Trauma and Orthopaedics Flashcards
How can spinal anaesthesia be adjusted to reduce the risk of intraoperative hypotension?
Lower dose of local anaesthetic
Coadminister with intrathecal fentanyl
Hyperbaric bupivacaine with fractured hip down
How long after hip fracture surgery should warfarin be restarted?
6-24 hours
What are the complications of a psoas compartment block?
Visceral damage
Retroperitoneal haematoma
Psoas abscess
Epidural spread
Intrathecal injection
What are accepted reasons for delaying hip fracture surgery?
Severe anaemia <80
Sodium <120 or >150
Potassium <2.8 or >6.0
Uncontrolled diabetes
Acute onset left heart failure
Chest sepsis
Reversible coagulopathy
Tachyarrhythmia >120bpm
When might you want an echocardiogram prior to hip fracture surgery?
Dyspnoea at rest or minimal exertion
Angina
Syncope
Slow rising pulse
Absent second heart sound
What investigations might be useful prior to hip fracture surgery?
Full blood count
Coagulation profile
ECG
Group and save
Urea and electrolytes
What cardiovascular changes are seen in bone cement implantation syndrome?
Reduced stroke volume
Reduced cardiac output
Reduced mean arterial pressure
Increased pulmonary vascular resistance
Reduced right ventricular ejection fraction
What are the two suggested pathophysiological mechanisms for bone cement implantation syndrome?
There is the monomer model and the embolus model
In the monomer model, little bits of methylmethacrylate get pushed into the circulation and trigger a vasodilatory response much like anaphylaxis
In the embolus model, marrow contents, air and cement can emoblise into the circulation and cause a pulmonary embolism-esque circulatory collapse
How can the surgeon reduce the incidence of bone cement implantation syndrome?
Not use cement
Thorough pulsatile lavage of intramedullary canal
Drilling a venting hole in the bone shaft
Ensuring proper haemostasis before cementing
Inserting cement with a cement gun
Retrograde cement insertion
What are the advantages of using bone cement?
Allows rapid confirmation that the joint is stable
Strengthens an osteoporotic joint
Can have impregnated antibiotics
Increased joint longevity
What is the triad of fat embolism syndrome?
Neurological - Confusion, drowsiness, seizures
Respiratory - dyspnoea, hypoxaemia
Dermatological - petechial rash, classically in the skin folds of the axilla and neck
What are Gurd’s criteria for diagnosing fat embolism syndrome?
To diagnose fat embolism syndrome, at least one major and four minor criteria must be present.
Major
- Petechial rash
- Hypoxaemia
- Neurological disturbance
- Pulmonary oedema
Minor
- Temperature greater than 38.5°C
- Tachycardia greater than 110 bpm
- Evidence of myocardial ischaemia
- Retinal emboli on fundoscopy
- Sudden unexplained thrombocytopenia or
anaemia
- Raised ESR
- Lipouria
- Fat in sputum
What are the two theories for the pathophysiology of fat embolism syndrome?
There are currently the mechanical theory and the biochemical theory
Mechanical theory
- Fat globules are forced into damaged
veins and venules
- This then embolises to the pulmonary circulation
- The physical presence of the fat globules lodged in the pulmonary, cerebral and skin arterioles then causes the triad of symptoms seen
- There is certainly visible material entering the chambers of the right side of the heart during orthopaedic surgery which may support this theory
- However it doesn’t explain why usually there is a 24-72 hour delay between the event and symptom onset
Biochemical theory
- This describes more of a ‘toxic inflammatory’ picture
- Excessive fat in the plasma produces toxic breakdown products such as free fatty acids
- This damages the endothelium in delicate capillaries
- This produces more of an inflammatory, endothelial dysfunction-type picture
What factors make a patient high risk for fat embolism syndrome?
This is broken down into two categories - ‘trauma and orthopaedics’ and ‘others’
Trauma and orthopaedics
- Long bone fractures
- Pelvic fractures
- Orthopaedic surgery
Others
- Liposuction
- Severe burns
- Substantial soft tissue injuries
- Bone marrow harvesting
- Bone marrow transplant
- Diabetes
- Pancreatitis
- Total parenteral nutrition
- Steroids
- Sickle cell
- Fatty liver disease
- Osteomyelitis
How can risk of fat embolism syndrome be minimised?
Early immobilisation
Early fixation
Drilling vent holes intraoperatively
Avoid intramedullary nailing where possible
How is acute spinal cord injury classified?
According to the internationally recognised ASIA impairment scale.
A = complete (no sacral sensory or motor function)
B = incomplete (sensory but no motor function)
C = incomplete (preserved motor function)
D = incomplete (more than half of muscles have power grade >2)
E = normal (normal sensory and motor function below the injury)
Neurological level
The level of the injury is classed as the lowest level with normal sensation and motor function on both sides of the body
What are the features of anterior spinal artery syndrome?
loss of motor function and pain and temperature, but intact fine touch, vibration and proprioception
What are the features of Brown-Séquard syndrome?
lateral cord damage with ipsilateral loss of motor function, fine touch, proprioception and vibration and contralateral loss of pain, and temperature
What are the features of central cord syndrome?
Damage to central grey matter, usually in cervical cord, causing upper motor neurone signs in the lower limbs and mixed upper and lower motor signs in the arms with loss of pain and temperature sensation in the upper limbs
What are the features of posterior cord syndrome?
Loss of vibration and proprioception due to compromise of posterior spinal artery
What are the sensory and motor neurological changes seen immediately after spinal cord transection at T4?
Sensory
Total sensory loss below T4 dermatome
Possible sensory loss above this if secondary neurological injury such as oedema
Motor
Flaccid paralysis below T4 (Lower limbs, trunk and lower intercostals)
Areflexia
What are the autonomic neurological changes seen immediately after spinal cord transection at T4?
Neurogenic shock due to sympathetic pathway damage and unopposed parasympathetic tone
If secondary injury extending to T1 then bradycardia and reduced cardiac output due to loss of T1-T4 cardio-accelerator fibres
Cutaneous vasodilatation and anhidrosis below T4 dermatome
Loss of bowel and bladder function
Priapism
What are the phases of spinal shock?
Phase 1 - Day 1 - areflexia due to loss of descending facilitation
Phase 2 - Day 2-3 - reflex return due to denervation supersensitivity
Phase 3 - Week 1-4 - hyperreflexia due to axon-supported synaptic growth
Phase 4 - Up to 12 months - hyperreflexia and spasiticity due to soma-supported synapse growth
What factors contribute to secondary neurological injury?
Local vasomotor changes
Free radical release
Oedema
Electrolyte disturbance
Cell metabolism dysfunction
Apoptosis and necrosis
Inflammation
When is suxamethonium contraindicated in spinal cord injury patients and why?
Between 72 hours and six months after injury
This is due to upregulation of extra-junctional nicotinic acetylcholine receptors, leading to excessive potassium release and life threatening hyperkalaemia
Why are acute spinal cord injury patients at increased risk of venous thromboembolism?
Immobility
Loss of soleus muscle activity leading to venous stasis
Stress response of trauma
Indwelling lines
Other interventions such as surgery
What are the features of neurogenic shock?
Hypotension - reduced inotropy and systemic vascular resistance
Bradycardia - unopposed vagal tone
Hypothermia - vasodilatation
Usually when the cardiac sympathetic fibres between T1 and T5 are affected
