Pathophysiology

What are the two common causes of joint injuries?

mechanical overloading

forcible twisting or stretching

What is a dislocation?

the displacement or separation of the bone ends of a point w/ loss of articulation

subluxation

partial dislocation

What is dislocation typically the result of? Where is it most often seen?

trauma

most often seen in the shoulder and acromioclavicular (AC) joints

dislocation manifestations

pain

deformity

limited movement/range of motion (ROM)

dislocation diagnosis

hx

pt assessment

radiologic findings

dislocation treatment

depends on the site, mechanism, and degree of injury

• reduction, immobilization, surgery

When do fractures occur?

when more stress is placed on the bone that it can absorb

What are the three fracture categories?

sudden injury (most common)

fatigue or stress

pathologic

comminuted fracture

bone broken into three or more pieces

fragments are present at the fracture site

lots of pain, crushing trauma

spiral fracture

the break spirals around the bone

common in a twisting injury

often from domestic abuse or sexual assault

compression fracture

bone is crushed

causes bone to be wider or flatter in appearance

two bones that are crushed/squeezed together

often in vertebrae

open (compound) fracture

if bone sticks out of skin

often needs surgery and IV abx

closed (simple) fracture

bone inside skin

less risk infection

greenstick fracture

incomplete break

transverse fracture

break is in a straight line across the bone

segmental fracture

the same bone is broken in two places, so there is a “floating” piece of bone

fracture clinical manifestations

pain, tenderness at the site

inflammation

loss of function: loss of nerve function (local shock)

abnormal mobility

deformity: long bones: angulation, shortening, rotation

fracture diagnosis

hx: mechanism, time of injury

physical assessment: shortening and rotation of extremities, like feet, is indicative of a fracture

imaging: XR, others may be indicated based on complications

fracture treatment

objectives for treatment

• reduction

• immobilization

• preservation and restoration of function

reduction and internal fixation

• closed manipulation

• surgical (open) reduction (ORIF)

immobilization and external fixation

• immobilization: splints, casts, traction

• external fixation: pins, screws

limb-lengthening systems

• used to widen or lengthen bones, correct angular/rotational defects, immobilize fractures

preservation and restoration of function

• active and passive ROM exercises

compartment syndrome etiology and pathogenesis

condition of increased pressure w/in a limited space that comprises the circulation and function of the tissues

What are the effects of fixed space (compartment) of an extremity?

increasing pressure can lead to death of nerve and muscle cells

permanent loss of function

What is the amount of pressure required to produce compartment syndrome dependent on?

duration of pressure elevation

metabolic rate of tissues

vascular tone

local blood pressures

acute compartment syndrome

can occur after a fracture or crushing injury

chronic compartment syndrome

may develop from exertion in long-duration of activity

compartment syndrome clinical manifestations

severe pain that is out of proportion to the injury

paresthesias, diminished reflexes, loss of motor function

compartment syndrome diagnosis

hx and physical assessment:

• pain score

• sensory assessment

• motor functioning testing

• peripheral vascular assessment: doppler pulses

compartment pressure

compartment syndrome treatment

removal of restrictive devices

• casts, splints, dressings

elevating extremity to reduce edema

fasciotomy

• incision of the fascia to separate it to allow for compartment to decompress

• re-establishes blood flow

What does a lower extremity fracture put one at risk for?

venous thromboemboli (VTE)

deep venous thrombosis (DVT) and/or pulmonary embolism (PE)

What is the recommended treatment for a thromboemboli?

thromboprophylaxis

pharmacological or mechanical

How often do VTE related to musculoskeletal system (MSK) injuries/procedures (hospital admissions) occur after discharge?

 ≥ 2 months after discharge

follow up assessment is indicated

fat embolism syndrome (FES)

refers to multiple life-threatening manifestations resulting from the presence of fat droplets in the small blood vessels of the lung, kidneys, brain after a long bone or pelvic fracture

FES pathogenesis

unclear mechanism

thought to result from fat droplets that are released from the marrow or adipose tissue at the fracture site into the venous system through a torn vein

FES clinical manifestations

respiratory failure: chest pain, SOB, tachycardia, cyanosis

cerebral dysfunction: confusion, change in behaviors, disorientation, seizures

skin and mucosal petechiae: chest, axillae, neck, shoulders

FES diagnosis

arterial blood gas (ABG)

other diagnosis as appropriate

FES treatment

correct hypoxemia

inflammation

maintaining fluid balance

osteopenia

characterized by a reduction in bone mass greater than expected for age, race, or sex

occurs d/t a decrease in bone formation, inadequate bone mineralization, or excessive bone deossification

osteopenia diagnosis

not a diagnosis, but a term used to describe an apparent lack of bone seen on XR studies

osteopenia major causes

osteoporosis

osteomalacia

malignancy (multiple myeloma)

endocrine disorders (hyperparathyroidism, hyperthyroidism)

osteoporosis

characterized by a loss of mineralized bone mass causing increased porosity of the skeleton and susceptibility to fractures

often associated w/ the aging process

imbalance between bone resorption and formation

resorption > formation

bone mineral density (BMD)

peak bone mass

determined by genetics, estrogen levels, exercise, calcium intake and absorption, and environmental factors

osteoporosis pathogenesis

poor nutrition and physical activity

age-related decreased in intestinal absorption of calcium d/t deficient activation of Vit. D may contribute towards osteoporosis

postmenopausal osteoporosis

• estrogen deficiency…loss of cancellous bone and predisposition to fractures of the vertebrae and distal radius

• males have ~8-10% more BMD

age-related changes: osteoblasts have reduced replicative potential in older adults

secondary osteoporosis pathogenesis

endocrine disorders: hyperthyroidism, hyperparathyroidism, Cushing syndrome, DM

malignancies: multiple myeloma

alcohol use disorder: alcohol is a direct inhibitor of osteoblasts and inhibits calcium absorption

medication use: corticosteroids (prednisone), aluminum-containing antacids, anticonvulsants

osteoporosis clinical manifestations

often a silent disorder…

• the first manifestations of the disease typically accompany a fracture

  • vertebral compression fracture

  • fracture of the hip, pelvis, humerus, etc.

loss of height

• wedging and collapse of the vertebrae: kyphosis

systemic symptoms (weakness, fatigue, pain) are suggestive that osteoporosis is caused by an underlying disease process

• secondary osteoporosis

osteoporosis diagnosis

WHO Working Group on Osteoporosis Screening Tool: Fracture Risk Assessment Algorithm

Dual-Energy X-Ray Absorptiometry (DEXA): spine and hip

serial height assessments

osteoporosis treatment

regular exercise

calcium supplementation

Vit. D supplementation

antiresorptive agents

• estrogens and selective estrogen receptor modulators (SERMs)

• biphosphonates

• calcitonin

anabolic agents

osteomalacia etiology

2 main causes:

• insufficient calcium absorption from the intestine d/t the lack of dietary calcium or deficiency of or resistance to the action of Vit. D

  • Vit. D deficiency is often caused by reduced Vit. D absorption as the result of biliary tract or intestinal diseases

  • cultural: northern China, Japan, northern India (less Vit. D from the diet)

• phosphate deficiency d/t increased renal losses or decreased intestinal absorption

  • chronic renal failure

    • renal rickets

osteomalacia clinical manifestations

bone pain and tenderness

fractures (w/ disease progression)

muscle weakness (severe cases)

slightly reduced serum calcium levels

osteomalacia diagnosis

XR

lab tests

bone scans

bone biopsy

osteomalacia treatment

treat the cause…

nutrition

sun exposure

rickets etiology

kidney failure

malabsorptive syndromes (celiac disease, cystic fibrosis)

medications (anticonvulsants, aluminum-containing antacids)

nutritional rickets: results from inadequate sunlight exposure or inadequate intake of Vit. D, calcium, phosphate

• prolonged breast-feeding w/o Vit. D supplementation

rickets clinical manifestations

bone deformities

• unmineralization

• enlarged and soft skull

  • delayed closure of fontanels

• deformities are likely to affect the spine, pelvis, and long bones

  • lumbar lordosis (curving of the lower spine) and bowing of the legs

rickets treatment

nutrition: diet w/ calcium, phosphorus, and Vit. D

• supplementation

sunlight exposure

Paget disease overview

osteitis deformans

• second most common bone disease

at the onset, marked by regions of rapidly occurring osteoclastic bone resorption

• followed by period of hectic bone formation w/ increased osteoblasts rapidly depositing bone in a chaotic manner

• poor quality bones…bowing and fractures

  • localized to the spine, skull, hips, pelvis

Paget disease etiology

genetic and environmental influences

15-40% have 1st degree relative w/ Paget disease

gene mutation

Paget disease clinical manifestations

often asymptomatic

• detected during wellness visit or during times of other illness presentation

skull

• HA, intermittent tinnitus, vertigo, eventual hearing loss

spine

• kyphosis of the thoracic spine

femur and tibia

• bowing

• coxa vara: reduced angle of the femoral neck d/t softening; waddling gait

nerve palsy syndromes

mental decline

cardiovascular disease

• high-output HF

• calcific aortic stenosis

• most common cause of death

osteogenic carcinomas

• femur → pelvis → humerus → tibia

Paget disease diagnosis

based upon bone deformity characteristics and XR changes

bone scans

bone biopsy

• differentiate other possibilities

  • infection vs carcinoma (primary vs metastases)

Paget disease treatment

based upon degree of pain and extent of disease

pain: NSAIDs, anti-inflammatory agents

• suppressive agents: biphosphonates, calcitonin

  • prevent further spread and neurologic deficits

rheumatoid arthritis (RA) etiology

systemic inflammatory disease

genetic predisposition

• first-degree relatives

  • gene: human leukocyte antigen (HLA) loci on the major histocompatibility complex (MHC)

immune-mediated joint inflammation

• activation of T-cell-mediated response to an immunologic trigger

  • antimicrobial agent (virus, bacteria, etc.)

RA pathogenesis

aberrant immune response leading to synovial inflammation and destruction of the joint architecture

• initiated by activation of helper T cells, release of cytokines (tumor necrosis factor [TNF], interleukin [IL]-1, an antibody formation

• rheumatoid factor (RF) (70% - 80%)

inflammatory response that begins w/ attraction of neutrophils, macrophages, and lymphocytes that then release lysosomal enzymes to destroy the joint cartilage

• progressive disorder

  • vasodilation and increased blood flow causes warmth and redness

    • joint swelling → reduced joint motion

    • irreversible

RA clinical manifestations

blend of systemic, articular (joint), and extra-articular (non-joint) manifestations

RA articular manifestations

symmetric and polyarticular

• fingers, hands, wrists, knees, and feet

• deformities

stiffness and pain

decreased joint motion

• pain → fibrosis

• subluxation

RA extra-articular manifestations

systemic: factor, weakness, anorexia, weight loss, low-grade fever

hematologic: thrombocytosis, anemia

• felty syndrome (rare): RA, splenomegaly, neutropenia

• rheumatoid nodules

vasculitis

• ischemic areas in the nail fold and digital pulp that appears as brown spots

• lower extremity ulcerations

• neuropathy

• visceral organ involvement

eyes

• keratoconjunctivitis sicca

• episcleritis

• uveitis

• nodular scleritis

RA treatment goals

prevent/reduce pain

decrease stiffness and swelling

maximize mobility

attempt to halt progression

RA treatment

pharmacological management

• disease-modifying antirheumatic drugs (DMARDs)

• NSAIDs

• corticosteroids

• biologics: anti-tumor necrosis factors (anti-TNFs)

surgery

• synovectomy

systemic lupus erythematosus (SLE) pathogenesis

characterized by the formation of autoantibodies and immune complexes

• B-cell hyperreactivity and increased production of antibodies against self and non-self antigens

  • autoantibodies can directly damage tissues or combine w/ other antigens to form tissue-damaging immune complexes

• autoantibodies

  • antinuclear antibodies (ANA)

SLE etiology

development of autoantibodies may result from a combination of factors

• genetics, hormones, immune factors, environment

How do SLE clinical manifestations occur?

in exacerbations and remissions

SLE musculoskeletal manifestations

arthralgias, arthritis

tenosynovitis

intrapatellar and Achilles tendon ruptures

avascular necrosis: femoral head

SLE integumentary manifestations

malar rash: butterfly rash

photosensitivity

fingertip lesions

• nail fold infarcts, splinter hemorrhages

hair loss

SLE renal manifestations

glomerulonephritis

• end-stage renal disease

interstitial nephritis

nephrotic syndrome

SLE pulmonary manifestations

pleural effusions

pleuritis

less common: pulmonary hemorrhage, interstitial lung disease, pulmonary embolism

SLE cardiac manifestations

pericarditis

myocarditis

HTN

ischemic heart diease

SLE neurologic manifestations

vasculitis leading to stroke or hemorrhage

seizures

psychosis

SLE hematologic manifestations

hemolytic anemia

leukopenia

lymphopenia

thrombocytopenia

lymphadenopathy

SLE diagnosis

hx, physical, labs

American College of Rheumatology criteria

diagnostics: ANA

SLE treatment priorities

prioritizes managing the acute and chronic symptoms

prevent progression

reduce exacerbations

minimize disability

prevent medication-related complications

SLE pharmacological management

NSAIDs

antimalarial agents

corticosteroids

immunosuppressive drugs

psoriatic arthritis etiology

unknown etiology

genetic, environmental, and immunologic factors appear to affect susceptibility and play a role in disease expression

• environmental: infectious agents, trauma

• immune: T-cell mediated immune response

psoriatic arthritis clinical manifestations

manifestations of arthritis w/ psoriasis

• detectable skin rash

• skin or nail changes

psoriatic arthritis treatment

similar to treatment of RA

pharmacological management

• NSAIDs: MSK symptoms

• DMARDs: methotrexate, sulfasalazine

• TNF inhibitors: indicated when there is inadequate response to DMARDs, NSAIDs, and steroid injections

osteoarthritis (OA) syndrome epidemiology and risk factors

age: primary OA affects 4% of people between the ages 18 - 24 years

• 85% of people in their 70s

sex: younger males are more commonly affected than females (45 years)

• after age 55, female

race

• hand OA is more common among Caucasian females

• knee OA is more common among African American females

obesity

OA syndrome pathogenesis

alterations in the homeostatic mechanisms that maintain articular cartilage

significant changes in both the composition and mechanical properties of cartilage

• increased water and decreased concentrations of proteoglycans (elasticity and stiffness) w/in the cartilage as compared to healthy tissue (early)

  • cytokine release which destroys the joint space

  • imbalance between joint building and breakdown

edematous changes in the cartilaginous matrix

• cartilage loses its smooth aspect and cracks begin to form

  • erosion…inability to absorb shock

secondary OA pathogenesis

repetitive impact loading resulting in joint failure

• high prevalence specific to vocational or avocational sites

  • shoulder and elbows of baseball pitchers

  • ankles of ballet dancers

  • knees of basketball players

immobilization

• cartilage degeneration from the loss of lubrication that occurs w/ joint movement

OA cervical spine manifestations

localized stiffness

radicular vs. nonradicular pain

vascular compression d/t posterior osteophyte formaiton

OA lumbar spine manifestations

low back pain/stiffness

muscle spasm

decreased movement

nerve root compression → radicular pain

spinal stenosis

OA hip manifestations

insidious onset of pain — localized to the groin/inner thigh

may be referred to buttocks, sciatic region, or knee

reduced ROM

gait changes

OA knee manifestations

localized discomfort w/ pain on motion

reduced ROM crepitus

quadricep atrophy

joint instability

joint effusion

OA first carpometacarpal joint

tenderness at base of thumb

squared appearance to joint

OA first metatarsophalangeal joint

irregular joint contour

pain and swelling

OA diagnosis

hx

physical assessment

labs: elevated inflammatory markers (if inflammation is present)

diagnostics: XR findings

• narrowed joint space, bony sclerosis, spikes, osteophytes

OA treatment

treatment goals: symptom management

nonpharmacologic management

• exercises and strengthening

• assistive devices: canes, walkers, splints

pharmacologic management

• NSAIDs

• intra-articular corticosteroid injections

surgery: severe disease

gout pathogenesis

the result of elevations in serum uric acid levels

• uric acid is the end product of purine metabolism

• overproduction of purines, augmented breakdown of nucleic acids, and decreased urinary excretion of uric acid

primary gout pathogenesis

90% of cases

overproduction of uric acid or inadequate elimination of uric acid (kidneys)

secondary gout pathogenesis

increased breakdown of nucleic acids

• chronic renal disease, thiazide diuretic use

gout attack

precipitation of monosodium urate crystals in the join which initiate the inflammatory response

• crystal deposition typically occurs in peripheral sites (great toe)

  • w/ prolonged hyperuricemia, crystals accumulate in the synovial joints and cartilage

    • results in cartilage destruction

repeated or untreated attacks lead to chronic arthritis and the formation of tophi

• large, hard nodules

gout clinical manifestations (4 stages)

1. Asymptomatic hyperuricemia

2. Acute gout arthritis

   • Typically, initial attack affects the first metatarsophalangeal joint

     • Tarsal joints, insteps, ankles, heels, knees, wrists, fingers, and elbows may also be initial sites

   • Abrupt onset of pain and inflammation

3. Intercritical gout

   • Early stages after the initial attack has subsided…asymptomatic

4. Chronic tophaceous gout

   • Recurrent attacks w/ permanent joint changes

gout treatment goals

termination and prevention of acute attacks

correction of hyperuricemia

gout treatment

Nonpharmacologic management

• Weight management

• Moderation in alcohol consumption

• Tobacco cessation

Pharmacologic management

• NSAIDs

  • Indomethacin, ibuprofen

• Colchicine

• Allopurinol

• Corticosteroid injections