General Principles ortho Flashcards
Principles of fracture management
(High-energy injuries resus following ATLS)
- Reduce - restoring anatomical alignment - reduce bleeding/ traction so swelling/ neuropraxia/ pressures on BVs
✅analgesia ✅conscious sedation - Hold - immobilising - simple splints/ plaster casts (not circumferential first 2wks, if axial instability needs cross joint above & below)
✅May thromboprophylaxis ✅advice compartment syndrome - Rehabilitate - intensive physiotherapy
✅May occupational therapists
How common is osteoarthritis? What is the pathophysiology?
Most common arthropathy
Leading cause of pain & disability in the western world
Knee OA 15% >55yrs
Radiographic incidence >80% >75yrs
Progressive loss articular cartilage & remodelling underlying bone - active response chondrocytes in cartilage & inflammatory cells in tissues -> enzymes break down collagen & proteoglycans-> subchondral bone exposed -> sclerosis -> remodelling -> osteophytes & bony cysts, loss of joint space
Clinical features of oesteoarthritis
Common joints: hands, feet, hip, knees
Insidious, chronic, gradually worsen, pain & stiffness, worsened with activity & relieved rest, pain worse through day stiffness improves
-> deformity, reduced range movement
Bourchard nodes (swelling PIPJs) Heberden nodes (DIPJs) Fixed flexion/ Varus malalignment knees
Crepitus
Reduction joint movement
Differentials for oesteoarthritis
Inflammatory arthropathy ex (RA) Crystal arthropathies (gout, CPPD) Septic arthritis Fractures Bursitis Malignancy
Hand - RA, gout, De Quervain’s tenosynovitis
Hip - trochanteric bursitis, radiculopathy, spinal stenosis, iliotibial band syndrome
Knee - referred hip, meniscal or ligament tears, chondromalacia patellae
Investigations for oesteoarthritis
Primary clinical diagnosis
Routine bloods - exclude inflammatory/ infective Radiograph: - loss joint space - osteophytes - subchondral sclerosis - subchondral cysts
Management of oesteoarthritis
Conservative:
Advice joint protection, strengthening & exercising,
WL
Heat/ ice packs
Joint supports
Physiotherapy
Medical: simple analgesics, topical NSAIDs, intra-articular steroid injections (may worsen few days)
Surgical:
Osteotomy
Arthrodesis (joint fusion)
Arthroplasty
What are the most common open fracture sites?
Tibial, phalangeal, forearm, ankle, metacarpals
How can the outcomes of open fractures be divided?
- skin if significant May need skin grafting/ local/ free flap
- soft tissues may muscle/ tendon/ ligament loss -> reconstructive surgery
- Neurovascular injury compressed/ arteriospasm/ intimal dissection/ transected
- infection contamination/ reduced vascularity/ systemic compromise/ insertion metalwork
Gustilo-Anderson Classification of open fractures
Type 1 <1cm wound & clean
Type 2 1-10cm wound & clean
Type 3A >10cm high energy, soft tissue coverage (orthopaedics alone)
Type 3B >10cm high energy inadequate ST coverage (plastics)
Type 3C vascular injury (vascular input)
Investigations for & management open fractures
G&S
Basic blood tests (clotting)
Radiograph
Complex/ communited CT
✅resus & stabilisation ✅realignment & splinting ✅document neurovascular status ✅broad antibiotics ✅ tetanus vaccine if not up to date ✅photograph wound ✅ remove gross debris ✅ wound dressed saline stacked gauze
Definitive management:
Debridement <12-24hrs if not contaminated
Washed out saline
Skeletal stabilisation
What is compartment syndrome? Where is most commonly affected?
Critical pressure increase within confined compartmental space
Any fascial compartment, most common: leg, thigh, forearm, foot, hand, buttock
Pathophysiology of compartment syndrome?
Typically following high-energy trauma, crush injuries or fractures -> vascular injury
Other causes: iatrogenic vascular injury , tight casts/ splints, DVT, post-reperfusion swelling
Closed non-distend-able space -> Fluid deposited -> ⬆️intracompartmental P -> compresses veins -> ⬆️hydrostatic P in veins -> fluid moves out of veins -> traversing nerve red compressed -> sensory/ motor deficit (paraesthesia) -> arterial inflow compromised -> ischaemia (cold, pale, pulsesless, paralysed) - late sign
Clinical features of compartment syndrome
Tend present within hrs - up to 48hrs post insult
Severe pain disproportionate injury, not readily improved, pain worse passively stretching muscle bellies, paraesthesia distal, compartment tense -> acute arterial insufficiency (5 Ps)
Investigations & management of compartment syndrome
Clinical diagnosis - intra-compartmental pressure monitor, creatine kinase elevated
Management:
Urgent fasciotomies -> skin incisions left open re-look 24-48hrs
- keep limb neutral level
- High flow O2
- augment BP crystalloid fluid bolus
- remove dressings/ splints/ casts
- opioid analgesia
- monitor renal function (rhabdomyolysis/ reperfusion injury)
What is the main cause of septic arthritis (infection of a joint)? How does it occur and what can it lead to?
Main causative organisms: staphylococcus aureus, streptococcus spp, gonorrhoea, salmonella (SCD pts)
Seed to join from: bacteraemia (cellulitis, UTI, chest infection), direct inoculation, adjacent osteomyelitis
- > irreversible articular cartilage damage
- > severe osteoarthritis