fractures and dislocations Flashcards by samson chin

difference between closed and open fracture

higher risk of infection

higher energy of injury

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determinants of classification

mechanism and velocity
degree of soft tissue damage
fracture configuration
degree of contamination

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open fractures gustilo grading

type 1- low energy, wound<1cm clean, often bone piercing skin from inside
type 11- moderate soft tissue damage, wound<10cm, no soft tissue flap or avulsion
type III-high enegy, extensive soft tissue damage, severe fracture,any gunshot, farm accident, bone loss, severe crush injury
-IIIA soft tissue damage+++ but not grossly containated
IIIB periosteal stripping, extensive muscle damage, heavy contamination
-IIIC assoc neurovascular complication

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type IIIB

common,

require flap cover

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management

tetanus, antibiotic prophylaxis
cover stabilise limb
surgery
early and thorough wound excision
do not close wound-leave skin open
review
fasciotomies
radiographs
early definitive skin cover

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definitive management

gustilo grades I-IIIA
same for closed fracture
IIB
external fixation to allow plastic surgery
IIIC- external fixator or primary amputation

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decision to amputate

duration of ishaemia

nerve damage

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surgical debridement and fixation

colour
contraction 
consistency
capacity to bleed
 4C

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MESS scoring system for amputation

skeletal soft tissue injury
limb ischaemia
shock
age
scores> 7 predict low limb liability

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dislocation

complete joint disruption

subluxation- partial dislocation

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common dislocation

shoulder 
Ant: squared off
Post: locked in internal rotation
Elbow
post- olecrannon prominent post
Hip
post: leg short flexed, internal rotation
knee
Anteropost extended
ankle
Lateral externally rotated
subtalar joints
lateral displaced os calcis

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complex regional pain syndrome type1

aetiology
trauma
surgery
infection
repetitive motion dis
IHD, MI

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incidence

after peripheral nerve injury
after colles fracture
higher in women

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CRPS 1

Pain
Oedema
Reduced ROM
Temperature colour changes
PORT
-extremity
-disproportionate to inciting event
-aggravated by activity
pain-severe
swolen +++, skin shiny, discoloured,hot
bone osteoporotic +++
joints osteoarthritic+++
muscles wasted
reduced NA levels
Alpha adrenocepter density increased
skin lactate increase

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allodynia

painful response to innocuous stimuli

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treatment

early active movement +++
regular analgesia and supervised physio
encourage normal use of limb
determine contribution of sympa nervous system
prevention

Pharmacological Therapy

Traditional analgesics
Tricyclic antidepressants
Gabapentin (other anticonvulsants)
Glucocorticoids
Transdermal clonidine
Intravenous bisphosphonates

Summary

Definition : Complex Regional Pain Syndrome

Recognition : PORT (sensitive but not specific)

Diagnosis : Clinical versus laboratory

Management: Early, medication, diagnostic blocks
functional restoration

Crush syndrome

Crush injury to a large muscle mass (thigh, calf, etc.)
direct muscle injury + muscle ischaemia + cell death with release of myoglobin ATN (acute tubular necrosis of the kidneys) ARF (acute renal failure)

clinical features

dark amber urine(test for Hb and Mb)

acute renal failure(hypovolaemia, metabolic acidoses, hyperkalaemia, hypocalcaemia, DIC)

management

IV fluids +++
early (protect kidney & prevent ARF)
Fluid expansion + osmotic diuresis (to maintain high tubular volume + urine flow – aim
-alkalisation of urine with sodium bicarbonate-> reduce tubular precipitation of myoglobin

acute compartment syndrome

Limb-threatening
HIGH INDEX OF SUSPICION!
Key pathology = ISCHAEMIA!
after trauma
also in vascular reperfusion of acutely ischaemic limb
burns
crush injuries
haemorrhage
drug injection

definition

A compartment syndrome develops when intramuscular pressure is elevated sufficiently to reduce nutritional blood flow significantly to tissues within the involved compartment.
A compartment syndrome develops when intramuscular pressure is elevated sufficiently to reduce nutritional blood flow significantly to tissues within the involved compartment.

at risk sites

lower leg
forearm
hand
foot
thigh

acute compartment syndrome

more common in low energy tibial fractures as fascial compartments more likely to be intact ACS occurs in open fractures as compartments will often remain intact

acute compartment syndrome 9ps

1. PAIN 2. Passive dorsiflexion 3. Paraesthesiae 4. Paresis or Paralysis 5. Pallor 6. Pulselessness 7. Perishing cold 8. Pressure 9. (Prompt decompression

missed compartment syndrome

``` If untreated leads to: Muscle ischaemia and necrosis Muscle contractures Delayed fracture healing May nessecitate limb amputation ```

ACS

if hypotensive, lower BP needed to produce ACSpatient with multiple trauma (incl. limb injuries) + hypovolaemic shock – may be in ITU paralysed and ventilated – therefore lost most important criteria for diagnosis of ACS

fat embolism syndrome

HIGH INDEX OF SUSPICION! Occurs after trauma – always with a fracture of a long bone – usually 24-72h Also seen in instrumentation of long bone, e.g. intramedullary nailing Key pathology = HYPOXIA!

definition

Fat within the systemic circulation that produces embolic phenomena, with or without clinical sequelae When associated with an identifiable clinical pattern of symptoms and signs, it is known as Fat Embolism Syndrome (FES) evidence of fat embolism (marrow fat + debris from fracture site) in 90% of patients with traumatic injury - but only 3-4% of long-bone fractures result in ‘FAT EMBOLISM SYNDROME’

risk factors

``` long bone fractures conservative management of long bone fractures multiple trauma associated abdominal injuries severe blood loss ```

pathophysiology

Mechanical Theory Bone marrow enters venous circulation and lodges in the lungs, smaller particles penetrate pulmonary capillaries and enter arterial circulation Biochemical Theory Circulating fatty acids directly affect pneumocytes altering gas exchange

diagnosis

Clinical - Blood Investigations - Hypoxia on ABGs - Fall in haemoglobin - Thrombocytopaenia - Fat droplets within blood clots - CXR

clinical features

``` Brain = most sensitive organ to hypoxia Confused/agitated fits drowsy  coma  dead Tachypnoeic + tachycardic Shock (hypotensive) – late Fever – low grade pyrexia Skin rash ```

investigations

``` Chest X-ray - serial Oxygen saturations + blood gases (PaO2) FBC – Hb + platelets  (thrombocytopenia <150) (Fat globules in blood clots) (Fat globules in sputum) (Fat globules in urine - “sizzle test” ```

FAT EMBOLISM SYNDROME

Pulmonary circulation – HYPOXIA Cerebral circulation – CONFUSION Cutaneous circulation – PETECHIAE Paradoxical embolisation through patent Foramen ovale

treatment

There is no current “Treatment” (i.e. cure) only SUPPORTIVE MANAGEMENT maintain cerebral and pulmonary perfusion. OXYGEN!! may require intensive gas and circulatory monitoring – therefore should be seen by ITU staff if necessary – mechanical ventilation – advanced circulatory support

prevention

PREVENTION - immobilisation/fixation of long bone fractures - possible role for prophylaxis with steroids? - monitoring with pulse oximetry