Aneurysms and Carotid Disease Flashcards
Define aortic aneurysms.
Dilatation of all layers of the aorta, leading to an increase in diameter of over 50%.
What arteries come off of the abdominal aorta and where?
Right
- hepatic artery
- left renal artery
- superior mesenteric arteru
Left
- left gastric artery and splenic artery
- `left renal artery
- inferior mesenteric artery
Bifurcation into common iliac arteries.
What are the causes of aneurysm disease?
Degenerative disease
Connective tissue disease (e.g. Marfan’s disease)
Infection (mycotic aneurysm)
What are the risk factors for degenerative AAA disease?
Male sex, increased age, smoking, DM, hypertension, family history (prevalence of 30% in 1st degree male relatives).
What is the overall prevalence of AAA in the UK?
3%
How can AAA present?
Asymptomatically
- may present with abdominal pain and can be palpated in the abdomen or picked up in screening.
Symptomatically
Where is the most common site for AAA?
just under the renal arteries.
Which areas are particularly susceptible to atherosclerosis?
Areas of bifurcation.
Where does true aneurysm disease affect?
All three layers of the artery wall.
Where does the aorta bifurcate into the two common iliac arteries?
L4 - just above umbilicus.
What are the different criteria for screening?
Definable disease
Reasonable prevalence
Needs to be severe (aneurysms can be fatal)
Natural history that can be interrupted after intervention and that gives you time to intervene afterwards
Reliable detection, tests with suitable sensitivity
Early detection confers advantage
Treatment available
Cost Effective
Feasible
What are the different outcomes in screening related to the size of the AAA?
1 - normal aorta, discharged
2 - small AAA (3-4.4cm) will be invited for annual USS scans
3 - medium AAA (4.5-5.5cm) will be invited for 3 monthly USS scans
4 - Large AAA (>5.5cm)
What symptoms might a patient with an AAA present with?
Impending rupture -
Increasing back pain
Tender AAA
Rupture - Abdo/back/flank pain Painful pulsatile mass Haemodynamic instability (single episode or progressive) Hypoperfusion
What are some of the more unusual presentations?
Distal embolisation - in aneurysms sac there is a lot of thrombus which can break of and lodge else where Aortocaval fistula - aorta erodes into IVC Aortoenteric fistula - aorta erodes into intestines/stomach = bloody stool and death. Ureteric occlusion Duodenal obstruction (both by compression due to aorta)
What are the considerations in management of AAA?
1 - Is the AAA a size to consider repair?
2 - Is patient a candidate for repair?
3 - Is the aneurysm suitable for endovascular or open repair?
How is the size of aneurysm related to risk of rupture?
As size of AA increases risk of rupture significantly increases.
Should surgery be carried out on aneurysms sized 4-5.5cm?
No, Lancet, 1998 showed that surgery did not confer any benefit (i.e. survival) for aneurysms <5.5cm.
30 day mortality 5.8% vs risk of rupture 1% per year.
How do you determine patient fitness for open or endovascular repair?
Full history and examination Bloods ECG ECHO PFTs MPS CPEX End of bed test? Patient preference
What are the imaging techniques used for assessment of AAA and what are their pros and cons?
USS Pros - No radiation or constrast Cheap Cons - Operator dependent Inadequate for surgical planning
CTA/MRA
Pros - Quick
Not operator dependent
Necessary for surgical planning (detailed anatomy)
Cons - Constrast
Radiation
What are the three different types of treatment for AAA?
Conservative
- patient/aneurysm not fit for repair
- plan what to do in case of rupture
Endovascular repair
Open repair
What are possible complications with open repair?
General - wound infection, dehiscence, bleeding, pain, scar.
Technical - damage to bowel, ureters, veins, nerves, incisional hernia, graft infection, distal emboli, renal failure, colonic ischaemia.
Patient factors - DVT/PE, MI, stroke, death.
What are the possible complications with endovascular repair?
General - wound infection, bleeding/haematoma, pain, scar, contrast (reaction/kidney injury), radiation.
Technical - endoleak, femoral artery dissection/pseudoaneurysm, rupture, distal emboli/ischaemia/colonic ischaemia, damage to femoral vein/nerve.
Patient factors - DVT/PE, MI, stroke, death.
What is an endoleak?
With endovascular repair you are relying on radial force to hold the tube in place, for young patients may be asking them to do this for 30/40 years and this can lead to leaking of the tube from different parts.
Discuss open vs EVAR.
3 fold reduction in operative mortality for EVAR vs OR.
Improved QoL initially with EVAR.
QoL improvements lost with increased intervention and surveillance for EVAR.
No difference in mortality overall.
Discuss EVAR vs no repair in unfit patients.
No difference in AAA related mortality, all cause mortality or QoL.
What is the initial route for management of symptomatic patients?
ABCDE
History, check records
Examination
CTA?
Discuss emergency open repair.
Straight to theatre (pre/post CT) Massive transfusion protocol Prep abdomen, rapid anaesthetic laparotomy xiphisternum to pubic symphysis Occlude aorta proximally 30-50% mortality, significant morbidity
Why do you try to keep patients awake for as long as possible during emergency open repair?
Awake to point of incision as tamponade reduces bleeding and stomach muscles relax after anaesthetics.
How does emergency EVAR differ from OR?
Need anatomic suitability, need to do CT scan and work out logistics.
Can use local anaesthetic, may be do percutaneous?
May lead to abdominal compartment syndrome.
What is abdominal compartment syndrome?
Abdominal compartment becomes subject to increased pressures.
What is atherosclerosis of the carotid arteries associated with?
TIA and ischaemic stroke.
Who manages stroke patients?
Specialised stroke teams.
Vascular surgeons are involved in management of carotid disease to prevent further events.
Define transient ischaemic attack.
Focal CNS disturbance caused by vascular events such as micro emboli and occlusion, leading to cerebral ischaemia. Symptoms last less than 24 hours and there are no permanent neurological sequelae.
Define stroke.
Clinical syndrome consisting of rapidly developing clinical signs of focal or global disturbances of cerebral function, lasting more than 24 hours, or leading to death with no apparent cause other than that of vascular origin.
What are the causes of stroke/TIAs?
Cerebral infarction (84%) - AF - Carotid atherosclerotic plaque rupture/thrombus Endocarditis MI Carotid artery trauma/dissection Drug abuse Haematological disorder, e.g. sickle cell disease
Primary intracerebral haemorrhage (10%)
Subarachnoid haemorrhage (6%)
What is Virchow’s triad?
The broad categories that are thought to contribute to thrombosis, they are:
Coagulability (blood too viscous)
Flow (stasis or turbulent flow)
Vessel wall (endothelial injury)
What are the risk factors for carotid artery atherosclerosis?
Smoking Diabetes Family history Male sex Hypertension Hyperlipidaemia/hypercholesterolaemia Obesity Age
Why does a previous DVT not put you at risk for getting carotid artery atherosclerosis?
Because DVT is a disease of the venous system, different from the arterial system.
What steps are important in the diagnosis of carotid artery atherosclerosis?
History
Examination
- neurological: remember contralateral symptoms of paralysis/paresis/visuospatial neglect, dysphasia, ipsilateral amaurosis fungal symptoms
- cardiac
- auscultate carotids - listen for bruit (sign of stenosis)
CT
Carotid USS
What does the velocity of BP in the carotid say about the level of stenosis?
As radius of vessel decreases (i.e. stenosis), velocity increases.
What is the best medical therapy for TIA and stroke?
Smoking cessation Control of hypertension Antiplatelet (e.g. aspirin or clopidogrel) Statin Diabetic control
How would you investigate a confirmed TIA with left sided symptoms?
Carotid doppler, which would probably show occlusion of the right internal carotid artery.
Even if the right internal carotid is occluded how is the brain still perfused?
Circle of willis.
Supplied by carotid, vertebral arteries on either side that all link together in a healthy patient, so brain is still perfused even if one is blocked.
Would you intervene if the internal carotid is completely occluded?
Risk of further stroke is from emboli being showered from high velocity flow in a diseased carotid artery causing distal ischaemia, but if no flow = no risk of emboli, so no need to remove clot.
Would you intervene if the internal carotid is completely occluded?
Risk of further stroke is from emboli being showered from high velocity flow in a diseased carotid artery causing distal ischaemia, but if no flow = no risk of emboli, so no need to remove clot.
How would you manage a patient with confirmed TIA, left sided symptoms, on carotid doppler, right internal carotid artery has 90% stenosis?
Need to remove atherosclerosis via carotid endarterectomy which may prevent a stroke if you have severely narrowed carotid artery. As there is still some flow risk of clot moving to brain.
What complications are associated with carotid endarterectomy?
Wound infection, bleeding, scar, anaesthetic risks.
Nerve damage - need to be careful with vagus and glossopharnygeal.
What may cause a preoperative stroke?
Plaque rupture, hypoperfusion, Virchow’s triad - raw intimal surface and thrombosis.
What is the process of stenting and when would you do it?
Cannulating the artery, putting a wire through it and releasing a stent (this initial part may cause emboli) so only do it when benefits outweigh risk of causing stroke.
Why should the procedure be done asap?
The sooner you do the operation the more advantages conferred to the patients, so try and do it urgently within two weeks.
