orthopaedic emergencies
DESCRIPTION
Orthopaedic Emergencies. Dr. Samuel Wong RMH Intern 2012. Orthopedic Emergencies. Open Fractures Acute Compartment Syndrome Neurovascular injuries Dislocations Septic Joints Cauda Equina Syndrome. Open Fractures. - PowerPoint PPT PresentationTRANSCRIPT
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Dr. Samuel Wong RMH Intern
2012
Orthopaedic Emergencies
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Orthopedic EmergenciesOpen FracturesAcute Compartment SyndromeNeurovascular injuriesDislocationsSeptic JointsCauda Equina Syndrome
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Open Fractures
An open (or compound) fracture occurs when the skin overlying a fracture is broken, allowing communication between the fracture and the external environment
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Open Fractures- Gustilo-Anderson Classification:
Type I:Small wound (<1cm), usually clean, no soft tissue damage and no
skin crushing (i.e. a low energy fracture) Type II:
Moderate wound (>1cm), minimal soft tissue damage or loss, may have comminution of fracture (i.e. a low-moderate energy fracture)
Type III:Severe skin wound, extensive soft tissue damage (i.e. high
energy fracture)Three grades: A – adequate soft tissue coverage, B – fracture
cover not possible without local/distant flaps, C – arterial injury that needs to be repaired.
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Open Fractures- Management
ABCDE – check neurovascular status (pulses, cap. refill, sensation, motor) , fluid resuscitation, blood
Antibiotics, tetanus prophylaxis – 48-72 hrs Surgical debridement – removal of de-vitalised tissue, irrigation Stabilization of fracture – internal/external, if closure delayed then
external prefered Early definitive wound cover – split skin grafts, local/distant flaps
(involve plastics)
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Open Fractures- Complications
Wound infection – 2% in Type I , >10% in Type III Osteomyelitis – staph aureus, pseudomona sp. Gas gangrene Tetanus Non-union/malunion
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Acute Compartment Syndrome
An injury or condition that causes prolonged elevation of interstitial tissue pressures
Increased pressure within enclosed fascial compartment leads to impaired tissue perfusion
Prolonged ischemia causes cell damage which leads to oedema Oedema further increase compartment pressure leading to a
vicious cycle Extensive muscle and nerve death >4 hours Nerve may regenerate but infarcted muscle is replaced by fibrous
tissue (Volkmann’s ischaemic contracture)
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ACS- Etiology
Crush injury Circumferential burns Snake bites Fractures – 75% Tourniquets, constrictive
dressings/plasters Haematoma – pt with
coagulopathy at increased risk
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ACS- Findings 5 Ps of ischaemia
Pain (out of proportion to injury)
ParesthesiasParalysisPulselessnessPallor
Severe pain, “bursting” sensation
Pain with passive stretch Tense compartment Tight, shiny skin
Can confirm diagnosis by measuring intracompartmental pressures (Stryker STIC)
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0 mm Hg
10 mm Hg
30 mm Hg
60 mm Hg
120 mm Hg
Pulse Pressure
Ischemia
Elevated Pressure
Normal
Difference between diastolic pressure and compartment pressure (delta pressure)< 30mmHg is indication for immediate decompression
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ACS - Mangement
Early recognitionMuscle necrosis at delta
pressure < 30mm HgIrreversible injury 4-6 hrs
Remove cast, bandages and dressings
Arrange urgent fasciotomy
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Fasciotomy
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ACS- Complications
Volkman ischaemic contractures Permanent nerve damage Limb ischaemia and amputation Rhabdomyolysis and renal failure
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DislocationsDisplacement of bones at a joint from their
normal positionDo xrays before and after reduction to look
for any associated fractures
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Dislocation- Shoulder
Most common major joint dislocation Anterior (95%) - Usually caused by fall on hand Posterior (2-4%) – Electrocution/seizure May be associated with:
Fracture dislocationRotator cuff tearNeurovascular injury
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Dislocation- Knee
Injury to popliteal artery and vein is common Peroneal nerve injury in 20-40% of knee dislocations Associated with ligamentous injury Anterior (31%) Posterior (25%) Lateral (13%) Medial (3%)
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Dislocation- Hip
Usually high-energy trauma More frequent in young patients Posterior- hip in internal rotation, most common Anterior- hip in external rotation Central - acetabular fracture May result in avascular necrosis of femoral head Sciatic nerve injury in 10-35%
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Neurovascular Injuries
Fractures and dislocations can be associated with vascular and nerve damage
Always check neurovascular status before and after reduction
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Neurovascular Injuries - Etiology
FractureHumerus, femur
DislocationElbow, knee
Direct/penetrating trauma Thrombus Direct Compression/
Acute Compartment SyndromeCast, unconscious
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Common vascular injuries Injury Vessel
1st rib fracture Subclavian artery/vein
Shoulder dislocation Axillary artery
Humeral supracondylar fracture Brachial artery
Elbow Dislocation Brachial artery
Pelvic fracture Presacral and internal iliac
Femoral supracondylar fracture Femoral artery
Knee dislocation Popliteal artery/vein
Proximal tibial Popliteal artery/vein
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Clinical Features & Mx
Paraesthesia/numbness Injured limb cold, cyanosed, pulse weak/absent Call for help!
Remove all bandages and splints Reduce the fracture/ dislocation and reassess circulation
If no improvement then vessels must be explored by operation If vascular injury suspected angiogram should be performed immediately
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Common nerve injuriesInjury Nerve
Shoulder dislocation Axillary
Humeral shaft fracture Radial
Humeral supracondylar fracture Radial or median
Elbow medial condyle Ulnar
Monteggia fracture-dislocation Posterior-interosseous
Hip dislocation Sciatic
Knee dislocation Peroneal
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Clinical Features & Mx Paraesthesia and weakness to supplied area Closed injuries: nerve seldom severed, 90% recovery in 4 months.
If not do nerve conduction studies +/- repair Open injuries: Nerve injury likely complete. Should be explored at
time of debridement/repair Indications for early exploration:
Nerve injury associated with open fractureNerve injury in fracture that needs internal fixationPresence of concomitant vascular injuryNerve damage diagnosed after manipulation of fracture
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Septic Joint/Septic Arthritis
Inflammation of a synovial membrane with purulent effusion into the joint capsule. Followed by articular cartilage erosion by bacterial and cellular enzymes.
Usually monoarticular Usually bacterial
Staph aureusStreptococcusNeisseria gonorrhoeae
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Septic Joint- Etiology
Direct invasion through penetrating wound, intra-articular injection, arthroscopy
Direct spread from adjacent bone abcess Blood spread from distant site
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Septic Joint- Location
Knee- 40-50% Hip- 20-25%*
*Hip is the most common in infants and very young children Wrist- 10% Shoulder, ankle, elbow- 10-15%
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Septic Joint- Risk Factors
Prosthetic joint Joint surgery Rheumatoid arthritis Elderly Diabetes Mellitus IV drug use Immunosupression AIDS
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Septic Joint- Signs and Symptoms
Rapid onset Joint pain Joint swelling Joint warmth Joint erythema Decreased range of motion Pain with active and passive ROM Fever, raised WCC/CRP, positive
blood cultures
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Septic Joint- Treatment
Diagnosis by aspirationGram stain, microscopy, cultureLeucocytes >50 000/ml highly
suggestive of sepsis Joint washout in theatre IV Abx 4-7 days then orally for another 3 weeks Analgesia Splintage
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Septic Joint- Complications
Rapid destruction of joint with delayed treatment (>24 hours) Growth retardation, deformity of joint (children) Degenerative joint disease Osteomyelitis Joint fibrosis and ankylosing Sepsis Death
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Cauda Equina Syndrome Compression of lumbosacral nerve roots below conus medullaris
secondary to large central herniated disc/extrinsic mass/infection/trauma
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Clinical Featuresmotor (LMN signs)
-weakness/paraparesis in multiple root distribution-reduced deep tendon reflexes (knee and ankle)-sphincter disturbance (urinary retention and fecal incontinence due to loss of anal sphincter tone)
sensory-saddle anesthesia (most common sensory deficit)-pain in back radiating to legs, crossed straight leg test-bilateral sensory loss or pain: involving multiple dermatomes
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Management Surgical emergency - requires urgent investigation and
decompression (<48 hrs) to preserve bowel and bladder function
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The End