chapter 11 - complications of fractures and dislocations Flashcards
2 examples of early complications
arterial injury
neural injury
when can arterial injury occur and why
early: immediate damage to arteries
late: later after injury due to displacement
how to prevent late arterial injury?
fracture splintage and reduction if needed
what can happen to the artery? 4 things
lacerated
avulsed
compressed
contused
why is there an absent pulse following arterial injury
thrombos formation and occludes blood supply
the 6ps of arterial injury to make a diagnosis
pain pallor parasthesia paralysis pulseless polar
what is the management after diagnosis?
- remove tight dressings and pops
- realignment and relocation of dislocation
- if no reversal of symptoms after 1+2 –> vascular angiography and surgical repair
what are the magic hours and how many hours post arterial injury?
6 hours - beyond which irreversible muscle ischaemia occurs
what types of nerve injuries may occur as a complication
neurapraxia
neurotemesis
causes of nerve complications
initial insult
inadequate splinting
causes of intermediate injuries
fat embolism syndrome
compartment syndrome
DVT
pulmonary embolism
define intermediate injury
occurs soon after injury but not at the time of injury
mehcanism of fat embolism syndrom
fat enters blood stream from marrow after a long bone fracture - the fat emboli occludes arteries and capillaries in all organs mechanically and as part of a systemic inflammatory response
clinical manifestations of fat embolism syndrome
agitation
tachypnoea
hypoxia
later - petechial hmg - ocular and skin
how to prevent fat embolism syndrome
adequate splinting and fluid resuscitation
how to manage fat embolism syndome
oxygen and respiratory support
aim: prev further fat immobilisation and manage fracture to prev resp and systemic insult
what is compartment syndrome
increased pressure in a closed osteofacial compartment may result from incresed contents - oedema, haematoma, fracture or increased extrinsic pressure - tight dressing, pop, tourniquet
mech is compartment syndrome
when intracompartmental pressure reaches capillary perfusion pressure then contents of compartment is rendered ischaemic
capillary pressure is usually 25mmhg
distal flow is not interrupted until compartment pressure reaches 100mhg
clinical features on hx of compartment syndrome
pain out of proportion to injury
paraesthesia
examination findings of compartment syndrom
woody hard compartment altered sensation muscle weakness and later paralysis pain on passive stretch distal pulses preserved till late limb not as cold as an arterial injiry
treatment of compartmen syndrome
immediate removal or splitting of pop
wait 10-15 min
open fasciotomy
when is intracompartmental pressure monitoring indicated
high risk patients who cannot communicate - intoxicated, infantile, unconscious
examination findings in a pt with a dvt
low grade pyrexia
swollen limb
pin with muscle stretching
how is the diagnosis of dvt made
venography
duplex doppler studies
- intramural clot seen
how to treat dvt - prophylxis and management
prophylaxis: elevation, dvt stockings, mechanical foot pumps
rx: anticoagulate with heparin, warfarin for 3 months
PE exam
pyrexia pleuritic chest pain tachypnoea hypoxia haemoptysis
investigations to help aid in diagnosis and investigations to confirm diagnosis
aid: cxr, ecg, blood gas
confirm: ventilation perfusion scans, pulmonary angiography
treatment of PE
respiratory support oxygen ventilation
thrombosis elimination - heparin/streptokinase/embolectomy
late complications
infection
disorders of union
joint complications
how to limit infection
early wash out and debridement
examples of infections
gas gangrene
necrotising fascitis
tetanus
organism in gas gangrene
clostridium wlechii - anaerobic
diagnosis of gas gangrene
odour and evidence of gas within tissues
clinical signs of gas gangrene
brownish discharge
rx gas gangrene
prompt surgical debridement/amputation and antibiotics- penicillin
hyperbaric oxygen - not always avail
necrotising fascitis cause ( NF)
symbiotic infection of any number of aerobic + anaerobic bacteria
where are the bacteria causing NF found and what do they do?
closed degloving injuries - area of relative anoxia
organisms result in seperation between the superficial and deep fascia and may cause massive devitalisation of skin
management of NF - prevention
early recognition of degloved tissue
debridement of dead tissue
insertion of drains
treatment of NF
fluid and electrolyte resus
appropriate antibiotics
skin grafting /flaps to defects
pathophysiology of tetatnus
clostridium tetani produce exotoxin which binds to anterior horn cells of the spinal cord after which it cannot be neutralised by tetanus immunoglobulins. organism flourishes in devitalised tissue
symptoms of tetauns
may present after injury has healed tonic clonic contractions risus sardonicus pooling of secretions/cannot swallow spasm of diaphragm and intercostals
treatment of tetanus
prevention: debridement and delayed wound closure
rx: tetanus toxoid
tetanus immunoglobulin
sedation
muscle relaxants
incubation and ventilation
D/O of union - 3
malunion
delayed union
non union
what is malunion and what is the cause? and complications
shortening, angulation or rotation after a fracture
cause: inadquate reduction of fracutre or failure to keep fracture reduced till union
complications: cosmetic, refracture, malaligns joints on either side of it
what is delayed union dependent on?
delayed union varies and depends on: host, local soft tissue, type of fracture
3 conditions which prolong healing and examples
3 conditions
- general: malnutrition, diabetes, smoking, peripheral vascular disease
local: compound fracture, comminution and gross soft tissue injury
iatrogenic: excessive soft tissue striping, inadequate stabilisation or large fracture gap
diagnosis of non union
pain at the # site on loading
motion at the # site
xray showing clear fracture gap
causes of non union
identical to malunion
two major forms of non union
atrophic: poor callus formation
hypertrophic: callus thrown out to try and heal fracture but due to too large a fracture gap or iadequate immobilisation the union fails
treatment of non union
eliminate causes for delaye dunion
bone grafting creates a scaffold for callus formation and provides osteoblast stimulating proteins
sound fracture stabilisation
growth disturbance in children - which fractures do no not cause complications and why
salter harris type 1 and 2 - in the zone of hypertrophy
which fractures can cause growth disturbance, where do they occur and what is the mechanism? and complications?
- salter harris 3,4,5,6
- germinal region of growth plate
- premature growth arrest
- entire plate arrests: limb length discrepancy/ if partial arest: angular deformity
joint complications
stiffness
myositis ossificans
avascular necrosis
osteoarthritis
causes of stifness and how to prevent it
periarticular adhesions
splints for shortest time possible, early physio
what is myositis ossificans? the most common areas?
heterotopic calcification within muscles adjacent to injured joint
elbow, biceps, brachialis
predisposing factors to myositis ossificans
severe head injruies
prophylaxis and rx of myositis ossificans
prophylaxis: nsaids, post op single dose radiotherapy
rx: surgical excision
what is avscular necrosis
ischaemic and death of bone subsequently with bony collapse and degeration of joint
areas of avascular necrosis
most common:: hip after dislocation or intracapsular fractures
other: scaphoid, lunate, talus
how tp prevent avascular necrosis
early reduction and fracture fixation
what happens to joints after trauma and the complication of this
cartilage destruction with trauma impossible to see on plain xray
- lead to early degenerative OA
mechanism of joint injury after trauma and how to prevent it
- malalignment of intra articular and long bone fractures results in abn joint loading
- accurate early intraarticualr fracture reduction and stable fixation
