intro lecture Flashcards

1
Q

what is claudication

A

Claudication, literally ‘limping’ (Latin), is a medical term usually referring to impairment in walking, or pain, discomfort or tiredness in the legs that occurs during walking and is relieved by rest.[1][2] The perceived level of pain from claudication can be mild to extremely severe. Claudication is most common in the calves but it can also affect the feet, thighs, hips, buttocks, or arms.[1] The word “claudication” comes from the Latin “claudicare” meaning to limp.

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2
Q

symptoms of chronic limb ischaemia

A

intermittent claudication

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3
Q

risk factors of chronic limb ischaemia

A

– Smoking, Diabetes, Hypertension, Stroke, IHD, hyperlipidaemia, renovascular disease,

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4
Q

best medical therapy for chronic limb ischaemia

A

– Stop smoking, Exercise, Control risk factor, Aspirin, Statin

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5
Q

symptoms of acute limb ischaemia

A
Pallor
Pulselessness
Perishing with cold
Paraesthesiae
Paralysis
Pain
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6
Q

what is critical limb ischaemia

A
• Gangrene
– Wet
– Dry
• Ischaemic Ulceration
• Rest pain
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7
Q

prognosis for critical limb ischaemia

A

 20% will be dead within a year

 More than 20% will have had an amputation at one year

 Only 56% will be alive with two legs at one year
 20% are not reconstructable angiography)

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8
Q

treatment of cricital limb ichaemia

A
 Early diagnosis (all the Ps)
 Heparinise, rehydrate, oxygenate
 Early imaging (duplex +
 Thrombolysis / Angioplasty / Surgery
 (Iloprost)
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9
Q

Reconstruction options in Critical Limb Ischaemia

A
• Thrombolysis
• Angioplasty
• Bypass
– In-situ vein
– Reversed vein
– Synthetic – ring-supported PTFE or dacron
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10
Q

indications for lower limb amputations

A
  • Indications include Irreversible ischaemia, refractory ulceration, loss of function, extensive rhabdomyolysis
  • 80% of leg amputations are a consequence of vascular disease
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11
Q

levels of lower limb amputation

A

• Levels: Above knee, (through knee), below knee, transmetatarsal, ray amputation of digits.

• Level is determined by
– Tissue viability for healing, suitability for prosthetic limb
• Digits may autoamputate
• Patients may experience phantom pain post-operatively

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12
Q

what is an aneurysm

A
  • A localised dilatation of an artery by greater than 50% of its normal diameter.
  • True vs False
  • Fusiform vs Saccular
  • Mycotic (is an aneurysm arising from bacterial infection of the arterial wall. It can be a common complication of the hematogenous spread of bacterial infection.)
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13
Q

Distribution of the location of true arterial aneurysms

A

Distribution of the location of true arterial aneurysms: aortoiliac are 71%, suprarenal are 5%, thoracoabdominal in 9%, femoral in 5%, popliteal in 4%, misc 6%.

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14
Q

AAA prognosis

A

• 1.8% all deaths in men
• 0.7% all deaths in women
(England and Wales)
• Rupture results in 80% mortality

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15
Q

AAA risk factors

A

• Risk factors – Age, Male (5:1), smoking, hypertension, family history, connective tissue
disorder (e.g.Ehlers Danlos)

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16
Q

AAA symptoms

A

• None until rupture or impending rupture
• Usually an incidental finding when presentingwith another complaint or found on screening
• Rupture
– Pain in back and/or abdomen
– Hypotension
– Tachycardia
– Confusion

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17
Q

Risk of rupture of AAA

A
Risk of rupture of AAA
• AAAs 5.0cm
• 3cm 0.4% at 1yr
• 4cm 1%
• 4.5cm 2%
• 5.5-5.9cm 9%
• 6.5-6.9cm 19%
• >7.0cm 34%
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18
Q

Treatment of AAA

A
  • Elective intervention considered at 5.5cm diameter
  • EVAR (EndoVascular Aneurysm Repair)
  • FEVAR (Fenestrated EVAR)
  • Open surgery
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19
Q

treatment of peripheral aneurysms

A
• Upper limb
– tend to embolise causing digital ischaemia
• Thoracic
– Tend to rupture. Treated with TEVAR
• Iliac
– Tend to rupture
• Femoral
– Tend to rupture
• Popliteal
– Tend to thrombose
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20
Q

what are varicose veins

A

Varicose Veins
• Abnormally dilated superficial veins
– Stem veins; long saphenous, short saphenous
– Reticular veins; tributaries of the saphenous veins
– Telangiectasia, thread veins; venules

21
Q

prevalence of varicose veins

A

• Common
– 50% of the population over 40yrs
– 10-20% of adults have significant VVs
– 0.5% have varicosities associated with chronic venous disease

22
Q

varicose vein risk factors

A

• Risk factors
– Family history (70% of first degree relatives), female (5:1 reducing to 2:1 after 6th decade), age over 50, multiparity, prolonged standing, Obesity

23
Q

symptoms and signs of varicose veins

A

• Symptoms
– Asymptomatic, aching, itching, heavy legs, swelling, cosmetic dissatisfaction

• Signs
– Distended veins on standing, telangiectasia, eczema, mild pitting oedema,

24
Q

treatment of varicose veins

A

• Treatment

– Elevation, support hosiery, laser /radiofrequency ablation, open surgery (ligation, stripping, avulsions)

25
Q

complications of varicose vein treatment

A

• Complications of treatment

– Recurrence, nerve damage, bruising, infection, bleeding, DVT, pigmentation,

26
Q

causes of chronic venous insufficiency

A

Chronic Venous Insufficiency
• Untreated primary varicose veins rarely results in CVI
• Post-thrombotic limb commonly does (Post Phlebitic Syndrome)

27
Q

clinical findings in chronic venous insufficiency

A

• Clinical findings

– Swelling, hyperpigmentation, lipodermatosclerosis, oedema, ulceration

28
Q

treatment f chronic venous insufficiency

A

Treatment

– Elevation, skin care, support hosiery, compression bandaging,

29
Q

what is the lymphatic system

A

The lymphatic system is the third circulatory system
• The lymphatic system (1) moves extracellular fluid from the interstitial space back into the
circulation (2) is a vehicle for the immune system
• Failure of (1) results in lymphoedema

30
Q

Lymphoedema clinical signs

A

– Painless diffuse swelling, distal to proximal distribution, hyperkeratosis, sausage-shaped
toes, Stemmers sign

31
Q

Lymphoedema DD

A

– Chronic venous insufficiency, lipidaemia, myxoedema, cardiac/hepatic/renal failure

32
Q

Lymphoedema classification

A

– Primary
• Congenital – from birth
• Praecox – 2nd or 3rd decade
• Tarda – after 35 yrs of age

– Secondary
• Infection, cellulitis, trauma, radiation injury, following LN dissection,

33
Q

Lymphoedema investigation

A

– Exclude other causes, lymphscintigram

34
Q

Lymphoedema treatment

A

– Supportive; skin care, elevation, support hosiery
– Manual lymphatic drainage
– Surgery

35
Q

types of leg ulcer

A

• Arterial
– Extremities/toes/lateral gaiter, severe pain, minimal or no bleeding, punched out margins

• Venous
– Above medial malleolus, moderate pain, may ooze, diffuse margins

• Neuropathic
– Pressure areas, no pain, may ooze, shape defined by location

• Mixed of the above

location and other hx/signs help differentiate between the sites. i.e. venous are most commonly over the medial malleolus and accompanied by the venous eczema skin changes (discolouration and thickened skin).

36
Q

what is the diabetic foot

A

a triad of neuropathy, infection and ischaemia

  • Ulceration at pressure points
    • Charcot foot with loss of function
    • Presents late due to reduced nociception
    • Spreads proximally un-noticed
    • Large vessel disease including calcification
    • Small vessel disease resulting in poor exchange of nutrients at tissue level
37
Q

treatment of the diabetic foot

A

• Treatment involves early drainage of infection and reconstruction of the arterial tree / amputation

38
Q

why is carotid disease important?

A

• 75% of strokes are thromboembolic and the carotid is a site of embolism.

39
Q

what is a TIA

A

• TIA- amaurosis fugax (fleeting) or speech deficit or lateralising neurological deficit lasting less than
24 hours

40
Q

what is a CVA

A

• CVA- focal neurological deficit lasting more than 24hrs

41
Q

management of carotid artery disease

A

• Significant stenosis of the internal carotid artery is 70%

• Medical management
– Aspirin, clopidogrel, control hypertension
• Symptomatic vs asymptomatic disease
• Surgical treatment
– Carotid endarterectomy (carries a 3-5% risk of stroke

42
Q

what is an ABPI

A

ankle-brachial pressure index

43
Q

How would you measure an ankle-brachial pressure index?

A

This is a measure of how well perfused the legs/feet are. Need a hand-held Doppler and a sphygmomanometer. Measure the brachial blood pressure and record the systolic pressure. Then put the Doppler over the three pedal arteries in turn (dorsalis pedis, posterior tibial and perforating peroneal) whilst inflating the cuff. The pressure at which the Doppler signal disappears is the systolic pressure of that artery as it passes under the cuff. Take the highest pedal artery pressure and work out: foot artery/brachial artery.

In health, ABPI should be 1+ in supine position.
Claudication: <0.4

44
Q

Peripheral vascular system examination

A
  1. Introduce yourself to the patient (you’ll probably be told they’re having pain in their legs), check problem and patient name, obtain consent.
  2. Get the patient lying down to start with – need the lower arms and all of the legs exposed.
  3. Inspect from the end of the bed. You are looking for: scars, obvious ulcers/gangrene etc, how the patient is holding their limbs, muscle atrophy.
  4. Examine the radial pulse’s rate, rhythm, volume and character. Assess both radial pulses at once for radial-radial delay.
  5. Feel the brachial pulse both sides.
  6. Say that you would like to measure the BP in both arms at this point.
  7. Feel the carotid pulse both sides and also auscultate for bruits/murmurs.
  8. Palpate and auscultate over the abdominal aorta.
  9. Inspect the legs fully for: signs of (pre) gangrene; ulceration (describe if present); skin changes inc. varicose eczema, loss of hair, pallor, damage from previous ulcers etc; scars from operations (groin, inner thigh); varicosities.
  10. Say if you thought you saw any varicosities you would ask the patient to stand so you could see them better (increased venous filling on standing) –see later notes.
  11. Ask the patient if they have any tenderness in their legs.
  12. Comment on any difference in skin temperature – use the back of your hand and compare the two legs. Start at the feet and move up – if it’s normal in the feet there’s little point in going on. Colder in ischaemia (unless there is infection).
  13. Look between the toes and at the heels for ischaemic changes and guttering (= chronic ischaemia of the limb is associated with onset of extreme pallor of the foot and emptying – ‘guttering’ – of dorsal foot veins with limb elevation.
  14. Look for reduced capillary return by compressing a nail bed on each of the feet.
  15. Palpate the arteries of the legs – comment on any difference in character between the two legs:

Femoral artery – feel both together, auscultate and also time with the radial artery.
The midpoint of the inguinal ligament, which stretches between the anterior superior iliac spine and the pubic symphysis.

Popliteal artery – feel in both flexed and extended positions.
Need to get the patient to relax hamstrings and calf muscles – flex the patient’s knee and place the thumbs of both hands on the tibial tuberosity. Use the pulps of the fingers to palpate the neurovascular bundle against the posterior surface of the upper end of the tibia.

Posterior tibial artery – feel.
Midway between the medial malleolus and the heel.

Dorsalis pedis artery – feel.
Felt along a line that extends between the middle of a line drawn between the two malleoli and the webspace between the first and second toe (congenitally absent in 10% of people).

  1. Elicit Buerger’s test – this is used as a rough guide to the degree of ischaemia in the leg. The leg is elevated passively to 45o (it becomes pale and blanched in a poor arterial supply because it can’t be perfused against gravity). Then ask the patient to hang their leg at 90o over the side of the bed – it becomes cyanosed as the dilated vascular bed fills with deoxygenated blood. Check the mobility of the patient’s leg before doing this.
  2. Say that you would like to measure the ankle/brachial pressure index and examine the foot for sensation.
45
Q

What is the basic anatomy of the long and short saphenous veins?

A

Long saphenous vein passes anterior to medial malleolus up the medial aspect of the calf to behind the knee, then up the middle aspect of the thigh to join the common femoral vein in the groin at the saphenofemoral junction. (ie. up medial aspect of leg)

Short saphenous vein passes behind lateral malleolus and up posterior aspect of calf. Commonly joins popliteal vein at the saphenopopliteal junction – 2cm above posterior knee crease. (ie. up back of calf)

46
Q

What other investigations might you want to do in a patient with varicose veins?

A

venous Duplex scan

Colour Doppler can identify retrograde flow of blood at incompetent valves and perforators.

47
Q

what is lymphoedema

A

●Lymphedema is a progressive disorder of the lymphatic system that results in the interstitial collection of protein-rich fluid (lymph) that can lead to adipose tissue hypertrophy and fibrosis.

●Primary lymphedema is associated with genetic or inherited conditions, all of which are associated with lymphatic disruption.

●Secondary lymphedema is due to underlying disease or as a consequence of prior treatment. In the United States, nearly all cases of lymphedema are secondary to malignancy or cancer therapy. The most common cause of lymphedema worldwide is filariasis, secondary to infection by the nematode Wuchereria bancrofti.

48
Q

presentation of AAA

A

Abdominal aortic aneurysm presents clinically in a variety of ways. Most individuals with AAA have no symptoms. When symptoms do occur, pain is the most common complaint. Pain may or may not be associated with AAA rupture or other associated symptoms.

49
Q

investigation of possible AAA

A

Although AAA may be suspected based upon these clinical features, a definitive diagnosis requires the demonstration of a focal, aortic dilation meeting the criteria for aneurysm (>1.5 times normal diameter) on imaging, or at the time of abdominal exploration. (See ‘Aneurysm definition and anatomy’ above.)

Although an imaging diagnosis is desirable, it is not an absolute requirement in the hemodynamically unstable patient with a known AAA who presents with classic symptoms and signs of rupture (abdominal/back/flank pain, hypotension, pulsatile mass). In this clinical scenario, patients who are candidates for repair are taken to the operating room for immediate management (intraoperative diagnosis) without an intervening diagnostic imaging study. (See “Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm”, section on ‘Introduction’.)

Although any imaging study that demonstrates the focal dilation can be used to make a diagnosis, abdominal ultrasound and computed tomography (CT) of the abdomen are the most useful. Each modality is sensitive and specific for establishing a diagnosis of AAA [67-69], but recommended under differing clinical circumstances (algorithm 1), depending upon the clinical presentation, and the hemodynamic status of the patient.