Trauma and Orthopaedics

Question 1

How can spinal anaesthesia be adjusted to reduce the risk of intraoperative hypotension?

Answer 1

Lower dose of local anaesthetic
Coadminister with intrathecal fentanyl
Hyperbaric bupivacaine with fractured hip down

Question 2

How long after hip fracture surgery should warfarin be restarted?

Answer 2

6-24 hours

Question 3

What are the complications of a psoas compartment block?

Answer 3

Visceral damage
Retroperitoneal haematoma
Psoas abscess
Epidural spread
Intrathecal injection

Question 4

What are accepted reasons for delaying hip fracture surgery?

Answer 4

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

Question 5

When might you want an echocardiogram prior to hip fracture surgery?

Answer 5

Dyspnoea at rest or minimal exertion
Angina
Syncope
Slow rising pulse
Absent second heart sound

Question 6

What investigations might be useful prior to hip fracture surgery?

Answer 6

Full blood count
Coagulation profile
ECG
Group and save
Urea and electrolytes

Question 7

What cardiovascular changes are seen in bone cement implantation syndrome?

Answer 7

Reduced stroke volume
Reduced cardiac output
Reduced mean arterial pressure
Increased pulmonary vascular resistance
Reduced right ventricular ejection fraction

Question 8

What are the two suggested pathophysiological mechanisms for bone cement implantation syndrome?

Answer 8

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

Question 9

How can the surgeon reduce the incidence of bone cement implantation syndrome?

Answer 9

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

Question 10

What are the advantages of using bone cement?

Answer 10

Allows rapid confirmation that the joint is stable
Strengthens an osteoporotic joint
Can have impregnated antibiotics
Increased joint longevity

Question 11

What is the triad of fat embolism syndrome?

Answer 11

Neurological - Confusion, drowsiness, seizures

Respiratory - dyspnoea, hypoxaemia

Dermatological - petechial rash, classically in the skin folds of the axilla and neck

Question 12

What are Gurd’s criteria for diagnosing fat embolism syndrome?

Answer 12

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

Question 13

What are the two theories for the pathophysiology of fat embolism syndrome?

Answer 13

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

Question 14

What factors make a patient high risk for fat embolism syndrome?

Answer 14

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

Question 15

How can risk of fat embolism syndrome be minimised?

Answer 15

Early immobilisation
Early fixation
Drilling vent holes intraoperatively
Avoid intramedullary nailing where possible

Question 16

How is acute spinal cord injury classified?

Answer 16

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

Question 17

What are the features of anterior spinal artery syndrome?

Answer 17

loss of motor function and pain and temperature, but intact fine touch, vibration and proprioception

Question 18

What are the features of Brown-Séquard syndrome?

Answer 18

lateral cord damage with ipsilateral loss of motor function, fine touch, proprioception and vibration and contralateral loss of pain, and temperature

Question 19

What are the features of central cord syndrome?

Answer 19

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

Question 20

What are the features of posterior cord syndrome?

Answer 20

Loss of vibration and proprioception due to compromise of posterior spinal artery

Question 21

What are the sensory and motor neurological changes seen immediately after spinal cord transection at T4?

Answer 21

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

Question 22

What are the autonomic neurological changes seen immediately after spinal cord transection at T4?

Answer 22

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

Question 23

What are the phases of spinal shock?

Answer 23

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

Question 24

What factors contribute to secondary neurological injury?

Answer 24

Local vasomotor changes
Free radical release
Oedema
Electrolyte disturbance
Cell metabolism dysfunction
Apoptosis and necrosis
Inflammation

Question 25

When is suxamethonium contraindicated in spinal cord injury patients and why?

Answer 25

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

Question 26

Why are acute spinal cord injury patients at increased risk of venous thromboembolism?

Answer 26

Immobility
Loss of soleus muscle activity leading to venous stasis
Stress response of trauma
Indwelling lines
Other interventions such as surgery

Question 27

What are the features of neurogenic shock?

Answer 27

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