Vascular Flashcards

1
Q

How can you distinguish between neurogenic and vascular claudication?

A

Intermittent vascular claudication should be differentiated from neurogenic
claudication, which can also present as pain in the lower limb on exertion. Neurogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is intermittent claudication?

A

Intermittent claudication is defined as a reproducible discomfort of a defined group of
muscles that is induced by exercise and relieved with rest.

Usually described by the patient as a cramping, aching pain in the muscle group on exertion such as walking,
and alleviated on stopping (patient does not have to sit down for pain to go away) – “shop window to shop window”.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Defintion of critical limb ischaemia?

A

Critical limb ischaemia is defined as a decrease in limb perfusion that causes a potential threat to limb viability (manifested by a greater than 2 week history of ischemic rest pain, ulceration, and/or gangrene).

Ankle brachial pressure index is typically <0.5.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Defintion of critical limb ischaemia?

A

Critical limb ischaemia is defined as a decrease in limb perfusion that causes a potential threat to limb viability (manifested by a greater than 2 week history of ischemic rest pain, ulceration, and/or gangrene).

Ankle brachial pressure index is typically <0.5.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Difference between wet and dry gangrene?

A

Gangrene is cyanotic, anaesthetic tissue associated with or progressing to necrosis, which occurs when arterial blood supply falls below the threshold to meet minimal metabolic requirements.

Dry gangrene is hard and dry with a clear demarcation between viable and necrotic tissue. Can be allowed to auto-amputate.

Wet gangrene occurs in the presence of infection and is moist, swollen, frequently blistered. This requires surgical debridement or amputation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is LeRiche’s syndrome?

A

LeRiche’s syndrome arises from occlusion of the aortoiliac arteries, and is composed of:

Tetrad of buttock claudication, impotence in men, absent femoral pulses (and distal pulses), and occasionally presence of aortoiliac bruits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the anatomical locations of the lower limb pulses?

A

Femoral pulse: Midpoint of the line joining the pubic symphysis to the anterior superior iliac spine (mid-inguinal point), just below the inguinal ligament

Posterior tibial pulse: one-third of the way down a line joining the medial malleolus to the heel

Dorsalis pedis pulse: just lateral to extensor tendon of hallux.

Popliteal pulse: Ask patient to bend the knee ~60 degrees, then palpate deeply in the popliteal fossa. [Suspect a popliteal aneurysm, if the pulse is strong.]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When is Burgers test significant?

A

A normal lower limb can be raised to 90 degrees without turning white; the lower the angle the greater the degree of peripheral vascular disease, if the Buerger’s angle is less than 20 degrees, this indicates severe ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is ABPI measured?

A

Brachial pressure is measured with a blood pressure cuff around the arm and a Doppler probe over the brachial artery.

The cuff is inflated until the arterial signal is obliterated, then slowly deflated until the signal just starts being detected, at which the pressure is recorded.

Ankle pressures are measured in a similar manner, with the cuff around the calf and the Doppler at the dorsalis pedis and posterior tibial arteries, taking one reading for each artery.

The ankle pressure to be used for each leg is the
higher of the two taken. Ankle pressure is then divided by the brachial pressure, to calculate the ankle-brachial pressure index

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the significant cut-off values for ABPI measurements?

A

> 1 Normal (or calcified vessels. e.g. diabetes)
0.5-1 Intermitted claudication
0.3-0.5 Rest pain/critical limb ischaemia
<0.3 Gangrene, ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are varicose veins?

A

Varicose veins are dilated tortuous superficial veins affecting the lower limb.

Most often found in distribution of the long saphenous vein (most common) and short saphenous vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes varicose veins?

A

Inherent weakness in the vein wall, leading to dilation and separation of valve cusps so they become incompetent. This may be aggravated by obstruction to venous return (secondary varicosities)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some RFs for primary varicose veins?

What is secondary varicose veins?

A
  • Age
  • Parity
  • Occupation – requiring long periods of standing
  • Weight
  • Increased abdominal pressure – constipation, chronic cough, etc

Varicose veins that develop after trauma or deep vein thrombosis are of secondary
cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is acute limb ischaemia?

A

Acute limb ischemia is defined as a sudden decrease in limb perfusion, that causes a potential threat to limb viability.

This is manifested by ischemic rest pain, ischemic
ulcers and gangrene, within two weeks of the acute event. (If >2 weeks it is considered chronic ischaemia).

Acute ischaemia is usually due to sudden occlusion of a feeding arterial vessel. It may occur in a setting of already narrowed vessel lumen (acute on chronic ischaemia) or in a normal lumen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 6 features of acute critical limb ischaemia?

A

Pain
Pallor
Pulselessness
Paraesthesiae
Paralysis
Perishing cold (poikilothermia)

In order of sensitivity to ischaemia, the tissues affected are nerves (most sensitive), muscle, and skin. So, early signs of ischaemia involve pain and numbness, with muscle paralysis and skin changes occurring much later.

The lower limb can survive about 6 to 8 hours in an ischaemic state before the injury becomes irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ix and mx for acute limb ischaemia?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the indications for surgery in AAA?

A
  1. Aneurysm > 5.5 cm diameter.
  2. Increase in diameter >1cm/year.
  3. Symptomatic aneurysm – back pain, tenderness on palpation, distal embolism,
    ruptured/leaking aneurysm.
18
Q

What are some complications of AAA?

A

Rupture

Thrombosis (causing lower limb ischaemia)

Embolism (trash feet)

Fistulation to bowel (aorto-enteric), to vena cava, renal vein

Pressure effects on adjacent organs (e.g. ureter)

Obstruction of branches from aorta e.g. iliac, renal, mesenteric, vertebral

Retroperitoneal fibrosis

19
Q

What is the definition of an aneurysm? What is the difference between fake and true aneurysms?

A

An aneurysm is a localised abnormal dilatation of a blood vessel or the heart.

True aneurysms are bound by all layers of the blood vessel wall

False aneurysm occurs as a result of a traumatic breach of the wall with the sac made up of the compressed surrounding tissue.

20
Q

What are some general complications of carotid endarterectomy?

A

Myocardial infarction
Arrhythmia
Congestive cardiac failure
Severe hypertension or hypotension

Thirty-day perioperative stroke and death rates between 5.8 and 7.3 per cent in symptomatic individuals (NASCET, ECST data)
Wound infection

21
Q

What are some specific complciations that can occur due to carotid endartectomy?

A

Cerebral ischaemia leading to neurological deficits in about 2 per cent

Hyperperfusion syndrome - Hyperaemic cerebral perfusion can cause cerebral oedema and haemorrhagic stroke

False aneurysm formation

Re-stenosis– lower if patch is used

Cranial nerve injury

Wound haematoma –there may be a risk of airway obstruction

22
Q

What are some mx options of claudication - conservative, medical and surgical?

A

Conservative:
- Smoking cessation.
- Exercise training - Walk until pain comes, rest 2-3 minutes, walk again

Medical:-
Anti-platelets e.g. aspirin.
- Statin.
- Control BP and diabetes

Surgical:
Critical ischaemia needs urgent revascularisation. Intermittent claudication should have at least 6 months of conservative treatment first. Monitor claudication distance and ABPI – intervene if deteriorates despite conservative management.
1. Angioplasty/stenting - Angioplasty only effective for focal stenotic lesions and better for large vessels, restenosis can occur.
2. Bypass grafting. Consider bypass when lesions cannot be treated by angioplasty i.e. lesion extends for long distance through the vessel. Needs a good “landing zone” for graft distally – if vessel is diffusely diseased, difficult to perform bypass.
3. Amputation

23
Q

What are the indications for surgical intervention in mx of varicose veins?

A

Symptoms – pain, discomfort

Complications – signs of chronic venous insufficiency, venous ulceration

Cosmesis – large unsightly varicosities

24
Q

What are some mx options of varicose veins?

A

Conservative
- Decrease the amount of time spent standing
- Graduated compression stockings

Surgical
- High tie with great saphenous vein stripping, and stab avulsion of varicosities
- Ultrasound-guided foam sclerotherapy
- Endovenous laser therapy (burns vein from within)

25
Q

What is the major CI for varicose vein surgery?

A

Do not operate if there is deep venous obstruction.

Obtain a venous duplex scan preoperatively to assess the deep system and to map out venous incompetence.

26
Q

What is May Thurners syndrome and when do you treat it?

A

May-Thurner syndrome is caused when the left iliac vein is compressed by the right iliac artery, which increases the risk of deep vein thrombosis (DVT) in the left extremity.

Treatment options include: Anticoagulation, catheter-directed thrombolysis, angioplasty and stenting

27
Q

What are the 4 causes of acute limb ischaemia?

A
  1. Arterial embolism:
    The most common cause of acute limb ischaemia (60-80% of the time). The most likely
    source of embolus is the heart, of which 70% is due to atrial fibrillation, 20% to AMI
    with left ventricular mural thrombus, and a small proportion to prosthetic heart valves
    - Non-cardiac emboli arise from other arteries where there are atherosclerotic plaques
    or an aneurysm.
    - After emboli obstructs the vessel, thrombus can propagate distally (due to stasis of
    blood) and proximally (due to turbulence of incoming blood hitting embolus) by
    derangements in the Virchow’s triad
  2. Acute thrombosis: Thrombosis of a previously stenotic but patent artery (atherosclerotic vessel). When thrombotic occlusion of a vessel does occur, the resulting ischaemia is usually less severe than in an embolic occlusion, because collaterals have had time to form around the chronically stenosed vessel. The other site where thrombosis occurs commonly is apopliteal aneurysm.
  3. Arterial trauma.
  4. Dissecting aortic aneurysm:
    As the blood dissects between the intima and media of the aorta, it can cause
    occlusion of the aortic branches at their origins
28
Q

Mx of ruptured AAA?

A

EMERGENCY.

ABC. Stabilise patient – resuscitation with fluid and blood products. (Do not raise the blood pressure to high as may reduce tamponade effect – we call this hypotensive resuscitation, most will say that as long as they are talking then the BP is OK even is very low. Similarly, neuromuscular blocking agents used in intubation will reduce tamponade effect, worsening haemorrhage.)

Call for vascular surgeon, who will often take to theatre for repair – either open or endovascular.

Ruptured AAA has a very high mortality. About 50% reach ED alive and have a leaking AAA with a tamponade effect by the retroperitoneal structures.

Mortality rate of repair operation in this setting is about 50%.

29
Q

2. How do most aneurysms present?

A

Most commonly asymptomatic, found incidentally during imaging or screening.

30
Q

What are the RFs for atherosclerotic aneurysms?

A

Male (4:1 ratio)
Age (>60 years old)
Smoking
Hypertension
Strong family history

31
Q

Can you name two treatment options for a non-ruptured AAA?

A

Open repair vs. endovascular aortic repair.

Endovascular stenting is an alternative to
open repair, as it is less invasive. It requires an adequate “neck” of the aneurysm proximally and a good landing site distally.

The results are not felt to be as good as open repair, and lifelong monitoring will need to be performed to check for complications such as stent migration or endoleaks.

32
Q

Can you name 6 complications of open aortic repair?

A

Intraoperative/early
- Acute myocardial infarction – atherosclerosis does not just affect the aorta
- Stroke (due to hypotension or embolism)
- Renal insufficiency
- Gut ischaemia – occurs in 2-6%
- Trash foot – embolism of thrombus from the aneurysm
- Infection of graft
- Spinal cord ischaemia.

Late
- Aortoenteric fisula – frank PR bleeding, torrential
- Late infection of prosthetic graft material

33
Q

What are two forms of peri operative monitoring for carotid endarterectomy?

A

Local anaesthetic and neurological assessment

General anaesthetic and transcranial Doppler

34
Q

What is a shunt in carotid endarterectomy and when might it be used?

A

If there is any evidence under local anaesthetic of neurological hemispherical symptoms, or under general anaesthetic of inadequate flow on transcranial Doppler (TCD), a shunt can be inserted as a conduit to enable blood flow during a greater proportion of the procedure time.

NASCET findings suggest overall rate of cranial nerve injury is 8.6 per cent, although 92 per cent are transient.

35
Q

What cranial nerves are at risk during carotid endarterctomy?

A

Hypoglossal (XII)
Vagus (X), Superior laryngeal nerve (X)
Mandibular branch of the facial nerve (V)
Spinal accessory nerve (XI)
Glossopharyngeal nerve (IX) – more common after high carotid artery dissections

36
Q

Name 2 general and 2 specific complications which can occur due to a carotid endarterectomy

A

General
- Myocardial infarction
- Arrhythmia
- Congestive cardiac failure
- Severe hypertension or hypotension
- Thirty-day perioperative stroke and death rates between 5.8 and 7.3 per cent in symptomatic individuals (NASCET, ECST data)
-Wound infection

Specific
- Cerebral ischaemia leading to neurological deficits in about 2 per cent
- Hyperperfusion syndrome - Hyperaemic cerebral perfusion can cause cerebral oedema and haemorrhagic stroke
- False aneurysm formation
- Re-stenosis– lower if patch is used
- Cranial nerve injury
- Wound haematoma –there may be a risk of airway obstruction

37
Q

What is compartment syndrome?

A

A progressive condition in which the elevated tissue pressure within a myofascial compartment exceeds the capillary pressure and compromises blood flow to
structures within that compartment.

38
Q

What can cause compartment syndrome?

A

Compartment syndrome can result from factors that either increase the volume of the compartment contents (swelling post ischaemia, fracture or soft tissue injury) or decrease the volume of the compartment itself (constricting cast, full thickness burns

39
Q

What is the most important indication of compartment syndrome?

A

Pain, pain, pain!

Elicited by passive flexion and extension of the distal joints.

40
Q

. What treatment is warranted? (compartment syndrome)

A

Urgent decompressive fasciotomies.

At a later date, closure of fasciotomies may well require skin grafting.

41
Q

What blood test can be used to measure muscle necrosis?

A

Muscle creatine kinase (CK) can be measured but note this may be low at the start of the ischaemic insult so can’t be used to gauge whether to act

42
Q

2 systemic complications of compartment syndrome?

A

Rhabdomyolysis leading to myoglobinaemia and subsequent renal failure
Shock
Hyperkalaemia
Hyperphosphataemia
Hyperuricaemia
Metabolic acidosis
Death.