Orthopaedic Emergency Flashcards
What are the orthopaedic emergencies?
-Compartment syndrome
-Open fractures
-Septic arthritis
-Necrotising fasciitis
-Neovascular injury
-Crush injury
Epidemiology and Aetiology of Compartment Syndrome
-Raised interstitial pressure within closed osseofacial/ anatomical space, eventually compromising tissue perfusion, leading to necrosis
-Blood:
=Fracture (supracondylar fractures, tibial shaft injury)
=Vascular injury
=Spontaneous haematoma (coagulopathy)
-Crush injury (long lie, tight circumferential dressings)
-Ischaemia
-Reperfusion in vascular patients
Presentation of compartment syndrome
-Pain!!!! Especially on movement (even passive stretch)- excessive use of breakthrough analgesia
-Paraesthesia
-Tense compartments: often anterior and deep posterior compartments of leg/ volar compartment of forearm
-No features of arterial insufficiency (presence of pulse does not rule out)
-Pallor
-Arterial pulsation may still be felt as necrosis occurs as a result of microvascular compromise
-Paralysis of muscle group may occur (late sign, prolonged nerve compression and ischaemia or irreversible muscle damage)
Investigation of compartment syndrome
-Clinical diagnosis
-Diastolic blood pressure- compartment pressure= Delta P
= Delta P <30mmHg concerning, measurement of intracompartmental pressure measurements.
=Pressures in excess of 20mmHg are abnormal and >40mmHg is diagnostic
=Compartment syndrome will typically not show any pathology on an x-ray
-Serum creatinine kinase: elevated as muscle cell lysis and muscle necrosis
-Elevated urine myoglobin
-Elevated troponin
Management of compartment syndrome
-Prompt and extensive fasciotomies to prevent muscle ischemia and rhabdomyolysis
-Resus, painkillers (minimise AKI so oxycodone hydrochloride IV) , elevate limb, cut off casts
-In the lower limb the deep muscles may be inadequately decompressed by the inexperienced operator when smaller incisions are performed
-Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason these patients require aggressive IV fluids
-Where muscle groups are frankly necrotic at fasciotomy they should be debrided and amputation may have to be considered
-Death of muscle groups may occur within 4-6 hours
Describe open fractures
-Direct communication between the fracture site and the external environment (disruption of the bony cortex associated with a breach in the overlying skin, any wound present in same limb as fracture)
-Whilst the skin is usually relatively resistant to trauma, underlying muscle can be damaged or devitalised, nerves, blood vessels and periosteum may all be disrupted the degree to which this occurs correlates with the severity of the injury and the outcome.
-May be ‘externally’ or ‘internally’ open:
=External – wound through the skin
=Internal – wound into the hollow viscera of the pelvis(i.e., vagina, rectum, bladder)
How?
-‘In-to-out’ – bone creates a deformity, causing the skin to break, or the sharp end of the bone penetrates the skin
-‘Out-to-in’ – an object penetrates the skin, causing the underlying bone to fracture
Clinical features of open fractures
-Size and location
-Contamination - ?marine or agricultural
-Soft tissue loss – skin / fat / fascia /muscle / periosteum
-Vascular status
Describe the Gustilo-Anderson Classification of open fractures
-Grade 1-3, 3 with A (adequate soft tissue coverage) , B (inadequate soft tissue cover), C (associated arterial injury)
-Energy of mechanism
=1 low, 2 moderate, 3 high
-Wound size
=1 <1cm, 2 >1cm, 3 usually >10cm
-Soft tissue injury
=2 moderate, 3 extensive
-Contamination
-Comminution/ fracture pattern
-Soft tissue coverage
-Vascular injury injury
=No except 3C so requires reparation
Investigation and management of open fractures
-Initial management should focus on careful patient examination to check for associated injuries, control of haemorrhage and the extent of injury
-Photograph (don’t have to keep undressing wound)
-Remove gross contaminants (do not irrigate open fractures of the long bones, hindfoot or midfoot in the emergency department before wound excision.)
-Cover (saline soaked gauze)
-Reduce fracture (apply slab)
-Early debridement- remove foreign material and devitalised tissue, stabilise fracture, external fixator
-Prescribe (IV antibiotic STAT like co-amoxiclav or clindamycin, with/without tetanus booster if not given within 5 years
-In Type IIIc injuries, the mangled extremity scoring system (MESS) can help to predict the need for primary amputation
Aetiology of septic arthritis
-Infection of native joint
=Bacterial, haematogenous spread, synovial joint
-Location: 50% knee, 20% hip, 8%shoulder, 7% ankle
-Neonates: strep, gram -ve
-Infants and children: S. aureus, H. influenza, Salmonella
-Adolescent: S. aureus, gonorrhoea (sexually active young- disseminated)
-Adults: S. aureus, strep, gram -ve
-IV drug abusers: suspect pseudomonas and atypical organisms
Clinical features of septic arthritis
-Pain
-Red, hot, acutely swollen (not shoulder or hip)
-+/- systemic features of infection
-Erythema, warm to touch/ fluctuant
-Fever
-Swelling
-Calor
-Grossly reduced ROM (pseudoparalysis)
Differentials for septic arthritis
-Vascular: haemarthrosis
-Infective/ inflam: osteomyelitis, necrotising fasciitis, abscess, gout, pseudogout
-Trauma: fracture (stress), tendinopathy
-Autoimmune: RA/ Psoriatic
-Degenerative: OA?
Investigation of septic arthritis
-Blood cultures
-Lactate
-Joint aspirate specimen for M&S: synovial fluid, prior to antibiotics if necessary, radiographic guidance
-Joint imaging
-Fever, non-weight bearing, raised ESR and WCC
Management of septic arthritis
-Do not give antibiotics until you have microbiological specimen (unless systemically unwell- immediate)
-Aspirate (needle) the joint to dryness to decompress joint
-Urgent surgical washout, arthroscopic lavage
-IV Abx (gram +ve cocci: flucloxacillin or clindamycin) 4-6 weeks, OPAT after 2 weeks
Pathophysiology of necrotising fasciitis
-Bacterial infection that can move unimpeded along the fascial planes -> rapid spread
-Endo- and exo- toxins result in:
=Thrombosis of the vessels -> ischaemia -> skin necrosis
=Acidic microenvironment -> impaired nerve conduction-> paraesthesia and anaesthesia
-Production of gas -> subcutaneous emphysema
Type 1: mixed anaerobes and aerobes (post-surgery diabetics) most common
Type 2: strep pyogenes
