Vascular Flashcards
4 types of ischaemic stroke?
- Thrombosis
- Embolic
- Systemic hypoperfusion
- Cerebral venous sinus thrombosis
In context of carotid artery atheroma
- Near total occlusion with thrombosis may elicit stroke
- Embolus of atheromatous plaque from carotid artery into ipsilateral cerebral artery may precipitate stroke
When should carotid endarterectomy be performed?
Following TIA or stroke
NICE recommends assessed carotid doppler and referred within 24hrs
Undergo surgery within 2 weeks
Complications of carotid endarterectomy?
Stroke - 2-5% risk
Periop MI, up to 4% risk
Bleeding
Infection
Cranial nerve injury
- Superior laryngeal and recurrent laryngeal nerve dysfunction
- Hypoglossal nerve
Cerebral hyPERperfusion syndrome
Advantages / disadvantages of GA for carotid endarterectomy?
Advan:
- Immobility
- Potential for neuroprotection
- Control of PaCO2 through ventilation
- Attenuated stress response (if stable GA)
Disad
- Lack of continuous direct neurological monitoring
- Higher rates of intraop shunt usage
- Intraop hypotension
- Post-op hypotension
- Delayed recovery may mask neurological symptoms and signs
Advantages / disadvantages of regional for carotid endarterectomy?
Advan:
- Awake patient therefore real-time neuro monitoring
- Avoids airway intervention
- Avoids pressor response to intubation
- Reduced shunt rate
- Surgical closure at normal BP therefore less haematoma
- Reduced LoS
Disad:
- LA block associated risks
- Heightened anxiety/pain may precipitate MI
- Risk of GA conversion
- Requires a co-operative pt.
GALA trial showed no difference, large multi-centre trial
Primary outcome identical
How to monitor cerebral perfusion under GA for Carotid Endarterectomy
Carotid artery stump pressure
Transcranial doppler
NIRS
EEG
What is cerebral hyperperfusion syndrome?
Dysregulated state of cerebral blood flow following restoration of blood flow to brain
1-3% of carotid endarterectomy patients
- Severe ipsilateral headache
- Seizures
- Focal neurological deficit
Often HYPERtensive
Can occur up to 1 month but commonly 5 days
Risk factors
- HTN, high grade stenosis, contralateral carotid stenosis, recent contralateral carotid endarterectomy
Potential benefits of EVAR over open AAA
- Less physiological disturbance
- Shorter surgery duration
- Reduced blood loss
- Less post op pain
- Reduced length of ICU and hospital stay
EVAR 2 = no survival benefit in EVAR vs no intervention in AAA open repair ineligible patients BUT dec. mortality in aneurysm related deaths
For planned abdominal aortic aneurysm (AAA) repair, endovascular aneurysm repair (EVAR) generally leads to lower early mortality and morbidity compared to open surgical repair, but long-term outcomes show EVAR has a higher risk of reintervention and aneurysm rupture
What are the risk factors for spinal cord ischaemia during aortic surgery?
Patient factors:
1. Atherosclerosis, diabetes, renal disease
2. Previous aortic surgery
Surgical factors:
1. Extent of aneurysm
2. Surgical difficulty
3. Cross clamp duration
4. Severity of hypotension
Incidence of spinal cord ischaemia during thoracoabdominal aortic aneurysm repair?
3-18%
Causes of poor blood supply to spinal cord?
- Trauma
- Aortic aneurysm rupture
- Aortic dissection
- Aortitis - vasculitis, collaged disorders
- Venous hypertension
- Degen spinal diseases and disc herniation
- Severe atherosclerosis
- Iatrogenic
- Vasoconstrictors in epidural space
- Cross clamping aorta
- Coeliac plexus block
- Severe Hypotension
What spinal cord protection strategies exist during AAA repair
Aim is to maintain SPINAL CORD PERFUSION PRESSURE (SCPP)
= MAP - CSFP
Therefore
1. Optimise MAP - vasopressors, fluid/blood
2. Minimise CSFP - use of lumbar drains
Other strategies
1. Mild systemic hypothermia 32-34 deg
2. Distal aortic shunting through fem fem bypass and L heart bypass
3. Pharmacological neuroprotection - steroids, opioids, free radical scavengers
4. Monitoring spinal cord function with MEPs/SSEPs
Risk factors for AAA
Age >65
Male
Smoker
Hypertension
Hypercholesterolaemia
Family hx. of AAA
Vascular disease elsewhere
Emergency Department management of AAA rupture
ABCDE assessment with including
- Applying high flow O2
- Establishing wide bore IV access
- Sending bloods for FBC, U+E, clotting and urgent x-match
- Awake arterial line if possible
Focussed history looking at:
- Co-morbidities
- Drugs and allergies
- Smoking and alcohol
- Functional status
- Previous anaesthetic complications
- Fasting status
Explain:
- Consent for anaesthesia
- Crit Care follow up
Organisation/logistics:
- Urgent vascular review
- Alert theatres and assemble team
- Senior on-call anaesthetist
- ICU pre-alert
IF STABLE consider CT for planning
Major haemorrhage activation
O-neg blood if delay
Why is induction of anaesthesia so risky in ruptured AAA
Myocardial depression and reduction in sympathetic tone/peripheral vasodilation in a hypovolaemic patient
Abdominal muscle relaxation = tamponade release
IPPV increases intrathoracic pressure and reduces preload
Therefore aim is to X-clamp aorta above aneurysm as soon as possible after induction
Talk through pre-induction and induction stage of ruptured AAA
Location - in OT, pt. on table with surgeons scrubbed and abdomen draped
Fluid resus aiming to correct conscious level and myocardial ischaemia
Infuse through level 1 warmer
AAGBI standard monitoring + art + IDC
Modified RSI, careful titration of agents
Consider ketamine
Surgery commence soon after induction
Maintain with volatile, titrate using BIS
Intraoperative issues of ruptured AAA
Aortic cross-clamping
Need for additional lines e.g. CVC
Coagulopathy - correct with products, TEG/ROTEM
Cell salvage
Maintanence of normothermia
Reperfusion injury
Complications post op ruptured AAA
Bleeding from anastamosis
Renal impairment
Abdominal hypertension and compartment syndrome
Ileus
Bowel ischaemia
Lower limb ischaemia and embolism
Talk through physiology of aortic cross-clamp application
Position of clamp depends on aneurysm anatomy and involvement of renal arteries - higher the cross clamp the greater the physiological disturbance
On application of cross clamp:
Proximal to clamp:
Increase in afterload, increase in SVR in upper limbs
Distal to cross-clamp: vasodilation due to ischaemia
Overall SVR decreases due to accumulation of local metabolites causing vasodilation
Increased afterload may precipitate ischaemia/arrythmia manage with increased volatile agent or GTN
Physiology of aortic cross clamp release
Vasculature below clamp maximally dilated due to ischaemia
Sudden decrease in afterload
Release of products of anaerobic metabolism into systemic circulation - lactic acid, K+
Profound hypotension / myocardial depression/ arrythmias may arise
Need to have vasopressors and inotropes prepared
May decrease risk by releasing one ‘leg’ of aortic graft at a time
Renal impairment following AAA surgery
Common following ruptured AAA
Causes:
Pre-existening renal artery /intrinsic renal disease
Supra-renal aortic clamp
Intraoperative renal artery trauma
Post-op abdominal compartment syndrome
Operative hypovolaemia
Why might patient with emergency AAA repair develop abdominal compartment syndrome and what is it?
IAP measured using special urinary catheter measuring intra-vesical pressure
IAP >12 = abdominal hypertension
IAP >20 = abdominal compartment syndrome
Consequences of abdominal compartment syndrome
Respiratory - diaphragmatic splinting, increased vent pressures, baro/volu trauma
Cardiovascular - IVC compression, reduced pre-load and reduced CO
Renal - compression renal veins, reduced filtration gradient
CNS - ICP increase by reduced venous drainage
Bowel wall ischaemia - oedema and bacterial translocation
