11/16 Flashcards
Type of Spondyloarthropathies
- Ankylosing arthritis: long term inflammation of the spine, fused vertebrae
- Reactive arthritis: inflammatory arthritis from an infection in another part of the body
- Psoriatic arthritis: long term inflammatory arthritis caused by the autoimmune disease psoriasis, common to have distal interphalanges joint coloration
- Enteropathic arthritis: long term arthritis with occurrence of inflammatory bowel disease
Features of Spondyloarthropathies
- Involvement of the axial skeleton, esp. sacroiliac joint
- Peripheral arthritis: lower limbs more common than upper limbs, asymmetric
- Enthesitis: inflammation of enthesis or where the ligament/tendon attaches to the bone
- Uveitis of the eye and mucocutaneous probs
Male predominance and familial clustering, autosomal dominance with 20% penetrance
HLA-B27 association and absence of autoantibodies, Haida Indians and eskimos have high prevalence of HlA-B27 positive people, not cause but may impact way we react to bacteria especially those in the gut, overzealous reactions to bacteria may trigger systemic inflammation
Inflammatory stuff for Spondyloarthropathies
Enthesitis: periosteal new bone formation, subchondral bone inflammation and resorption
Dactylitis: sausage digit, tendons and ligaments of the digit becomes inflammed and causes swelling, also seen in sarcoidosis and sickle cell
Uveitis: red painful eye
Urethritis or Cervicitis: from chlamydia or gonorrhea that triggers reactive arthritis, may have circinate balantis
Schooner Test
Have limited ROM of flexion with spondyloarthropathies, mark lower back by L5, want to turn 10 cm line segment into 15 cm line segment by flexion
Ankylosing spondylitis
Males more affected than females, normally 20-40 at diagnosis but there is juvenile AS
Diagnosis: inflammatory lower back/butt pain, peripheral arthritis
Uveitis, GI ulcers, lung disease or aortic valve insufficiency is rare
Psoriatic Arthritis
Males and females affected equally, 20-40 at diagnosis, there’s a juvenile PsA
Diagnosis: skin and nail lesions, enthesitis, uveitis, axial and peripheral inflammatory arthritis, peripheral is oligo or polyarticular and involves DIP joints
Silvery plaques over elbows and umbilicus, onycholysis on nails
Enteropathic Arthritis
Complication of inflammatory bowel disease, arthritis can be axial or peripheral
Clinical signs: pyoderma gangrenosum, symptomatic uveitis, oral ulcers,erythema nodosum
Reactive Arthritis
Aseptic peripheral or axial arthritis occurring within a month of infection (GI, urethral, cervical or other)
Self limited or chronic, HLA-B27 positive increases risk of chronicity
Signs: Keratoderma blenorrhagicum (scaly pustules on feet), urethritis, cervicitis, vulvitis, circinate balinitis, inflammatory eye disease
Radiographic findings of Spondyloarthropathies
Sacroilitis: unilateral or bilateral, has widening/irregularity of joint space, sclerosis, erosions
Lumbar spine: bridging syndesmophytes, bamboo spine, new bone forms along interosseous ligaments
Enthesitis: new bone and erosion where attach
Treatment for Spondyloarthropathies
Intraarticular/topical steroids, PT, OT
Anti-TNF Agents are most effective for moderate to severe forms
NSAIDS then sulfasalazine and methotrexate (often ineffective for axial disease but work for peripheral) then anti-TNF agents
Biomechanics of Fractures
- Extrinsic Factors: magnitude, duration, and direction of force
Stress: load/area on which load acts
- Intrinsic Factors: energy absorbing capacity, modulus of elasticity, fatigue strength
Bone is a two phase material with type I collagen and hydroxyapatite, strength of bone depends on density, mineral content, and amount of collagen
Classifications of Fractures by Injury
- Direct trauma-
Nightstick fracture: small force over a small area, minimal soft tissue damage
Direct crush: large force over a large area, comminuted fracture, extensive soft tissue trauma
Penetrating fractures: large force over small area, gunshot, depends on velocity
- Indirect trauma-
Tension fracture: bone pulled apart, muscles and tendons, transverse fracture line
Compression fracture: short oblique fracture line, 45° shear strain, failure of cancellous in spine
Bending fractures: tension/compression, butterfly fragment on compression side
Rotational Fractures: spiral pattern, torsional stresses
Fracture Clinical Evaluation and Care
Soft tissue care: primary goal to halt the continued trauma to the tissues, get pressure off soft tissue, may immobilize fracture with splint
Reduction: sooner is better, imperative in neurovascular injuries
Pediatric Fractures
Thicker periosteum, more amenable to closer reduction and casts, more rapid healing
Physis-
Growth plate injury can be limb/life altering, leads to decreased growth
Nonphyseal-
Torus (buckle) fracture: More ductile so incomplete fracture, one side of bone/cortex broke
Greenstick fracture: bone bends but doesn’t break
Apophysis
Small projection on a bone without an independent center of ossification
Can be tendon/bone interface, due to infused nature of structure when subject to high force, ischial tuberosity or ASIS
Occult fracture
Often not easily seen on X-rays, hard to differentiate between and soft tissue injury
Present with pain/difficulty if weight bearing
Treat like fracture if think maybe, immobilize and re-examine (diagnosis is - if symptoms resolve)
Get MRI or other imaging if high stress area like femoral neck
Why a concern: can displace if at weight bearing joint, can violate blood supply, lead to nonunion or malunion
Bone Fracture Treatment
- Primary- rigid fixation
Direct attempt by cortical bone to reestablish itself, need fracture fragments to be anatomically near each other, no callus
New osteoid on bone closes gals, cutting cones to allow new blood vessel entry
- Secondary-
Periosteum is important, enhanced by some motion and decreased by rigidity, endochondral/intramembranous, rapid, bridge lap gaps
6 Stages of Secondary Bone Healing
- Hematoma/Inflammation: direct bone formation via osteoprogenitor cells at periosteum (hard callus), Inflammatory Signaling
- Angiogenesis/cartilage form: angiogenesis, mesenchymal Cells differentiate to chondrocytes to deposit cartilage
- Cartilage calcification
- Cartilage removal
- Bone formation
- Remodeling
Fracture Fixation Stability
- Cast/Splint- least stable
Splints allow swelling and aren’t circumferential while casts are opposite, use for fractures with little displacement, limit motion, maintain alignment to limit soft tissue damage
More common in kids, secondary bone healing
- External Fixation-
Middle stable, temporary
Open fractures, intrarticular fractures, fractures with soft tissue swelling and injury - Intermedullary Nails-
Long bone fractures/diaphyseal (femur, tibia, humerus), closed reduction techniques, greater preservation of soft tissue compared to ORIF
Secondary bone healing, will see callus
- Open Reduction Internal Fixation (ORIF)-
Incision, realign bone/joint, plates and screws, middle stability
Plating method determines rigidity, can be 1° or 2° healing
- Compression plating-
Most stable, transverse or oblique fractures, compress bones to decrease gap bone must bridge which creates stability, need anatomic fixation
Bridge plating for comminution with proximal/distal fixation and little fixation in zone of injury, non-anatomic fixation, Secondary healing
4 Sources of Blood Supply to Long Bones
- Nutrient artery and branches: divide into multiple small branches when reach medullary cavity, some supply medullary cavity and others enter cortex to supply inner 2/3 via Haversian System, anastomoses with metaphyseal artery
- Metaphyseal Artery: subdivide into numerous small branches,
- Epiphyseal artery: pass through reserve zone of cartilage but no Capillaries, supply blood to proliferating zone of cartilage and the distal zones are less vascularized
- Periosteal Artery
Growing vs. Mature Bone Circulation
Blood doesn’t flow through physis and intramedullary vessels don’t reach epiphysis, direct epiphyseal artery is main blood supply to epiphysis (loses prominence when growth plate closes at skeletal maturity
Metaphyseal Blood Supply provides nutrients for active cells in enchondral ossification, doesn’t cross physis
Disruption of Blood Supply to Bones
Medial circumflex humeral Artery is main blood supply to femoral head, branches transverse neck and may be torn by fracture, artery to the head of the femur is insufficient for blood supply when fractured so get avascular necrosis
Most nutrient arteries enter the neck of the talus, fracture can create osteonecrosis
Some people only have nutrient arteries on distal half of scaphoid, fracture of scaphoid makes osteonecrosis of proximal scaphoid
Common cause of secondary arthritis
Osteocytes disappear from lacunae
Revascularization extends inward from adjacent live bone
Dead bone is more opaque than live bone: new bone formation and collapse with old bone compression
Osteonecrosis
Osteoclastic resorption: vessels approach and dead bone resorbed, articular surface weakens and a portion of it can collapse leading to degenerative arthritis
History/Physical: pain with activity, younger patient, limited joint ROM
Imaging: need MRI for early stage but radiographs work for later stages
Prevention and Treatment: restore Anatomy in fracture, total hip for end stage
Risk Factors: trauma, corticosteroid use, alcohol abuse, smoking, sickle cell, high cholesterol, organ transplant, Gaucher disease
Osteonecrosis Etiology and Treatment
- Etiology-
Idiopathic is most common
Arterial compromise from fracture or heminoglobinpathies/arterial thrombosis
High intraosseous pressure: pressure in bone rises above capillary pressure from steroids, alcohol abuse, or Gaucher’s disease
- Treatment-
Early: core decompression
Later: bone grafting with vascularized fibula, osteotomy vs. total hip arthroplasty
Osteonecrosis Stages
I: no X-ray changes but clinical symptoms are suspicious
II: some bone remodeling, subchondral sclerosis, and cysts
III: crescent sign on X-ray, subchondral fracture
IV: narrowing, osteophyte development, deformation of bone (flattening of femoral head with normal joint space)
V: narrowing of joint space, loss of articular cartilage on femoral head
VI: arthritis involving femoral head and acetabular sides of the joint
Osteochondrosis
Vascular insult to growing bone (osteonecrosis if to mature bone)
Degenerative change in ossification center of epiphysis that goes on to avascular necrosis, perthes for femoral head, Freiberg on 2nd metatarsal involves flattening of the head
Pathophysiology-
Obliteration of the epiphyseal Blood Supply results in necrosis of the epiphysis
1. Cartilage cells deep in growth plate deprived of nutrients
2. Longitudinal growth stops
3. If collateral circulation not restored, growth plate closes
Osteochondritis Dissecans
Damage at the articular cartilage due to blood deprivation of the subchondral bone, lose support for overlying articular cartilage
Etiology can be traumatic (overuse) but is often idiopathic, could be underlying avascular necrosis
Use plain radiographs or MRI
Presents commonly in distal humerus, distal femur, and talus
Osteochondritis Dissecans Stages
- Normal X-ray and scintigraphically invisible
- Bulge on medial femoral condyle due to partial separation of bone fragment, articular cartilage intact but show up on X-ray, no scintigraphically
- Fragment demarcated by separation of articular cartilage, scintigraphically visible
- Fragment of cartilage/bone completely separated, increased isotope uptake in lesion and femoral condyle
- Increased uptake in adjacent tibial plateau
Osteochondritis Dissecans Presentation and Treatment
- Presentation-
Mild aching to severe pain with joint effusion and sometimes a mechanical block - Treatment- depends on fragment status and child age
Observation and stop activities, drilling, osteochondral allograft, mosaic plasty, ORIF
Primary Survey for MSK Emergency
ABCDE
A- airway
Move air between mouth/nose to lungs, mechanical block or lost due to unconsciousness
Treatment: endotracheal, nasotracheal, circothyroid intubation
B-breathing
Ability of lungs to exchange oxygen to the blood for transport to the tissues
Impaired by hemothorax, pneumothorax, flail chest from multiple rib fxs, pulmonary contusions/pain
Treatment: address specific injury, possible intubation with mechanical support
C-circulation
Assessing for shock when the body can’t deliver adequate oxygenated blood to tissues
Evaluate for bleeding, cardiac tamponade, neurogenic shock from spinal cord injury
Clinical signs: tachycardia, faint peripheral pulse, lower skin temp, sweating, loss of consciousness
D-neurologic disability
Give brief neuro exam
E-exposure
Remove all clothes to see all injuries
Secondary Survey for MSK Emergencies
Systematic head to toe examination
Immobilized on a spine board
Rectal exam, Foley catheter, do every hole
Do X-rays or act scans as needed
Orthopedic Emergencies
Crush injuries
Compartment syndrome
Open fractures
Bite wounds
Pelvic/acetabulum fractures
Dislocations
Crush injuries
Earthquake, prolonged extremity compression, too much beer/drugs
Continuous pressure on muscle causes cellular ischemia and death
Cells leak K+ and myoglobin, while absorb Na/Ca/water, metabolic acidosis from hypotension and
hyperkalemia/calcemia
Renal failure as myoglobin precipitates in renal tubules, Metabolic abnormalities cause cardiac failure and arrhythmia
Be wary of Compartment syndrome
Treatment: prevention of renal failure, aggressive fluid resuscitation, sodium bicarbonate to prevent myoglobin precipitation, dialysis
Pelvic and Acetabular Fractures
- Pelvic fractures-
Can injure multiple other areas, hemorrhage is leading cause of death and mainly comes from intra-abdominal source
Manage hypotension: fluid resuscitation, evaluate chest/abs, sheet immobilization, angiography
Fairly high mortality
- Acetabular Fracture-
High energy with associated injuries, not associated with ongoing blood loss, check for dislocation
Compartment Syndrome
Increased pressure: ischemia, oxygen deprivation, damage to muscle and nerve tissue
Extrinsic Factors: tight dressing/cast, burns, occlusive dressings
Intrinsic factors: bleeding from injury or fracture, iatrogenic fluid infusion, swelling from tissue injury
Often with closed Tibial shaft fractures, swelling can cause compression of muscles/neurovasculature
Medical emergency, death of muscle and injury to nerves if untreated, can be reversible if release pressure
Signs and Symptoms of Compartment Syndrome
Pain out of proportion
Pallor
Parathesia (late)
Paralysis (progressive weakness)
Pulselessness
Others: elevated muscle compartment pressures, tense swollen area (porkiness), poikilothermia (cold)
Open fractures
Emergency, infection increases greatly without prompt treatment, antibiotics help
Generally high energy with multiple associated injuries like soft tissue loss and compartment syndrome
Staph aureus most common, Cephalosporin for Grade I/II, add aminoglycosides (Gent) when Grade III, add penicillin if high contamination
Thorough irrigation and debridement, skeletal stabilization
Bite wound
Human: From punching, examine with hand in fist, Staph is common
Cat bites have Pasteurella multocida
Plan: local wound care, debridement open joints, antibiotics, rabies, tetanus
Flexor tenosynovitis
Caused by puncture wound, very painful
Staph aureus is most common, high index of suspicion, need prompt treatment
Treatment-
Prompt IV antibiotics, nonoperative Treatment should see improvement after 2 days but operate if not help after a day, can do closed continuous irrigation, open treatment
Kanavel’s 4 Cardinal Signs of Flexor Tenosynovitis
- Symmetric swelling of the entire digit
- Exquisite tenderness along the sheath
- Digit with semi-flexed posture
- Pain with attempted passive extension
Effusions
Abnormal collection of fluid in a joint, aspirate synovial fluid
Immobilize, antibiotics, irrigate and debridement since infection damages cartilage
History important and most effusions are benign
Arthrocentesis: >50k WBC indicates infection, pain upon palpating and weight bearing
Deep Vein Thrombosis
Diagnosis is clinically hard-
Swelling, calf tenderness, Homan’s sign is unreliable, fever, elevated WBCs
Can use Doppler ultrasound
Virchow’s Triad
- Hypercoagulable state-
Malignancy, IBD, pregnancy or postpartum, oestrogen therapy, trauma of LE, sepsis, nephrotic syndrome - Vascular wall injury-
Trauma or surgery, venipuncture, atherosclerosis, chemical irritation - Circulatory stasis- decreases blood flow rate
Atrial fibrillation, immobility or paralysis, venous obstruction from tumor/obesity/pregnancy
