * Amputation * Deep Vein Thrombosis (DVT) * Pulmonary embolism * Fat embolism * Sarcoma * Hypovolaemia Shock → Large bone fractures increase this risk eg) femur or pelvis * Death → Can result from damage to underlying organs or vascular structures
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PREVENTION of FRACTURES
* Consume adequate amounts of Calcium and Vitamin D * Lifestyle changes ○ Healthy amounts of exercise ○ Minimise alcohol intake ○ Cease smoking ○ Avoid misadventure ○ Avoid falls, pay attention to surroundings, avoid high risk-taking behaviours * Regular review with GP ○ Bone mineral density tests ○ General wellness ○ Medications to slow bone loss and reduce fracture risks ○ Vision tests
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PATHOPHYSIOLOGY of FRACTURES
* Force exceeds what the bone can absorb (which is bone strength) ○ eg) falling onto an outstretched hand * Normal force is exerted on a bone that has not developed correctly ○ eg) Osteogenesis imperfecta * Normal bone is weakened secondary to deterioration from structural changes ○ eg) Osteoporosis * Normal bone is fatigued secondary to repeated force on a bone ○ eg) Marathon runners Regardless of the list above, all of them share the same fracture pathophysiology: * Periosteum, cortex blood vessels, marrow, and surrounding soft tissue are disrupted * Bleeding occurs from damaged ends of the bone and surrounding soft tissue * Blood loss from fractures can be extreme and life-threatening. Below are some approximate amounts of blood loss: ○ Humerus # → 200 - 300 mLs blood loss ○ Femur # → 500 - 1000 mLs blood loss ○ Pelvis # → 1000 - 1500 mLs blood loss
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Inflammatory Phase [0 - 2 weeks post-fracture]
○ Immediately at the time of fracture, bleeding occurs due to damage of the blood vessels in the cortex, marrow, periosteum, and surrounding tissue ○ Formation of a fracture haematoma between the medullary canal and beneath the periosteum, so the fractured end of the bone seals ○ Damaged blood vessels disrupt oxygen supply resulting in bone tissue death immediately adjacent to the fracture ○ This triggers the inflammatory response: vasodilation, increased permeability, exudation of plasma, infiltration of inflammatory mediators such as leukocytes and mast cells ○ This decalcifies the fractured bone end resulting in the formation of a procallus
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Reparative Phase [2 - 6 weeks post-fracture]
○ A capillary network forms within the haematoma from surrounding soft tissue and the marrow cavity into the fractured area which increases blood flow to the area ○ Phagocytes start 'cleaning up' debris whilst granulation tissue develops ○ Fibroblasts (collagen-forming cells create fibrocartilaginous callus) and osteoblasts (bone-forming cells create bone matrix) create a bridge of spongy bone between the bone ends ○ Osteoblasts migrate inwards to mineralise this new bone resulting in a bone callus
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Remodelling Phase [>6 weeks post-fracture, several months]
○ Gradual spread of the callus with creation of compact and cancellous bone structures (which takes several months, up to 2 years) ○ Osteoclast cells absorb fragments of dead bone tissue and unnecessary callus ○ Finally, this 'new bone' has reformed its internal and external structure
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FACTORS THAT AFFECT BONE HEALING POST-FRACTUR
* Complexity or type of fracture ○ Displacement ○ Comminuted ○ Compound * Genetics can impact healing * Advancing age makes it harder to heal * Lifestyle choices ○ High alcohol consumption ○ Smoking ○ Illicit drug use ○ Medication → steroids are known to inhibit inflammation, bone formation, and delay wound healing slowing everything down ○ Exercise → light, supervised exercise can help with blood flow thus healing but the repetitive movement that caused the fracture in the first place, eg) to continue running on a runners' injury will delay healing ○ Poor nutrition * Endogenous factors ○ Comorbidities ○ Hormones ○ Inflammation / Infection elsewhere in the body or secondary to fracture ○ Blood supply to area * Immobilisation * Internal Fixation Devices.
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HIP FRACTURES- CLINICAL MANIFESTATIONS
* Pain → hip and groin or in the medial side of the knee * Decreased range of movement * Limited ability to weight-bear * Muscle spasms * Change in neurovascular status * The patient is normally most comfortable with their leg slightly flexed in external rotation
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MEDICAL TREATMENT- FRACTURES
* Surgery on fractured bone * Reduction of the fracture * Immobilisation * Traction * Open fractures require additional treatment to prevent infection
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Sprains & Strains
Soft tissues connect, support and surround structures and organs of the body. This can include: * muscle → attached to bone by tendons → made up of fibres that shorten and lengthen to produce movement of a joint * tendon → tough bone of slightly elastic connective tissue that connect muscle to bone. * ligament → strong bands of inelastic connective tissue that connect bone to bone * other soft tissues include fascia, fibrous tissue, blood vessels, nerves, synovial membranes, fat
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Sprains & Strains Injuries
* many activities can result in an injury to soft tissue, including everyday activities such as during ADLs, exercise, sports or even by a direct blow * most common → sports injury * types of injuries include sprains, strains, tendonitis, contusions, bursitis
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SPRAIN
* occur in response to a tear or the stretching of a ligament surrounding a joint * usually results from a traumatic event, such as a fall or an external force that displaces the surrounding joint from it's normal alignment ○ inversion / eversion of the ankle during sport ○ fall after stepping in a hole * can be mild to severe * can occur in any joint ○ most common in ankle (2 million each year), knee, wrist, fingers
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STRAIN
* occurs in reaction to a tear, twist, or excessive stretch of a muscle, its muscle sheath and / or its tendon * usually results from activity involving overexertion (overstretching or over contraction), trauma or repetitive movement ○ lifting an item that is too heavy, commencing exercise without warming up, performing repetitive movements at work * can be mild to severe * mostly occurs in large muscle groups ○ lower back, calf, hamstrings
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DIAGNOSIS- Sprains & Strains
Diagnosis is achieved through taking the patient's history and performing a physical exam. Grouping of subjective and objective data obtained from current clinical presentation, clinical manifestations and physical assessment is key to a clear diagnosis. Imaging: * x-ray to exclude fracture * ultrasound * CT scan * MRI
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RISK FACTORS- Sprains & Strains
* advancing age * obesity * poor physical fitness → sedentary lifestyle * smoking * medications → steroids * poor posture * comorbidities that result in muscle fatigue / tightness / imbalance * not warming up before activity
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COMPLICATIONS- Sprains & Strains
* severe sprains can result in a # → ligament pulls off a fragment of bone from the joint * dislocation * chronic instability * loss of function / strength * chronic pain and swelling * arthritis * muscle atrophy * muscle fibrosis * compartment syndrome
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PREVENTION- Sprains & Strains
* balanced nutrition * maintain a healthy weight * regular exercise * avoid playing sports / exercising when fatigued or in pain * avoid traumatic injuries → be aware of falling hazards * maintain strength * warm up and stretch before exercise / sports * wear good fitting and good quality shoes * wear protective braces / equipment during sports
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MEDICAL MANAGEMENT- Sprains & Strains
Most sprains and strains resolve with conservative management and little intervention. Severe injuries may require surgical intervention if: * There is poor recovery from conservative management and clinical manifestations persist * Severely torn ligament with an unstable joint, for example, anterior cruciate ligament rupture * A complete tear in the muscle and it has become unattached from the bone, for example, severe hamstring in
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PATHOPHYSIOLOGY - SPRAIN
The severity of a sprain is graded according to how badly the ligament has been damaged and whether or not the joint has been made unstable. The joint can become unstable when the damaged ligament is no longer able to give it the normal support: * Grade I - mild stretching of the ligament (only a few fibres torn) without joint instability. * Grade II - partial tear (rupture) of the ligament but without joint instability (or with mild instability). * Grade III - a severe sprain: complete rupture of the ligament with instability of the joint.
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CLINICAL MANIFESTATIONS- Sprains & Strains
Similar signs and symptoms for both sprains and strains: * pain / tenderness * swelling / oedema * ecchymosis (bruising) * loss of function → limited / decreased range of movement, loss of strength * difficulty weight bearing * antalgic gait * contusion * altered sensation with severe oedema * muscle spasms
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NURSING ASSESSMENTS- Sprains & Strains
Patients with a musculoskeletal injuries can either be managed by their GP, or at the Emergency Department. Patients will be either discharged home after simple intervention, or they will be admitted to hospital and may require surgical intervention. Nursing assessment and management of a patient with a fracture will depend on the type of fracture, treatment plan, and the healthcare setting. Regardless of the setting, nursing assessment and management must include a combination of obtaining a thorough history and completion of assessments and observations, prior to implementing nursing interventions.
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Primary Assessment
Obtain brief patient history Obtain subjective and objective information as part of this conversation you have with your patient. You can ask questions relating to: * Are you normally well, do you have any existing illnesses? (Limiting jargon, but what we want to know are their comorbidities) * What was the mechanism of injury today? (How did you do it?) * What was the position of the patient post-injury? (We need this question to rule out other injuries) * Were you alone at the time? (We are identifying whether there were witnesses eg) head strike with accurate history-telling) ○ If not, am I able to ask them what happened as well? * Then document all your clinical findings in this time (which will be your secondary assessment) and review all medical notes regarding their clinical presentation and patient's treatment plan.
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Secondary Assessment
Performed at the start of a shift, for every patient, particularly important to rule out any injuries that may have been missed in the primary assessment. * Can include: general appearance - Looks well vs unwell, comfortable vs any discomfort, skin colour: pale / pallor or redness / flushed face, sometimes patient's can be described as 'grey-looking' (very unwell) Full set of vital signs We are particularly looking out for injury being warm or hot to touch, changes to heart rate and respiratory rate as this could indicate high levels of pain
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Focused Neurovascular Assessment
When assessing your patient's limb, you are obtaining baseline observations which should be performed at admission or the start of your shift so you can compare other findings to this baseline. * Neurovascular observations may need to occur very frequently if there is a risk to the perfusion of a limb. It may be hourly. * Neurovascular observations should be completed post-interventions at higher frequencies, eg) the compression bandage has just been applied to your patient, then your neurovascular observations increase to: ○ 15 minutely for the 1st hour ○ Hourly for the next 3-4 hours
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The 6 P's
- Pain - Paresthesia - Pallor - Paralysis - Polar - Pulses
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NURSING MANAGEMENT FOR SPRAINS & STRAINS Pharmacological
* Simple analgesia including NSAIDs: ○ Paracetamol ○ Ibuprofen § Narcotics are rarely required * Ensure multimodal approach to the management of pain
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NURSING MANAGEMENT FOR SPRAINS & STRAINS Non-pharmacological
* RICE ○ Rest § weight bear as tolerated but avoid sports / exercise for 4-6 weeks § aides to support mobility or non-weight bearing instructions → crutches § splinting → sling, brace, splint ○ Ice § to reduce swelling and decrease pain ○ Compression § crepe bandage § casting may be required for more severe sprains / strains ○ Elevation of extremity * Avoid HARM for first 72 hours ○ Heat → vasodilation will increase pain, bruising and inflammation ○ Alcohol → increases risk of bleeding and swelling → decreases recovery ○ Running → or other activity → may cause further injury only return to activity on medical advice ○ Massage → can increase bleeding and swelling * Education ○ How to manage injury at home ○ Safe use of medicines ○ When to seek additional review / help or support
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NURSING MANAGEMENT FOR FRACTURES
* Managing and relieving pain * Identifying mechanism of injury - Used to determine type and severity of injury and possible complications * Assess clinical Presentation * Improving joint function * Correcting deformity and malalignment * Increase functional capacity * The patient may have X-rays, CT scans, or MRI scans depending on the presentation. Nurses can not order these but may have to assist with transfer and ensure adequate pain relief prior * Assess past medical / surgical history for any comorbidities * Reduce the risk of complications - DVT, chest infection etc * When to seek additional review / help or support * RICE * Open fractures → saturate gauze with normal saline → apply over wound and / or cover with sterile dressing → aseptic technique to reduce risk of contamination and osteomyelitis * Do not attempt to reduce fractures
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NURSING MANAGEMENT FOR FRACTURES Pharmacological
* Paracetamol & NSAIDs * Severe fractures will be managed with opioids once reviewed
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Preoperative Nursing Management of Fractures
* keep the patient NBM until plan of care is finalised by the admitting/treating team * 1/24 vital signs, pain and neurovascular assessments * fluid balance chart * urinary catheter if clinically required → an IDC is routinely inserted when a patient has a #NOF (more so for women than men to reduce need for movement in the immediate postoperative period). However this can increase the risk of a UTI particularly in the elderly. * for # NOF - use pressure relieving mattress to ensure patient comfort and to decrease risk of pressure sores * VTE risk assessment * pharmacological management as directed by orthopaedic team * non-pharmacological management
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Postoperative Nursing Management of a Fractures
* assessment / observation frequency as per all postoperative patients and organisation policy * DVT prophylaxis * Indwelling catheter (IDC) * Mobilisation * FBC * IVC care and assessments * Attend to hygiene needs * Prevention of constipation * Address psychosocial needs (immobility, pain and loss of independence)
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Postoperative nursing care for surgery to manage hip fractures
○ the patient will need to commence mobilising, with full weight-bearing as tolerated, the day after surgery, unless contraindicated § first time out of bed is usually under the guidance from the physiotherapist * pressure area care * removal of catheter 24/24 after surgery
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Logroll
* performed for either hygiene needs or for pressure area care * with # NOF - aim is to avoid internal or external rotation of the hip * analgesics should be administered prior
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Analgesia
Analgesics are commonly used to treat pain, especially the pain associated with musculoskeletal disorders. Some analgesics will be discussed in the 'Introduction to Surgical Nursing' module, please ensure you review the content so that you are familiar with additional analgesics. Here, we will focus on non-opioids and non-steroidal anti-inflammatory medications.
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ANALGESICS NON-OPIOIDS
These medications are considered first-line analgesics for acute pain and are extremely effective for mild to moderate pain * also effective in managing severe pain when used in a multi-modal approach ○ when used as a multi-modal approach, less opioids are required * non-opioids have an analgesic ceiling → administering above upper dose limit will not provide additional analgesia * no tolerance or dependence produced * most are available over-the-counter (OTC) Examples → paracetamol, aspirin, non-steroidal anti-inflammatory agents (NSAIDS) such as ibuprofen
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Paracetamol
Not fully understood but has inhibitory action on central prostaglandin synthesis. not an anti-inflammatory. Anti-pyretic – fever reduction Used for mild to moderate pain Use with caution and reduced doses in patients with liver failure - hepatotoxicity. Patients will require a lower dose. Safe to use in pregnancy and breast feeding. Minimal adverse effects. Increased aminotransferases (liver disorders) Educate re no more than 4 grams (8 500mg tablets) in a 24 hour period. Ensure patients are aware to look out for medications containing paracetamol including cough and cold products.
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Aspirin
Non-selective NSAID, preventing synthesis of prostaglandins. Antipyretic, analgesic, antiplatelet Dosing for analgesic effect is 300-900mg 4-6/24. Avoid using in patients with gout, renal disease and peptic ulcer disease. Contraindicated in severe active bleeding or disease states with increased risk of severe bleeding. Avoid using in children <16, pregnancy and breastfeeding. Nausea, dyspepsia, vomiting, GI ulceration or bleeding, asymptomatic blood loss, increased bleeding time Headache, dizziness, tinnitus (common in high doses). Skin reactions, iron deficiency anaemia, renal impairment, oesophageal ulceration. Educate patients to take with or after food to avoid GI upset. Aspirin can break down rapidly if out of protective packaging so remove immediately prior to taking them. Stop taking aspirin 7 days prior to surgery and some dental procedures after discussion with doctor/dentist. Ensure those on long term therapy are monitored for GI bleeding, renal failure or hepatic dysfunction.
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Non-steroidal Anti-Inflammatory Drugs (NSAID)
Inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX-1 and COX-2. COX-1 – impaired gastric cytoprotection and antiplatelet effects. COX-2 anti-inflammatory and analgesic effect Have little or no effect on COX-a at therapeutic doses – GI adverse effects still occur. Use cautiously in those who are dehydrated, those with asthma and with coagulation disorders. Avoid when possible for those with cardiovascular disease or ^risk factors, Contraindicated in patients with severe heart failure, active peptic ulcer disease, significant renal and hepatic impairment. Seek specialist advice regarding use in pregnancy and breast feeding. Nausea, dyspepsia, GI ulceration or bleeding, ^liver enzymes, diarrhoea Headache, dizziness Salt and fluid retention, hypertension Route and formulation of NSAID does not reduce the risk of GI ulceration. Educate patients to take the lowest effective dose, try topical if appropriate before oral, combine with paracetamol to lower dose required. Consider use of GI protective medication if required to take NSAID for a prolonged period of time.
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Biphosphonates
- Inhibit the resorption of bone by impairing osteoclast function and decreasing osteoclast numbers. - Incorporated into bone matrix where they may continue to act for some months, even after therapy has stopped. - Indicated for OP, Osteogenesis imperfecta, Paget’s disease - Calcium supplements, antacids and other oral medications may decrease absorption - Caution with NSAIDs due to increased risk of gastric irritation/ulceration - Caution with aminoglycosides as they may decrease serum calcium - Abdominal pain, nausea, diarrhoea, flatulence, dysphagia, constipation - Oesophagitis, oesophageal ulcer/erosion - Headache, dizziness, fatigue, malaise - Asymptomatic or symptomatic hypocalcaemia, hypophosphataemia, hypokalaemia - Bone, joint and muscle pain, muscle cramps - Instruct patient to take the medication in the morning on an empty stomach with a full glass of water, not to suck or chew the tablet and remain sitting or standing for at least 30 minutes after taking the medication.
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Calcitonin Salmon
- Inhibits activity of osteoclasts – decreased bone resorption. - Inhibits tubular resorption of calcium – increases calcium excretion. - Treatment of established OP, not prevention. - Contraindicated to those allergic to the preparation. - Nasal dryness and irritation - Nausea - Inflammatory reaction at injection site - Flushing of face and hands - Instruct patient on proper use of IN spray - Instruct patient on how to inject S/C preparation and importance of rotating sites.
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Selective estrogen receptor modulator (SERM)
- Estrogen agonistic effect on bone mass and lipid. - Prevention and treatment of postmenopausal osteoporosis - Contraindicated in patients with history of venous thromboembolism (VTE). - Caution in patients with prolonged immobilisation (^VTE risk) - Caution in patients with or increased risk of heart disease - Contraindicated for pregnant or breast feeding women. - Hot flushes, sweating - Leg cramps - Peripheral oedema - Sleep disorders - VTE - Ensure adequate intake of calcium and vitamin D. - Ensure regular bone marrow density (BMD) screening - Advise patients of the need to stop taking medication 72 hours prior to any prolonged period of immobility – surgery, long distance travelling.
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Romosozumab
- Increases bone formation and decreases bone resorption. - Treatment of OP in postmenopausal women at high risk of fracture. - Treatment of OP in men with high risk of fracture. - Correct serum calcium before commencing treatment. - Avoid in patients with cardiovascular risk factors (MI or stroke in last 12 months) - Injection site reaction - Hypocalcaemia, - Urticaria - Cataract - Cardiovascular events - Ensure calcium and vitamin D status are adequate - Monitor calcium concentration - Treatment is restricted to a total of 12 months after which it is recommended that the patient commence another antiresorptive medication such as a bisphosphonate.
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Teriparatide
- Promotes bone formation and increases BMD - Postmenopausal OP when there is a high risk of fractures and other agents are unsuitable - Primary OP in men with high risk of fractures and other agents are unsuitable - Corticosteroid-induced OP in patients with high risk of fractures. - Contraindicated in people with hyperparathyroidism, skeletal malignancies, hypercalcaemia. - History of skeletal radiation treatment, Paget’s disease - Treatment with alendronate – may decrease effectiveness - Contraindicated in both pregnancy and breastfeeding as no human data. - Nausea - Headaches, dizziness - Muscle cramp, arthralgia - Hyperuricaemia - Injection site reactions - Hypercalcaemia - Allergic reactions - Inform patient of adverse effects to watch out for and inform GP. - Can only be used for a maximum of 24 months. - Ensure adequate intake of calcium and vitamin D - Ensure on completion of treatment that a antiresorptive medication is commenced.
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Nonbiologic DMARDs
Action for RA unsure. - Suppresses inflammation and immune response Contraindicated in serious or untreated infection/ renal disease with CrCl <10ml/min; chronic liver disease; pregnancy and breastfeeding Leucopenia, thrombocytopenia, GI toxicity, malaise, alopecia (reversible) Instruct patient to take medication on the same day each week. Limit alcohol intake as it will increase side effects. Avoid sun exposure, wearing protective clothing and using sunscreen. Patient should take high dose folic acid to reduce GI and hepatic toxicity. Instruct patient to take medication with food to reduce GI upset and warn that urine may become orange.
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Sulfasalazine
- Action for RA unsure. - anti-inflammatory, immunosuppressant Use with caution in renal and hepatic impairment. Safe to use during pregnancy and breastfeeding. Contraindicated if maculopathy is present and if allergic to sulpha medications. Use with caution in patients with diabetes as it can reduce HbA1C resulting in severe hypoglycaemia. Vomiting, diarrhoea, pruritis, rash, urticaria, headache Avoid sun exposure, wearing protective clothing and using sunscreen. Patient should take high dose folic acid to reduce GI and hepatic toxicity. Instruct patient to take medication with food to reduce GI upset and warn that urine may become orange.
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Hydroxychloroquine
Action for RA unsure. Often combined with methotrexate and may improve long-term outcomes. Use with caution in children and those with renal impairment. Cautious use during pregnancy and breastfeeding. Retinal damage, rash, GI upset Instruct patient to take medication with food to reduce GI upset. Inform patient of side effects and the importance of monitoring vision. Monitor renal and hepatic function and full blood count
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Cyclosporine
Immunosuppressant Used as a last resort for severe, progressive RA not responding to safer DMARDs. Contraindicated in uncontrolled hypertension, malignancy, renal impairment. Adjust dose due to increased drug clearance for children. Seek specialist advice in pregnancy and breastfeeding. Gingival hyperplasia, hirsutism Nephrotoxicity, hypertension, hypercholesterolaemia, neurotoxicity and more. For IV – administer as slow IV infusion with a glass bottle and non-PVC giving set. Instruct patients to swallow tablets whole and 12 hours apart at the same time each day. Ensure good oral hygiene is maintained. Avoid grapefruit as it may interact with the medication. Avoid sun exposure and wear protective clothing and sunscreen.
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Tumor Necrosis Factor (TNF) antagonists
Bind to TNF alpha and inhibits its activity, anti-inflammatory, immunosuppressant Used for both RA and psoriatic arthritis to reduce symptoms and slow progression of joint damage. Contraindicated for patients with MS, heart failure, concomitantly with other immunosuppressant medications, serious and untreated infections, pregnancy Seek specialist information if breastfeeding. - Nausea, weakness, flu-like syndrome - Allergy, hyperlipidaemia - infections, injection site reactions - Rash, itch - headache Educate patient regarding observing for signs of persistent fever, infection, bruising or bleeding.
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B-lymphocyte-depleting agents
Suppresses immune response and inflammation by reducing T cell activation and resulting cytokine production. Monitor patients with cardiac and respiratory disease closely Avoid combining with other similar medications. Avoid in those who are pregnant or breastfeeding. Infusion-related reactions including fever, chills/rigors, nausea, vomiting, urticaria, itch, headache, bronchospasm, dyspnoea, angioedema, rhinitis, hypotension Infections, neutropenia, lymphopaenia. Educate patient regarding observing for signs of infusion-related reactions. Ensure ongoing monitoring of FBC.
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T-cell Activation inhibitors
Reduction of cytokine production hence inflammation Normally used in conjunction with methotrexate Avoid combining with other similar medications. Use cautiously in those with COPD. Contraindicated if serous or untreated infection present. Seek specialist advice if patient pregnant or breastfeeding. Infections Headache, dizziness Educate patient regarding observing for signs of infusion-related reactions. Ensure ongoing monitoring of FBC, ALT, AST and creatinine.
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Interleukin-6 Receptor Antagonist
Reduction of cytokine production hence inflammation Normally used in conjunction with methotrexate Use cautiously in patients with neutropenia and thrombocytopaenia or with a history of gastrointestinal (GI)ulceration. Contraindicated in the presence of serious or untreated infection. Seek specialist advice if patient pregnant or breastfeeding. Infections, neutropenia, increased liver enzymes Gastritis, mouth ulcers, ^lipids Hypertension Infusion-related reactions, rash, itch, headache, dizziness GI perforation, thrombocytopenia Educate patient regarding observing for signs of infusion-related reactions as well as adverse effects. Ensure FBC and liver functions are monitored regularly.
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Interleukin-1 Receptor Antagonists
Reduction of cytokine production hence inflammation Normally used in conjunction with methotrexate Use cautiously in patients with neutropenia. Contraindicated in the presence of serious or untreated infection. Seek specialist advice if patient pregnant or breastfeeding. Injection site reactions Headache Serious infections, neutropenia, thrombocytopenia, ^cholesterol Educate patient regarding importance of dosing at the same time each day and to rotate injection sites. Educate patient regarding signs and symptoms of injection site reactions and infection and to report them immediately to their doctor.
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Uric acid production reduction
Inhibits xanthine oxidase which promotes the conversion of xanthine to urate. Used to treat chronic gout. Avoid using in those taking azathioprine/mercaptopurine or reduce dosage. Use lower doses in those with renal impairment. Seek specialist advice in pregnancy. Considered safe with breastfeeding. Gouty flare up, raised liver enzymes, oedema, rash Arthralgia, dizziness, drowsiness, taste disturbance, abdominal pain Medication should not be commenced during an acute gouty attack. Commence low dosing to avoid flare ups. Educate patient to take medication with or after food to reduce GI upset. Inform patient that there may be an increase in flare-ups for the first 6 months but to continue to take medication as these will reduce and tophi will disappear. Educate patient on importance of maintaining a high fluid intake but avoiding high purine products such as aspirin and fish. Ensure renal and liver function are monitored and medication altered according to results.
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Increased uric acid secretion
Blocks renal tubular reabsorption of uric acid. Contraindicated in those with a history of blood dyscrasias. Avoid during an acute flare-up of gout. Seek specialist information for patients who are pregnant or breastfeeding. Rash, nausea, vomiting Headache, dizziness, flushing, sore gums, alopecia, urinary frequency, uric acid kidney stones. Educate patient to take medication with food to reduce GI upset and to drink lots of fluids to prevent kidney stones. Tell the patient that flare-ups may initially increase in the first few months but that this will improve. Monitoring of urate levels, renal function and complete blood count undertaken regularly.
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Colchine
Inhibits leucocyte migration in gouty joints thereby decreasing inflammatory response to urate crystals. Whilst not an analgesic, provides relief of pain in acute gout. Used in lower doses than previously prescribed with similar results and fewer side effects. Contraindicated in those with blood dyscrasias and those with severe GI disease. Avoid in those with corneal wounds or ulcers as may prevent or delay healing. Avoid in those with renal and hepatic impairment those undergoing eye surgery and in the elderly. If needing to be used, adjust dose. Not used for long-term treatment. Safe to use in pregnancy and breast feeding Diarrhoea, nausea, abdominal discomfort, vomiting, pharyngolaryngeal pain. GI haemorrhage, rash Educate patient to avoid grape juice as it may increase serum colchicine levels, to stop taking the medication if severe diarrhoea, vomiting, muscle pain, numbness or tingling in fingers or toes or any evidence of unusual bleeding, bruising or infection and avoid alcohol as it can inhibit the effects. It is important to monitor complete blood count 1-6 monthly. Most effective when commenced within 24 hours of onset of flare-up.
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Physiotherapists- Musculoskeletal Disorders
* In conjunction with regular nurse-initiated pressure area care and encouraging our patients' to sit out of bed, physiotherapists can assist in their recovery by strengthening their bones and muscles during the acute phase * Exercise has been proven to assist with maintaining bone strength and density and often lifts the spirits of our patients encouraging them to get better to return home sooner ultimately assisting in the smooth transition and preparation for their discharge
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Occupational Therapists- Musculoskeletal Disorders
* Due to the mobility challenges, for example from a fall, general limb pain or loss of sensation, occupational therapists work together with physiotherapists to gather equipment for the home, in preparation for their transition back into community post-discharge from the hospital * This equipment might be bathroom assist devices, handles for the steps at the front of their house, even handles for their bed frames to assist with turning while they maintain good pressure area care techniques at home
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Pharmacists- Musculoskeletal Disorders
* Pharmacists are crucial in the admission and discharge process of our patients' to ensure everything required for the patient is smoothly transitioned from the start of their inpatient journey so they can get back into community and into their homes while the interprofessional team prioritises maintaining good pain management * Pharmacists are involved with risk management of certain medications as well. For example, if steroid use was increasing your patient's risk of developing osteoporosis, or you required the patient to take the right supplements to support bone development, this would be a good reason to seek early referral to a pharmacist
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Dieticians- Musculoskeletal Disorders
* Some patients' will be making lifestyle changes to their diet for the first time since diagnosis during their admission with you, a referral to the dietician can be a handy way for the patient to discuss any necessary changes to their diet, especially when there are many vitamins, minerals, and electrolytes that are crucial for healthy bones
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Social Workers- Musculoskeletal Disorders
* When learning of a new diagnosis, it may have a lifelong impact. Social workers can converse with patients to ease their concerns, establish any relationships that may outlive their inpatient stay and possibly community supports our patients' might need on discharge: such as meal services, at-home physiotherapy, and more * Social workers are important to the whole family when a patient has been admitted to hospital, holistically they can gauge where support systems already exist for the patient and support other members of their family in providing the best care possible