Aortic Aneurysms and Carotid Artery Disease- Presentation, Investigation and Therapy Flashcards

1
Q

What is an aneurysm

A

Dilatation of all layers of the aorta, leading to an increase in diameter of >50% (abdominal aorta >3.5cm)

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2
Q

Branches of descending aorta (6)

A
  1. Left gastric artery
  2. Hepatic artery
  3. Splenic artery
  4. Right and Left renal artery
  5. Superior and Inferior mesenteric artery
  6. Bifurcation and iliac vessels
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3
Q

Causes of aneurysm disease (3)

A

Degenerative disease
Connective tissue disease- Marfan’s
Infection (mycotic aneurysm)

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4
Q

Risk factors

A
Smoking
Age
Male 
Hypertension
Family history
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5
Q

How prevalent is the disease in 1st degree male relatives

A

30%

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6
Q

Why is a screening programme used

A

To detect dangerous swelling of the aorta, the largest blood vessel in the body

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7
Q

Who is the screening programme aimed towards (2)

A

Men

65+

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8
Q

What is the criteria for screening (10)

A
  1. Definable disease
  2. Prevalence
  3. Severity of disease
  4. Natural history
  5. Reliable detection
  6. Early detection confers advantage
  7. Treatment options available
  8. Cost
  9. Feasibility
  10. Acceptability
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9
Q

Outcomes for screening (4)

A

Normal
Small AAA
Medium AAA
Large AAA

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10
Q

Small AAA

A

3.4-4cm invited for annual USS

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11
Q

Medium AAA

A

4.5-5.5 invited for 3 monthly USS scans

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12
Q

Large AAA

A

> 5.5cm

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13
Q

Impending rupture symptoms (2)

A
  • Increasing back pain

* Tender AAA

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14
Q

Rupture Symptoms (4)

A
  • Abdo/back/flank pain
  • Painful pulsatile mass
  • Haemodynamic instability (single episode or progressive)- perfusion failure leading to shock and advanced heart failure
  • Hypoperfusion- decreased blood flow through an organ
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15
Q

Presentation (5)

A
Distal embolism- Trash foot
Aorticaval fistula
Aortoenteric fistula
Ureteric occlusion
Duodenal obstruction
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16
Q

UK Small Aneurysm Trial (Lancet 1998)

A
  • Surgery did not confer any benefit (e.g. survival) for aneurysms <5.5cm
  • 30 day mortality 5.8% vs risk of rupture 1% (per year)
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17
Q

How is patient fitness assessed for surgery (9)

A
Full history and examination
Bloods
ECG
ECHO
PFTs
MPS
CPEX
End of bed test
Patience preference
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18
Q

USS (5)

A
No radiation
No contrast
Cheap
Operator dependent
Inadequate for surgical planning
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19
Q

CT/MRA (5)

A
Quick
Not operator dependent
Necessary for surgical planning
Contrast
Radiation
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20
Q

General complications of open repair (4)

A

 Wound infection / dehiscence
 Bleeding
 Pain
 Scar

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21
Q

Technical complications (6)

A
	Damage to bowel, ureters, veins, nerves
	Incisional hernia
	Graft infection
	Distal emboli
	Renal failure
	Colonic ischaemia
22
Q

Complication of open repair involving patient factors (4)

A

 DVT/PE
 MI
 Stroke
 Death

23
Q

Management (symptomatic) (4)

A
  • ABCDE
  • History, check records
  • Examination
  • Computed Tomography Angiography (CTA)
24
Q

Emergency open repair procedure

A

Laparotomy (xiphisternum to pubic symphysis)

25
Q

Emergency EVAR (3)

A

Local anaesthetic
Percutaneous
Abdominal compartment syndrome

26
Q

EVAR1 Lancet 2005

A

3-fold reduction in operative mortality for EVAR vs OR. Improved QOL initially with EVAR. QOL improvements lost with increased reintervention and surveillance for EVAR. No difference in overall mortality

27
Q

EVAR2 Lancet 2005

A

No difference in AAA related mortality, all cause mortality of QOL. 9% operative mortality vs 9% person year rupture if no repair

28
Q

IMPROVE trial BMJ 2014 (3)

A
  • EVAR vs open repair for rAAA
  • No difference in 30 day mortality between the 2 interventions
  • Women may benefit more than men from EVAR
29
Q

Atherosclerosis of carotid arteries results in

A

Ischaemic attacks and strokes

30
Q

transient Ischaemic Attack

A

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

31
Q

Stroke

A

clinical syndrome consisting of rapidly developing clinical signs of focal or global disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin

32
Q

Causes of stroke

A

Cerebral infarction
• Primary intracerebral haemorrhage
• Subarachnoid haemorrhage

33
Q

What can cause cerebral infarction (7)

A

AF
Carotid atherosclerotic plaque rupture/thrombus (15%)
Endocarditis
MI
Carotid artery trauma/dissection
Drug abuse
Haematological disorder e.g. sickle cell disease

34
Q

Risk Factors for Carotid Artery Atherosclerosis

A
  1. Smoking
  2. Diabetes
  3. Family history
  4. Male sex
  5. Previous DVT secondary to slight
  6. Hypertension
  7. Hyperlipidaemia
  8. Obesity
  9. Age
35
Q

Diagnosis of Carotid artery disease

A

History
Examination (neurological, Cardiac and auscultate carotids)
CT
USS of Carotids

36
Q

Poiseuille’s Law

A

• As radius of a vessel decreases, resistance increases and velocity increases

37
Q

Best Medical Treatment

A
  • Smoking cessation
  • Control of hypertension
  • Antiplatelet
  • Statin
  • Diabetic control
  • Carotid doppler
38
Q

Circle of Willis

A

• Provides collateral circulation: If one part of the circle becomes blocked or narrowed (stenosed) or one of the arteries supplying the circle is blocked or narrowed, blood flow from the other blood vessels can often preserve the cerebral perfusion well enough to avoid the symptoms of ischemia

39
Q

What is the Circle of Willis Composed of

A

 Anterior cerebral artery (left and right)
 Anterior communicating artery
 Internal carotid artery (left and right)
 Posterior cerebral artery (left and right)
 Posterior communicating artery (left and right)

40
Q

What is an endarterectomy

A

incision is made in carotid artery and plaque is removed. It may prevent a stroke if the carotid artery has been narrowed severely

41
Q

Complications of endarterectomy (6)

A

wound infection, bleeding, scar, anaesthetic risks, nerve damage (Vagus nerve and Hypoglossal nerve) Complications (perioperative): Plaque rupture, hypoperfusion,

42
Q

Branches of the External carotid (5)

A
  • Posterior auricular
  • Occipital
  • Facial
  • Lingual Ascending pharyngeal
  • Superior thyroid
43
Q

NASCET, NEJM 1998

A

No benefit of surgery is stenosis is less than 50%. Dramatic benefit to CEA with stenosis greater than 70%. Risk of reduction of 17% for stroke in 2 years following CEAT compared

44
Q

ECST, Lancet 1998

A

Risk of major stroke or death in 70-79% stenosis is similar between CEA and BMT (best medical treatment). With 90-99% stenosis BMT was more effective

45
Q

CREST, NEJM 2010

A

No difference in composite endpoint. Risk of periprocedural stroke high in CAS (coronary artery stenting). Risk of perioperative MI higher in CEA

46
Q

ACAS trial, Lancet 2004

A

CEA vs BMT in asymptomatic stenosis >60%. 26% of BMT patients went on to develop symptoms and have CEA in the next 10 years

47
Q

NNT

A

: number of patients needed to treat to prevent 1 bad outcome

48
Q

Management in Women

A
  • The NNT to prevent one stroke at 5 years is 9 for men and 36 for women
  • Clear benefit in women with 70-99% stenosis but not in those with 50-69% stenosis
  • This is driven by a high operative risk in women and more rapid reductions in risk of stroke recurrence on medical therapy in women
49
Q

When should CEA be considered (2)

A

asymptomatic patients with high grade carotid stenosis

more beneficial for male patients less than 70 or those with bilateral disease

50
Q

When should asymptomatic CEA be performed

A

low perioperative stroke or death rate

51
Q

What kind of surgery is CEA

A

Prophylactic