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4th year everything > Vascular Flashcards > Flashcards

Vascular Flashcards

1
Q

Incidence of chronic limb ischaemia?

A

5% of males >50 yrs have intermittent claudication

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2
Q

Definition of chronic limb ischaemia?

A
  • Ankle artery pressure <50mmHg (toe <30mmHg)
  • And either:
    Persistent rest pain requiring analgesia for >2 weeks
    Ulceration or gangrene.
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3
Q

Causes of chronic limb ischaemia?

A

Atherosclerosis

  • Typically asymptomatic until 50% stenosis
  • Vasculitis and fibromuscular dysplasia are very rare causes.
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4
Q

Atherosclerosis summary - pathophysiology?

A
  1. Endothelial injury: haemodynamic, HTN, icnreased lipids.
  2. Chronic inflammation
    - Lipid-laden foam cells produce GFs, cytokines, ROS and MMPs.
    - lymphocyte and SMC recruitment.
    - SM proliferation: conversion of fatty streak to atherosclerotic plaque.
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5
Q

Difference between Arteriosclerosis and atherosclerosis?

A 
Arteriosclerosis = general arterial hardening
Atherosclerosis = Arterial hardening specifically due to atheroma
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6
Q

Atheroma pathology?

A

Fibrous cap: SM cells, lymphocytes, collagen

Necrotic centre: Cell debris, cholesterol, Ca, foam cells.

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7
Q

Risk factors for chronic limb ischaemia?

A

Modifiable: Smoking, BP, DM control, hyperlipidaemia, decreased exercise.
Non-modifiable: FH and PMH, Male, increased age, genetic.

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8
Q

Associates vascular diseases with chronic limb ischaemia?

A 
IHD: 90% 
Carotid stenosis: 15% 
AAA. 
Renovascular disease. 
DM microvascular disease.
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9
Q

Presentation of chronic limb ischaemia?

A

Intermittent claudication

  • Cramping pain after walking a fixed distance
  • Pain rapidly relieved by rest
  • Calf pain = superficial femoral disease (commonest)
  • Buttock Pain = Iliac disease
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10
Q

What is the presentation of critical limb ischaemia?

A

Fontaine 3-4

1 or more of: 
Rest pain  
- Especially @ night 
- >2 weeks
- Usually felt in the foot
- Not helped by analgesia
- Pt hangs foot out of bed 
- Due to decreased CO and loss of gravity help.

Ulceration
Gangrene

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11
Q

What is Leriche’ syndrome?

A

Leriche’s syndrome: aortoiliac occlusive disease

  • Atherosclerotic occlusion of abdominal aorta and iliacs

Presents with triad

  • Buttock claudication and wasting
  • Erectile dysfunction
  • Absent femoral pulses
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12
Q

What is Buerger’s Disease?

A

Thomboangiitis Obliterans

  • Young, male heavy smoker
  • Acute inflammation and thrombosis of arteries and veins in the hand and feet.
  • Leads to ulceration + gangrene.
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13
Q

Signs of chronic limb ischaemia?

A

Pulses: Pulse and increased CRT (normall <2sec)
- Ulcers: painful, punched out, on pressure points.
- Nail dystrophy/onycholysis.
- Skin:cold, white, atrophy, absent hair.
- Venous guttering (veins collapse)
- Muscle atrophy
Decreased Buerger’s Angle
- >90: normal
- 20-30: ischaemia
- <20: Severe ischaemia.

+ve Buerger’s Sign - Reactive hyperaemia due to accumulation of deoxygenated blood in dilated capillaries.

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14
Q

What is Buerger’s test?

A

Patient is positioned supine.
Standing at bottom of bed, raise both of the patient’s feet to 45 degrees for 2-3mins.
- Look for pallor - Note at what angle this occurs. If less than 20 degrees indicates severe limb ischaemia.

Then drop leg over side.
- Look for reactive hyperaemia.

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15
Q

Clinical classification? - Fontaine?

A
  1. Asymptomatic
  2. Intermitted claudication
    a. >200m
    b. <200m
  3. Ischaemic rest pain
  4. Ulceration/gangrene
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16
Q

What is the rutherford classification?

A 
Mild claudication 
Moderate claudication
Severe claudication 
Ischaemic rest pain 
Minor tissue loss
Major tissue loss.
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17
Q

What are the investigations for chronic limb ischaemia?

A

Doppler Waveforms

  • Normal: triphasic
  • Mild stenosis: biphasic
  • Severe stenosis: monophasic
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18
Q

What if ABPI is high? >1.4

A

Calcification: CRF, DM
>1.4 . Diabetes leading to high ABPI. Neuropathic and duplex shows its normal.
Can use toe pressure <30mmHg.

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19
Q

What is normal ABPI?

A

> or equal to 1.

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20
Q

What is asymptomatic ABPI?

A

Fontaine 1: 0.8-0.9

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21
Q

What is claudication ABPI?

A

Fontaine 2: 0.6-0.8

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22
Q

What is rest pain ABPI?

A

Fontaine 3: 0.3-0.6

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23
Q

What is ulceration and gangrene ABPI?

A

Fontaine 4 <0.3.

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24
Q

Walk Test

A

Walk on treadmill @ certain speed and incline to establish max claudication distance.

ABPI measured before and after: 20% decreased is significant

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25
Q

Bloods for chronic limb ischaemia?

A

FBC, U+E, lipids + glucose, ESR: arteritis, G+S: possible procedures.

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26
Q

Imaging for Chronic limb ischaemia?

A

Assess site, extent and distal run-off.

  • Colour duplex US
  • CT/MR angiogram: gadolinium contrast.
  • Digital subtraction angiography
    Invasive therefore not commonly used. USed when performing therapeutic angioplasty or stenting.

May also do ECG looking for ischaemia.

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27
Q

What is the conservative management of chronic limb ischaemia?

A
  • Most patients with claudication can be managed conservatively
  • Increased exercise and employ exercise program - very important.
  • Stop smoking - must quite smoking.
  • Weight loss
  • Foot care
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28
Q

Medical management of chronic limb ischaemia

A
  • Risk factors: BP, Lipids, DM
    B-B don’t worsen intermittent claudication but used with caution in CLI.
  • Atorvastatin 80mg regardless of baseline cholesterol.
  • Anti-platelets:
    clopidogrel (75mg) over aspirin
  • Analgesia: may need opiate
  • parenteral prostanoids decreased pain in patients unfit for surgery.

Can use naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life.
Cilostazol: phosphodiesterase III inhibitor - not recommended.

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29
Q

What is the endovascular management of chronic limb ischaemia?

A

Percutaneous Transluminal Angioplasty ± stenting.

Good for short stenosis in big vessels: E.g iliacs, SFA.

Lower risk for patients: performed under LA as day case.

Improved inflow –> decreased pain but restoration of foot pulses is required for Rx of ulceration/gangrene.

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30
Q

What are the surgical reconstruction used in chronic limb ischaemia?

A

Indications

  • V.short claudication distance (e.g <100m)
  • Symptoms greatly affecting pts QoL
  • Development of rest pain.
  • Critical limb ischaemia should cannot have angioplasty.
  • Pre-op: need good optimisations as likely to have cardioresp co-morbidities.
  • Practicalities: need good proximal supply and distal run-off. Saphenous vein grafts preferred below the IL. More distal grafts have increased rates of thrombosis.
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31
Q

What is the classification of surgical reconstructions?

A

Anatomical: fem-pop, fem-distal, aortobifemoral.

Femoral popliteral bypass.

Extra-anatomical: axillo-fem/ bifem, fem-fem crossover.

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32
Q

What other surgery can be used for chronic limb ischaemia?

A

Endarterectomy: core-out atheromatous plaque
Sympathectomy: chemical (etoh) or surgical.

Amputation.

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33
Q

What is the prognosis of chronic limb ischaemia?

A

1 yr after onset of CLI

  • 50% alive without amputation
  • 25% will have had major amputation
  • 25% dead (MI/Stroke).
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34
Q

What is acute limb ischaemia?

A

Acute: ischaemia <14d
Acute on chronic: worsening symptoms and signs <14 d
Chronic: ischaemia stable for >14 days.

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35
Q

Severity of acute limb ischaemia ?

A
  • Incomplete: Limb not threatened
  • Complete: limb threatened
    Loss of limb unless intervention within 6hrs.
  • Irreversible: requires amputation
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36
Q

Causes of acute limb ischaemia?

A

Thrombosis in situ (60%)

  • A previously stenosed vessel with plaque rupture.
  • Usually incomplete ischaemia

Embolism

  • 80% from LA in AF
  • Valve disease
  • Iatrogenic from angioplasty/surgery
  • Cholesterol in long bone fracture
  • Paradoxical (venous via PFO)
  • Often complete ischaemia

Graft/stent occlusion
Trauma
Aortic dissection

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37
Q

Presentation: 6Ps

A 
Pale 
Pulseless
Perishingly cold 
Painful 
Parasethesia 
Paralysis
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38
Q

Difference between a thrombosis and embolus?

A 
Thrombosis 
= hrs to days. 
- is less severe 
- History of claudication 
- Contralateral pulses absent 
- Diagnosed on angiography
- Thrombolysis management and bypass surgery.

Embolus

  • Sudden
  • Profound ischaemia
  • Present with AF
  • Absent claudication hx
  • present contralateral pulses
  • Diagnosed clinically
  • Manage = Embolectomy + warfarin.
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39
Q

Investigations for acute limb ischaemia?

A

Blood

  • FBC, U+E, INR, G+S
  • CK

ECG

Imaging
- CXR, Duplex Doppler

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40
Q

General management of acute limb ischaemia?

A
  • In an acutely ischaemic limb discuss immediately with a senior as time is crucial.
  • NBM
  • rehydration: IV fluids
  • Analgesia: morphine + metoclopramide
  • Abx: e.g augmentin if sings of infection
  • Unfractionated heparin IVI: prevents extension

Is there complete occlusion

  • Yes: urgent surgery: embolectomy or bypass.
  • No- angiogram + observe for deterioration.
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41
Q

When is angiography performed?

A

Not performed if there is complete occlusion as it introduces delay: take straight to theatre

If incomplete occlusion, pre-op angio will guide any distal bypass.

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42
Q

Management of an embolism?

A
  1. Embolectomy
    - Under LA or GA
    - Wire fed through embolus
    - Fogarty catheter fed over the top
    - Balloon inflated and catheter withdrawn to remove embolism.
    - Send embolism for histo (exclude atrial myxoma)
    - Adequacy confirmed by on-table angiography.
  2. Thrombolysis
    Consider if embolectomy unsuccessful
    - E.g local injection if TPA

Other option

  • Emergency reconstruction
  • Amputation

Post embolectomy

  • Anticoagulate: heparin IVI –> warfarin
  • ID embolic source : ECG, echo, US aorta, fem and pop
Complications 
- Reperfusion injury 
Local swelling --> compartment syndrome 
Acidosis and arrhythmia 2ndry to increased K
ARDS 
GI oedema --> endotoxic shock.

Chronic pain syndromes.

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43
Q

Management of thrombosis?

A
  • Emergency reconstruction if complete occlusion
  • Angiography + angioplasty
  • Thrombolysis
  • Amputation
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44
Q

Carotid artery disease definition?

A

Stroke: Sudden neurological deficit of vascular origin lasting >24hrs

TIA: sudden neurological deficit of vascular origin lasting <24hrs (usually last <1hr) with complete recovery.

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45
Q

What is the pathogenesis of carotid artery disease?

A

Turbulent flow –> decreased shear stress at carotid bifurcation promoting atherosclerosis and plaque formation.

Plaque rupture –> complete occlusion or distal emboli.

Cause 15-25% of CVA/TIA

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46
Q

Investigations of carotid artery disease?

A

Duplex carotid doppler

MRA

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47
Q

Management of Carotid artery disease?

A

Conservative

  • Aspirin or clopidogrel
  • Control risk factors
Surgical: Endarterectomy 
- Symptomatic 
>70% (5% stroke risk) 
>50% if low risk (<3%) 
Perform with 2week of presentation

Asymptomatic
- >60% benefit if low risk

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48
Q

Complications of Endartectomy?

A 
Stroke or death: 3% 
HTN: 60% 
Haematoma 
MI 
Nerve injury 
- Hypoglossal: ipsilateral tongue deviation 
- Great auricular: numb ear lob
- Recurrent laryngeal: hoarse voice, bovine cough
49
Q

Stenting of carotid artery disease?

A

Less invasive: decreased hospital stay, decreased infection, decreased CN injury.

There is concern over increased stroke risk
Meta-analysis shows no sign

Younger pts have best risk/benefit ratio.

50
Q

What is an aneurysm?

A

Abnormal dilatation of a blood vessel >50% of its normal diameter.

51
Q

What is a true aneurysm?

A

Dilatation of a blood vessel involving all layers of the wall and is >50% of its normal diameter.

  • Fusiform: AAA
  • Saccular: Berry aneurysm
52
Q

What is a false aneurysm?

A

Collection of blood around a vessel wall that communicates with the vessel lumen.

Usually iatrogenic: puncture, cannulation.

53
Q

What is a dissection?

A

Vessel dilatation caused by blood splaying apart the media to form a channel within the vessel wall

54
Q

Causes of aneurysms?

A

Congenital

  • ADPKD –> Berry aneurysms
  • Marfan’s, Ehler’s-Danlos.
Acquired 
- atherosclerosis 
- Trauma, e.g penetrating trauma 
- Inflammatory: takayasu's aortitis, HSP 
- Infection 
Mycotic: SBE
Tertiary syphilis (esp thoracic).
55
Q

Complications of aneurysms?

A 
Rupture 
Thrombosis
Distal embolisation 
Pressure: DVT, oesophagus, nutcracker syndrome. 
Fistula (IVC, intestine)
56
Q

What is a popliteal aneurysm?

A

Loss common than AAA
50% of patients with popliteal aneurysm also have AAA.

Presentation

  • Very easily palpable popliteral pulse
  • 50% bilateral
  • Rupture is relatively rare
  • Thrombosis and distal embolism is main complication –> acute limb ischaemia

Management

  • Acute: Embolectomy or fem-distal bypass
  • Stable: Elective grafting + tie off vessel.
57
Q

Epidemiology of AAA?

A

Prevalence: ~5% ?50 yrs
Mortality: 10,000 deaths/yr
Sex: M>F = 3:1

Causes

  • HTN, Diabetes or Smokers
  • Also connective tissue disease and Marfan’s.
58
Q

Pathology of AAA?

A

Dilatation of the abdominal aorta >3cm
90% infrarenal
30% involve the iliac arteries

59
Q

Presentation of AAA?

A

Usually asymptomatic: discovered incidentally
- May –> back pain or umbilical pain radiating to groin

Acute limb ischaemia

Blue toe syndrome: distal embolisation
Acute rupture

60
Q

Examination of AAA?

A

Expansile mass just above the umbilicus
Bruit may be heard
Tenderness + shock suggests rupture

61
Q

Investigations of AAA?

A

AXR: calcification can beseen
Abo US: screening + Monitoring

CT/MRI: gold-standard
Angiography

  • Won’t show true extent of aneurysm due to endoluminal thrombus
  • Useful to delineate relationship of renal arteries.
62
Q

Management of AAA?

A

Conservative

  • Manage CVS risk factors: Esp BP
  • AAA <5.5 cm is max diameter that can be monitored by US/CT
  • <3 = Normal - no action
  • 3-4.4cm: yearly monitoring
  • 4-5.5cm: 3 monthly monitoring
  • > =5.5 = Refer in 2 weeks.

Refer people with an abdominal aorta diameter of 5.5 or later to regional vascular service within 2 weeks.

Refer people with an abdominal aorta diameter of 3-5.6 to be seen in 12 weeks of diagnosis.

63
Q

Surgical AAA?

A

Aim to treat aneurysms before it ruptures

  • Elective mortality: 5%
  • Emergency mortality: 50%

Low rupture = asymptomatic, aortic diameter <5.5.
- Abdo US surveillance

Operate when risk of rupture >risk of surgery.
Indications
- Symptomatic (back pain = imminent rupture)
- Diameter >5.5
- Rapidly expanding: >1cm
- Causing complications e.g emboli
- Refer within 2 weeks for surgery.

Open or EVAR

  • EVAR has decreased perioperative mortality
  • No decreased in mortality by 5yrs due to fatal endograft failures
  • EVAR not better than medical management in unfit patients.
  • Midline/Transverse incision.
  • bowel + Distal duodenum mobilised to access aorta.
  • Systemic heparinization
  • Cross clamp
  • Insert graft either tube or bifurcated depending upon anatomy.
  • Suture using prolene
  • Clamps off
  • Haemostasis
  • Closure of aneurysm sac to minimise risk of aorto-enteric fistula.

Supra renal AAA requires clamp therefore carries high risk.

64
Q

Screening of AAA?

A

UK men offered one-time US Screen @ 65yrs.

65
Q

Ruptured AAA Rates?

A 
<5.5cm = 1% / yr
>6cm = 25% / yr
Increased risk if 
- BP increased 
- Smoker 
- Female 
- Strong FH
66
Q

Rupture of AAA presentation?

A

Sudden onset severe abdominal pain

  • Intermittent or continuous
  • Radiates to back or flanks (don’t dismiss as colic
  • Collapse –> Shock
  • Expansile abdominal mass.
67
Q

Management of ruptured AAA?

A
  • High flow O2
  • 2x large bore cannulae in each ACF
  • Give fluid if shocked by keep SBP <100mmHg
  • Consider giving 6 units of blood. -
  • Give O- blood if desperate
  • Blood: FBC, U+E, Clotting, amylase, xmatch

Instigate the major haemorrhage protocol.
Call vascular surgeon, anaesthetist and warn theatre.
Analgesia
Abx prophylaxis: cef+met
Urinary catheter + CVP line
If stable + Dx: US or CT may be feasible

Take to theatre: Clamp neck, insert dacron graft.

Suprarenal is bad - due to risk of renal failure.

68
Q

What is a thoracic aortic dissection?

A
  • Blood splays apart the laminar planes of the media to form a channel within the aortic wall.
69
Q

Aetiology of a thoracic dissection?

A

Atherosclerosis and HTN cause 90%

Minority caused by connective tissue disorder

  • Marfan’s, Ehlers Danlos
  • Vitamin C deficiency
70
Q

Presentation of thoracic aortic dissection?

A

Sudden onset, tearing chest pain

  • Radiates through to the back
  • Tachycardia and HTN (primary and sympathetic)

Distal propagation –> sequential occlusion of branches

  • Left hemiplegia
  • Unequal arm pulses and BP
  • Paraplegia
  • Anuria

Proximal propagation

  • Aortic regurgitation
  • Tamponade

Rupture into pericardial, pleural or peritoneal cavities
- Commonest cause of death.

71
Q

What is the Stanford Classification?

A

Type A: Proximal

  • 70%
  • Involves ascending aorta + descending
  • higher mortality due to probable cardiac involvement
  • Usually requires surgery

Type B: Distal

  • 30%
  • Involves descending aorta only: distal to L SC artery.
  • Usually best managed conservatively.
72
Q

Investigations of Thoracic Dissection?

A

ECG: Exclude MI

TTE/TOE: can be used in haemodynamically unstable patients.

CT/MRI: not suitable for unstable pts.

73
Q

Management of Thoracic Aortic Dissection?

A

Resuscitation
- investigation
Bloods: X-match 10u, FBC, U+E, Clotting, amylase

ECG: 20% shows ischaemia due to involvement of the coronary ostia

IMaging

  • CXR
  • CT/MRI: not if hemodynamically unstable
Treat 
- Analgesia 
- Decreased SBP 
Labetalol or esmolol (short t1/2) 
Keep SBP 100-110mmHg

Type A: open repair. Acute operative mortality :<25%

Type B: conservative initially

  • Surgery if persistent pain or complications
  • Consider TEVAR if uncomplicated.
74
Q

What is Gangrene?

A

Death of tissue from poor vascular supply

75
Q

Classification of gangrene?

A

Wet: tissue death + infection Dry: tissue death only
Pregrangrene: tissue on the brink of gangrene

76
Q

Presentation of gangrene?

A

Black tissue ± slough

May be suppuration ± Sepsis.

77
Q

Gas gangrene presentation?

A

Clostridium perfringens myositis

RF: DM, trauma, malignancy

Presentation

  • Toxaemia
  • Haemolytic jaundice
  • Oedema
  • Crepitus from surgical emphysema
  • Bubbly brown pus.

Management

  • Debridement
  • Benzylpenicillin + metronidazole
  • Hyperbaric O2
78
Q

What is synergistic gangrene?

A

INvolves aerobes + anaerobes

Fournier’s: Perineum
Meleney’s: post-op ulceration

Both progress rapidly to necrotising fasciitis + myositis.

79
Q

Management of gangrene?

A
  • Take cultures
  • Debridement (including amputation)
  • Benzylpenicillin ± clindamycin
80
Q

What is a varicose vein?

A

Tortuous, dilated veins of the superficial venous system

81
Q

Pathophysiology of varicose veins?

A

One-way flow from sup –> deep maintained by valves

Valve failure –> increased pressure in superior veins –> Varicosity

3 main sites where valve incompetence occurs:
- SFJ: 3cm below and 3 cm lateral to pubic tubercle.

  • SPJ: popliteral fossa

Perforatiors: Draining GSV

  • 3 medial calf perforators
  • 1 medial thigh perforator
82
Q

Causes of varicose veins

A

Primary

Secondary

83
Q

What are the primary causes of varicose veins?

A

idiopathic

  • Prolonged standing
  • Pregnancy
  • Obesity
  • OCP
  • FH

Congenital valve absence

84
Q

Secondary causes of varicose veins?

A

Valve destruction –> reflux: DVT, thrombophlebitis.

Obstruction: DVT, foetus, pelvic mass
Constipation
AVM
Overactive pumps (cyclist)

85
Q

Symptoms of varicose veins?

A 
Cosmetic defect 
Pain, cramping, heaviness
-Tingling 
Bleeding: May be severe
Swelling
86
Q

Signs of varicose veins?

A

Skin changes

  • Venous stars
  • Haemosiderin deposition
  • Venous eczema
  • Lipodermatosclerosis (paniculitis)
  • Atrophie blanche
  • Champagne bottle ulcers
  • Ulcers: medial malleolus/gaiter area
  • Oedema
  • Thrombophlebitis
87
Q

Investigation for varicose veins?

A

Duplex US

  • anatomy
  • Presence of incompetence
  • Caused by obstruction or reflux

Surgery: FBC, U+E, Clotting, G+S, CXR, ECG.

88
Q

Referral criteria for varicose veins?

A 
Bleeding 
Pain 
Ulceration 
Superficial thrombophlebitis 
Severe impact on QoL
89
Q

What is the CEAP classification?

A

Chronic venous disease can be classified according to

  • Clinical signs
  • Etiology
  • Anatomy
  • Pathophysiology
90
Q

Conservative management of varicose veins?

A

Treat any contributing factors

  • lose weight
  • relieve constipation

Education

  • avoid prolonged standing
  • regular walks

Class II graduated compression stocking

  • 18-24mmHG
  • Symptomatic relief and slows progression

Skin care

  • Maintain hydration with emollients
  • Treat ulcers rapidly (compression banding after exclusion of arterial disease or surgery)
91
Q

Minimally invasive therapies?

A

Indications
- Small below knee varicosities not involving GSV or SSV.

Techniques

  • Local or GA
  • Injection sclerotherapy: 1% Na tetradecyl sulphate
  • Endovenous laser or radiofrequency ablation.
  • Foam therapy

Post-operatively
Compression banding for 24hr
Compression stocking for 1mon

92
Q

Surgical management of Varicose Veins?

A

Indications

  • SFJ incompetence
  • Maor perforator incompetence
  • SYmptomatic: ucleration, skin changes, pain
93
Q

Procedure for surgical management of varicose veins?

A

Trendelenberg: saphenofemoral ligation

SSV ligation: in the politeral fossa

Multiple avulsion
Perforator ligation
Subfascial endoscopic perforator surgery

Post-op

  • Bandage tightly
  • Elevate for 24hrs
  • Discharge with compression stockling + walk daily
94
Q

Complications of surgery for varicose veins?

A 
Haematoma
Wound sepsis 
Damage to cutaneous nerve (long saphenous) 
Superficial thrombophlebitis 
DVT
Recurrenece: 15%
95
Q

What is a leg ulcer?

A

Interruption in the continuity of an epithelial surface

96
Q

What are the causes of leg ulcers?

A 
Venous: commonest 
Arterial: large or small vessel 
Neuropathic: EtOH, DM
Traumatic: pressure 
Systemic disease: pyoderma gangrenosum 
Neoplastic: SCC
97
Q

What is a venous ulcer?

A

75%

  • Painless, sloping, shallow ulcers.
  • Usually on medial malleolus “gaiter area”
  • associated with haemosiderin deposition and lipodermatosclerosis
  • RF: venous insufficiency, varicosities, DVT, obesity
98
Q

What is an arterial ulcer?

A

History of vasculopathy and risk factors

Painful, deep, punched out lesions

Occur at pressure points

  • Heal
  • Tip of and between toes
  • Metatarsal heads

Other sign of chronic leg ischaemia.

99
Q

What is a neuropathic ulcer?

A

Painless with insensate surrounding skin

Warm foot with good pulses.

100
Q

Complications of leg ulcers?

A

Osteomyelitis
Development of SCC in the ulcer (Marjolin’s ulcer) - leading to an ulcer that gradually gets worse despite different topical therapies.

101
Q

Investigations for ulcers?

A

ABPI - must do this first to ensure this is not an arterial ulcer.
Duplex US
Biopsy may be necesary

102
Q

Management of Venous ulcer?

A

Refer to leg ulcer community clinic
- Focus on prevention

Graduated compression stocking
Venous surgery

Optimising risk factors: nutrition, smoking

103
Q

Specific management of venous ulcers?

A 
Analgesia 
Bed rest + elevated leg 
4 layer graded compression bandage (If ABPI >0.8
Pentoxyfylline PO 
- increased microcirculatory blood flow 
- Improves healing rates.
104
Q

Other options for venous ulcers?

A

Desloughing: e.g larval therapy, hydrogel
Topical antiseptics: iodine, manuka honey
Split-thickness skin grafting may be considered.

105
Q

Bilteral Leg swelling differentials?

A 
Bilateral
 - increased venous pressure 
RHF
Venous insufficiency 
Drugs (nifedipine)

Decreased oncotic pressure

  • Nephrotic syndrome
  • Hepatic failure
  • Protein losing enteropathy

Lymphoedema
Myxoedema (hyper/hypothyroidism)

106
Q

Unilateral leg swelling?

A

Venous insufficiency
DVT
Infection or inflammation
Lymphoedema

107
Q

What is lymphoedema?

A

Collection of interstitial fluid due to blockage or absence of lymphatics

108
Q

Primary lymphoedema?

A

Congenital absence of lymphatics
May or may not be familial

Presentation

  • Congenital: Evident from birth
  • Preacox: after birth but <35
  • Tarda >35
109
Q

What is milroy’s syndrome?

A

Familial AD subtype of congenital lymphoedema

110
Q

Secondary lymphoedema?

A
  • Fibrosis: post-radiotherapy
  • Infiltration (Ca: prostate, lymphoma or filariasis
  • Infection: TB
  • trauma: block dissection of lymphatics
111
Q

Investigations of lymphoedema?

A

Doppler US
Lymphoscintigraphy
CT/MRI

112
Q

Management of Leg swelling?

A

Conservative

  • Skin care
  • Compression stocking
  • Physio
  • treat or prevent comorbid infections

Surgical
- Debulking operation

113
Q

73 yr old male presents with collapse and is brought into ED. Cold, painful left hand and forearm.

A

Sudden axillary artery embolus. Usually as a result of AF.

If patient collapses more central cause.

50% lodge into the brachial artery. Most likely to be embolus.

30% in the axillary artery.

Pain, pallor, paresis, pulselessness, paraesthesia.

114
Q

A 23-year-old man presents with intermittent symptoms of altered sensation in his arm and discomfort when he uses his hands. He works as an electrician and his symptoms are worst when he is fitting light fixtures.

A

Cervical rib

Basis of the Adson’s test.

115
Q

Arterial occlusions normally more intermittent, and allows development of collaterals.

A

Features may include claudication, ulceration and gangrene. Proximally sited lesions may result in subclavian steal syndrome

116
Q

Upper limb venous thrombosis?

A

Gradual upper limb swelling and discomfort.

Sensation and motor function are normal. Condition may complicate pre-existin malignancy.

Diagnosis with Duplex US.

Treat with anticoagulation.

117
Q

Subclavian steal syndrome?

A

Due to proximal stenotic lesion of the subclavian artery

Results in retrograde flow through vertebral or internal thoracic arteries.

Decreased cerebral blood flow may occur and produce syncopal symptoms.

118
Q

Takayasu’s arteritis?

A

Large vessel granulomatous vasculitis
Results in intimal narrowing
Most commonly affecting young asian females.
treatment is with systemic steroids.

Patients present with pulseless phase with symptoms of vascular insufficiency

4th year everything (43 decks)

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