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Year 3 Surgery > Vascular Surgery > Flashcards

Vascular Surgery Flashcards

1
Q

Regarding the Acutely Painful limb, Identify the likely diagnosis if;

  • Cold+Pale
  • Hot+Swollen

What are 2 other types of causes?

A
  • Acute Limb Ischaemia
  • DVT

Trauma
Neurological pathology

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2
Q

Radiculopathies can cause an Acutely Painful Limb.

How do these present

A

Back pain radiating to affected area- Worse on movement

Can have;

  • Muscle weakness
  • Parasthesia
  • Altered reflexes
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3
Q

Other than Radiculopathy, outline classes of Neurological causes of Acutely Painful Limb

A

Central- MS
Spinal- Disc hernia
Peripheral- Infective/ Traumatic

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4
Q

Most Lower Limb Ulcers have Venous Origin (80%)

List 2 other common causes

A

Arterial insufficiency

Diabetic-related neuropathy

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5
Q

List some rarer causes of Lower Limb Ulcers

A

Infection, Trauma, Vasculitis, Malignancy

In hospital: Pressure ulcers- Prolonged/ excessive pressure over bony prominence-> Skin breakdown+Necrosis

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6
Q

Briefly compare Venous, Arterial and Neuropathic ulcers

A

Venous;
- Shallow w/ granulated base + irregular borders

Arterial;
- Deep w/ well defined borders, Necrotic base

Neuropathic;

  • Painless, over areas of abnormal pressure
  • Often due to joint deformity in Diabetics
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7
Q

Outline the possible pathophysiology of venous ulcer formation

A

Valvular incompetence/ Venous outflow obstruction-> Impaired venous return, causing WBC “trapping” in capillaries

Inflammatory mediators released-> Tissue injury, poor healing, necrosis

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8
Q

List RFS for Venous Ulcers

A 
Increasing age
Pre-existing venous incompetence/ VTE history 
Pregnancy
Obesity/ Inactivity 
Severe trauma
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9
Q

How do venous ulcers present

A

Can be painful- worse at end of day
Often around Medial Malleosus

Associated chronic venous disease symptoms: Aching, Itching, Bursting sensations

O/E: 
- Varicose Veins w/ Ankle or Leg Oedema
Features of Venous insufficiency;
- Varicose eczema/ Thrombophlebitis 
- Haemosiderin skin staining 
- Lipodermatosclerosis, Atrophie Blanche
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10
Q

Outline venous ulcer investigations

A

V Insufficiency confirmed by Duplex USS

ABPI to assess for an arterial component, and if compression therapy is suitable

Swab cultures if infection suspected

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11
Q

Outline Conservative Venous Ulcer Management

A

Leg elevation, Improved exercise+Nutrition, W loss

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12
Q

Outline the main management of Venous Ulcers

A

Compression bandaging changed 1-2x/week
(30-75% will heal after 6mths of compression)

ABPI must be >0.6 before any bandaging done

Use appropriate dressings and emollients to maintain surrounding skin health

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13
Q

How should concurrent varicose veins be managed in venous ulcer treatment

A

Endovenous techniques or open surgery

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14
Q

List RFs for Arterial Ulcers

Same as for Peripheral Arterial Disease

A

Smoking, Obesity, Inactivity, DM
HyperT, Hyperlipidaemia
Fhx

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15
Q

How does an Arterial Ulcer present

Presenting complaint, Exam, PMHx

A

May be painful
Develops gradually
Little or no healing (granulation tissue)

O/E:

  • Limbs cold, reduced/absent pulses
  • If Pure Arterial, Sensation maintained

PMHx of 1 of;

  • Intermittent Claudication (Pain on walking)
  • Critical Limb Ischaemia (Pain at night)
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16
Q

Outline Arterial Ulcer investigations

A

ABPI (>0.9=normal, 0.8-0.9=mild, 0.5-0.8=moderate, <0.5=severe)

To identify anatomical location, exam+imaging;
- Duplex USS, CT Angiogram and/or MR Angiogram

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17
Q

Outline Conservative management of Arterial ulcers

A

Lifestyle change- Smoking, Weight, Exercise

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18
Q

Outline Medical management of Arterial ulcers

A

CVD risk modification;

  • Statin (80mg as CVD 2ndary prevention)
  • Antiplatelet agent (Clopidogrel 75mg preferred to Aspirin)
  • BP, Glucose management
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19
Q

Outline Surgical management of Arterial ulcers

A

Angioplasty (W/ or w/o Stenting)
OR
Bypass grafting (For more extensive)

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20
Q

List RFs for Neuropathic Ulcers

A

Any condition causing Peripheral Neuropathy (Mostly, DM and B12 deficiency)

Foot deformity
Peripheral Vascular Disease

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21
Q

How do Neuropathic ulcers present

History, Exam

A

Burning/ tingling in legs
Single nerve involvement
Amotrophic neuropathy (painful proximal Quad wasting)

O/E;

  • Variable size + depth
  • “Punched out” appearance
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22
Q

How are Neuropathic Ulcers investigated

A

Check Blood glucose, Serum B12
Assess arterial disease w/ ABPI +/- Duplex USS

Swab if sign of infection (If Deep, may warrant X-Ray to assess for Osteomyelitis)

Assess extent of Peripheral Neuropathy (10g monofilament or Ipswich touch test, Vibration sensation- 128Hz fork)

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23
Q

How are Neuropathic ulcers managed

A

Diabetic foot clinics- Blood Glucose, Diet, Exercise, CVD RFs managed

Regular Chiropody- Foot hygiene, correct footwear

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24
Q

How does Charcot’s Foot present

A

Swelling
Deformity
Pain
Loss of function

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25
Q

List 4 types of Arterial Disease

A

Aortic Dissection
Thoracic Aortic Aneurysm
Abdo Aortic Aneurysm
Carotid Artery Disease

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26
Q

What are the 3 layers of an Arterial Wall?

Describe an Aortic Dissection

A

Tunica Intima, Media, Adventitia

Tear in Tunica Intima of Aortic wall, so blood flows in and splits apart the T. Intima and Media

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27
Q

Aortic Dissections peak between 50-70

Compare Acute and Chronic
List RFs

A

Acute: Diagnosed = 14 days
Chronic: Diagnosed >14 days

Male
CT Disorder (Marfan’s or Ehlers-Danlos)
HyperT, Atherosclerosis
Bicuspid Aortic Valve

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28
Q

Aortic Dissections can progress Proximally and/or Distally from initial tear.

Compare Anterograde and Retrograde Dissections

A

Anterograde: Propagate towards Iliac Arteries

Retrograde: Propagate towards Aortic Valve (at root of Aortic)

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29
Q

List complications of Retrograde Dissection

A

Aortic valve prolapse
Bleed into Pericardium
Cardiac tamponade

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30
Q

Aortic dissections are classified anatomically by two systems, DeBakey and Stanford.

Outline the Stanford Classification
(Into 2 groups)

A

Group A;
- Includes DeBakey Types I + II
- Involves Ascending Aorta, can propagate to Aortic Arch + Descending Aorta
(Tear can originate anywhere along this path)

Group B;

  • Don’t involve Ascending Aorta
  • Include DeBakey Type III
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31
Q

Aortic dissections are classified anatomically by two systems, DeBakey and Stanford.

Outline the DeBakey Classification

(Groups dissections anatomically)

A

Type I;

  • Starts in Ascending Aorta, propagates at least to Aortic Arch
  • Usually in <65s, Highest mortality

Type II;

  • Confined to Ascending Aorta
  • Usually in elderly w/ Atherosclerotic disease + HyperT

Type III;

  • Starts distal to the Subclavian Artery in the Descending Aorta
  • IIIa: Extends distally to Diaphragm
  • IIIb: Extends past Diaphragm into Abdominal Aorta
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32
Q

How does an Aortic Dissection present

A

Tearing chest pain- usually radiates to back

Tachycardia
Aortic regurgitation murmur
Hypotension (Blood loss into dissection)

Signs of Organ hypoperfusion (Less urine, Ischaemia, Consciousness deterioration)

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33
Q

How will Pericarditis usually present

A

Pleuritic chest pain
ECG showing diffuse ST elevation

Possibly, Pericardial rub on Auscultation

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34
Q

How is an Aortic Dissection investigated

A

Bloods- FBC, LFT, U&E, Clotting, Crossmatch (≥4 units), ABG

CT Angiogram (Diagnose + Classify)
Transoesophgeal Echo can be useful, but operator dependent
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35
Q

Outline General Management for Aortic Dissections

Specifics different for Type A and B

A

High flow O2, Careful IV Fluids (If ruptured, goal is to maintain cerebral perfusion. If stable, <110 Systolic)

Lifelong Antihypertensive + Surveillance imaging (At 1, 3 and 12mth post-discharge, then at 6-12mth intervals)

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36
Q

Outline Type A Aortic Dissection management- Higher mortality

(Urgent transfer to Cardiothoracic centre + discussion with cardiac/ vascular surgeon)

A

Removal of Ascending Aorta, replaced with Synthetic Graft (w/ or w/o Aortic Arch removal)

If damaged, repair suspensory apparatus of valve

Any other Aortic Arch branches involved, need reimplantation into Graft

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37
Q

Outline Uncomplicated Type B Aortic Dissection management

A

HTN management IV;

  • B-blockers as 1st line (Labetalol)
  • CCBs as 2nd line
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38
Q

Why is Endovascular Repair not recommended in treating Acute Type B Aortic Dissections

A

Risk of Retrograde Dissection

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39
Q

When is Surgical intervention indicated in Type B Aortic Dissecions

A

Rupture
Organ/ Limb Ischaemia
Uncontrollable Pain or HyperT

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40
Q

Type B Dissections can become Chronic w/continued leakage into the dissection, even if a stent has been placed.

The most common complication of chronic disease is what?

A

Formation of an aneurysm

Endovascular repair offers better survival chance

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41
Q

List complications of Aortic Dissection

(Depend on Site + Spread, Branches + Organs affected

A

Aortic Rupture/ Regurgitation
MI (Due to Coronary artery dissection)
Cardiac tamponade

Stroke/ Paraplegia (Spinal/ Cerebral Artery affected)

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42
Q

TAAs are less common than AAAs.

Which segments can be affected? Different segments affected= different symptoms

A 
Ascending Aorta/ Aortic root (60%)
Aortic Arch (10%)
Descending Aorta (40%)
Thoraco-abdominal Aorta (10%(
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43
Q

TAAs develop due to degradation of which layer of the artery wall?

List the 2 main causes

A

Tunica Media

CT Disease (Marfan’s or Ehlers-Danlos)
Bicuspid Aortic Valve

(Other causes: Trauma, Aortic Dissection, Tertiary Syphilis, Aortic/ Takayasu’s Arteritis)

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44
Q

TAAs grow at a mean rate of 1-2mm/ year

List 3 groups in which they grow faster

A

Those with;

  • Marfan’s
  • Descending Aneurysms (vs Ascending)
  • Dissected Aneurysms (vs non-dissected)
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45
Q

List RFs for TAA development

A

Fhx, Male, Increasing age
HTN, Atherosclerosis
Smoking, High BMI

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46
Q

TAAs are usually Asymptomatic and found incidentally.

List possible symptoms if Symptomatic

A

Pain- Most common

Hoarse voice- L RLN damage in Arch Aneurysms
Distended neck veins- SVC Compression
HF symptoms- Aortic valve affected
Dyspnea/ Cough- Tracheal/ Bronchial compression

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47
Q

In TAA, Back Pain can be caused by Spinal Compression

What do Pain in Neck, Ant Chest, Between Scapulae suggest

A

Neck- Aortic Arch

Ant Chest- Ascending Aorta

Between Scapulae- Descending Aorta

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48
Q

TAAs are diagnosed through imaging, but what tests should an initial work-up include

A

Bloods, ECG, CXR

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49
Q

Outline Imaging and results of a TAA

A

CXR (not enough to diagnose):

  • Wide mediastinal silhouette
  • Enlarged Aortic knob
  • Possibly, Tracheal deviation
  • CT-Chest w/ Contrast: Preferred modality
  • TOE
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50
Q

Outline Medical Management of TAAs

A

Statin + Antiplatelet therapy

BP Control, Smoking cessation

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51
Q

Surgical Management/ Indication of TAAs is dependent on Location.

Outline for Ascending Aorta, Aortic Arch and Descending Aorta

A

Ascending;

  • When >5.5cm
  • Excision, replaced with Dacron Graft
  • If Aortic root involved: Bentall procedure w/ Prosthetic Aortic Valve

Arch;

  • Consider surgery when >5.5cm
  • Replaced w/ multi-limbed graft

Descending;

  • When >6cm, Open or EV repair
  • EV safer+more effective
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52
Q

Outline post-op monitoring for those treated for a TAA surgically

A

Outpatient CT/ MRI imaging, as development of a 2nd Aneurysm isn’t uncommon post-op

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53
Q

List AAA RFs

Is DM a RF?

A

Male, Increasing age, Fhx
Smoking, HyperT, Hyperlipidaemia

DM is not a RF, but is PROTECTIVE against AAA

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54
Q

How can an AAA present if symptomatic?

Many are Asymptomatic, found incidentally/ on screening

A

Pain- Abdo/ Back/ Loin
Distal Embolisation-> Limb ischaemia
Aortoenteric Fistula

O/E;

  • Abdo Pulsatile mass
  • Rarely: Retroperitoneal Haemorrhage signs
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55
Q

Outline AAA screening in the UK, offered by NAAASP

A

Abdo USS for all Men aged 65

Most men with AAA detected wait 3-5yrs in surveillance before qualifying for elective repair

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56
Q

How should an AAA be investigated

A

USS to confirm

CT w/ Contrast: When 5.5cm in diameter

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57
Q

Outline Monitoring and Management of an AAA <5.5cm

Surgery before 5.5.cm offers no survival benefit

A

Monitored via Duplex;

  • 3 to 4.4cm: Yearly USS
  • 4.5 to 5.4cm: 3-monthly USS

Smoking, Weight, Exercise
BP Control, Statin + Antiplatelet

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58
Q

An AAA of what diameter requires;

  • the DVLA to be notified
  • Not driving until repaired
A

> /= 6cm

> /= 6.5cm

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59
Q

List 3 AAA pt groups who surgery would be considered in

A
  • Diameter >5.5.cm
  • Expanding at >1cm/year
  • Symptomatic AAA in a pt, otherwise fit
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60
Q

Describe Open and EV repair in AAA treatment

A

Open;

  • Midline Laparotomy/ Long Transverse Incision
  • Clamp Aorta proximally, Iliac arteries distally
  • Segment replaced with Prosthetic graft

EV;

  • Graft inserted via Femoral arteries
  • Stent fixed across aneurysm
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61
Q

Compare outcomes of Open and EV AAA Repair

A

EV;

  • Higher rate of Re-intervention and Aneurysm rupture
  • Decreased hospital stay and 30-day mortality

Similar long-term outcomes
Same mortality after 2yrs

(Consider Open repair in younger pts)

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62
Q

Outline an important complication of EV AAA Repair

A

Endovascular leak/ Endoleak;
- Incomplete seal forms around aneurysm, blood leaks around graft

Often asymptomatic, so need regular surveillance (USS)

If left untreated, can-> Expansion + Rupture

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63
Q

Other than Rupture, list complications of an AAA

A

Retroperitoneal leak
Embolisation
Aortoduodenal Fistula

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64
Q

List RFs for AAA Rupture

Symptoms: Pain, Shock/ Syncope, Vomit, Pulsatile mass, Tenderness

A

Increasing diameter
Smoking, HyperT
Female gender

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65
Q

50% of AAA rupture pts present with the classic triad- Flank/ back pain, HypoT, Pulsatile abdo mass

What proportion rupture;

  • Into Retroperitoneal space
  • Anteriorly to Peritoneal Cavity (V poor prognosis)
A

Peritoneal Cavity- 20%

Retroperitoneal- 80%

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66
Q

Outline AAA Rupture management

A 
Blood transfusion (After Cross-matching)
Keep BP <100, to prevent more bleeding via clot displacement

High Flow IV O2

Transfer to Vascular unit;

  • If Stable, CT Angiogram to determine if EV repair possible
  • If Unstable, Immediate Open Surgical repair
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67
Q

What is Carotid Artery Disease?

Responsible for 10-15% of Ischaemic strokes, due to plaque rupture and/or thromboembolism

A

Atherosclerotic plaque in one/ both CCAs + ICAs-> Stenosis or Occlusion

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68
Q

Correlated Degree of Stenosis with Diameter Reduction

Carotid Artery Disease

A

Mild Stenosis: <50% Reduction
Moderate: 50-69% Reduction
Severe: 70-99% Reduction
Total: 100%

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69
Q

List RFs for Carotid Artery Disease

A

Age (>65). Fhx
Smoking, HyperT, Hypercholesterolaemia
Obesity, DM, CVD history

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70
Q

Carotid Artery Disease is often asymptomatic (even if totally occluded on on side)

It may present as a neurological deficit.

What 2 forms can this take
What vascular features may be seen

A

TIA or Stroke

Carotid bruit in neck (<50% of cases)
May have Amaurosis Fugax

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71
Q

Atherosclerosis is the most common form of Carotid Artery Disease.

List 4 other pathologies that can be involved

A

Carotid Dissection (Pts often <50 w/ CT disease, event triggered by Trauma/ Sudden neck movement)

Thrombotic Occlusion of Carotid Artery (Need imaging to differentiate from plaque)

Fibromuscular Dysplasia (Non-atheromatous angiopathy-> Wall hypertrophy)

Vasculitis (Usually systemic symptoms w/ other vessels affected)

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72
Q

Outline Initial Investigations for Carotid Artery Disease

A

Non-contrast CT Head for signs of infarction, treatable by Thrombolysis

Bloods- FBC, U&E, Coag, Glucose, Lipids
ECG- AFib

CT-Head Contrast Angiography, if considering Thrombectomy

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73
Q

Outline Follow-up investigations for Carotid Artery Disease

A

Duplex USS;
- After TIA/ Stroke diagnosis, need to screen arteries to asses degree of stenosis

Lesions in Carotid Artery may be further characterised via CT Angiography

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74
Q

Outline Acute Management of Carotid Artery Disease

Thrombectomy: If confirmed ischaemic stroke + Proximal Ant Circulation on angiography

A

High flow O2, Blood glucose optimisation, Swallowing screen assessment on admission

Ischaemic stroke;

  • IV Alteplase (if <4.5hrs of symptoms onset)
  • 300mg Aspirin

Haemorrhagic stroke;

  • Correction of coagulopathy, referral to neurosurgery
  • Vessel repair may be needed
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75
Q

Outline Long Term Management of Carotid Artery Disease

CVD RF reduction

A
  • AP therapy: Aspirin 300mg OD for 2wks, then Clopidogrel 75mg OD
  • Statin therapy: High dose Atorvastatin
  • Aggressive HyperT and DM Management
  • Smoking cessation, Exercise, Weight
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76
Q

Carotid Endarterectomy (CEAs) are now considered better than Stenting.

Who should be referred for assessment for a CEA

A

All pts with Acute TIA or Non-disabling stroke, who have symptomatic carotid stenosis between 50-99%

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77
Q

CEAs involve removing Atheroma and damaged T. Intima.

What are the main risks of CEA

A

Stroke, MI
Nerve damage to CN 9/ 10/ 12
Bleeding/ Infection

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78
Q

Whats a Pseudo-aneurysm

A

Blood gathers between T. Media and Adventitia, due to Arterial Wall breach

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79
Q

What typically causes Pseudo-aneurysms

A

Vasculitis, Regional Inflammation

Damage to vessel wall, e.g;

  • Puncture after Cardiac Catheterisation
  • Repeated injections to vessel
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80
Q

Where are Pseudo-aneurysm most common?

A

Femoral artery

Can be at Radial artery, Carotid artery, Abdo/Thoracic Aorta

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81
Q

What can happen if a Pseudo-aneurysm gets infected

A

Pts can become Septic

Increased chance of Rupture

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82
Q

How does an uninfected Pseudo-aneurysm present?

A

Pulsatile lump- Tender + Painful

May be Distal Arterial Occlusion, due to compression (check distal pulses)

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83
Q

How can an infected Pseudo-aneurysm present?

A
  • Area will be Red + Tender
  • Pt likely Septic (Fever, Tachycardia)
  • Purulent material may discharge from any sinus opening
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84
Q

What do you do if a pt reports they had Bleeding from a Pseudo-aneurysm that has now stopped

A

Close monitoring + urgent management, as this may be a ‘Herald Bleed’ that could re-bleed at any time

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85
Q

Outline uninfected Pseudo-aneurysm investigations

A

Distal pulses before any intervention

Gold standard- Duplex USS;
- Turbulent Forward and Backward flow (Yin-Yang sign)

CT can be used if access difficult with USS

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86
Q

Outline investigations, specific to infected Pseudo-aneurysm

A

Bloods
Blood culture
MC&S, if discharging

Cross-match sufficient amount of blood (High rupture risk)

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87
Q

List treatment options for Pseudo-aneurysms

A

Small ones can be left alone

Larger/ Symptomatic ones;

  • USS-guided Thrombin injection
  • USS-guided Compression
  • EV Stenting
  • Surgical repair/ Ligation
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88
Q

Describe USS-Guided Thrombin Injections

Pts can have follow-up imaging to ensure resolution

A

Thrombin injected directly into Pseudo-aneurysm lumen under US-Guidance

This forms a Thrombus within the Pseudo-aneurysm, so it can be closed off

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89
Q

Options of EV Stenting or Surgery depend on pt and location of Pseudo-aneurysm

Describe suitability of deploying EV Covered Stents

A

Good success rates, but can leak causing persistent perfusion of Pseudo-aneurysm, or they can migrate

Often not possible, due to Pseudo-aneurysm location, meaning there is insufficient space to land stent w/o covering a major branch

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90
Q

Describe use of Surgical repair/ Ligation in treating Pseudo-aneurysms

A

Control the healthy artery Prox+Distal to the PA

May be possible to repair artery defect;

  • Directly
  • w/ a Vein or Bovine patch

Ligation;
- Occasionally needed, but may cause distal ischaemia and require a bypass graft

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91
Q

Outline management of an infected Pseudo-aneurysm

A

If discharge: Pressure dressing + Urgent imaging

Surgical ligation;

  • Most pts won’t get Acute Limb Ischaemia
  • Occasionally a Bypass graft needed, recommended to Tunnel the graft through a non-infected area
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92
Q

When using a Graft in treating a Pseudo-aneurysm, which graft types are more resistant to infection

A

Vein or Bovine grafts

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93
Q

Outline Complications following Surgical Ligation of a Pseudo-aneurysm

A

Small % of people will need Amputations

Mostly however, collateral supply will provide adequate blood flow distally

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94
Q

Define an Aneurysm

Peripheral and Vascular Aneurysms can occur, but AAAs are most common

A

Persistent abnormal dilation of an artery >x1.5 its normal diameter

95
Q

List RFs for Peripheral+Vascular Aneurysms

A

Trauma, Infection
CT/ Inflammatory Disease

Smoking
HyperT, Hyperlipidaemia
Fhx

96
Q

Briefly, outline Investigations for Peripheral + Visceral Aneurysms

A

Usually, CT Angiography
MR Angiography: Good alternative, as less Radiation and Nephrotoxicity

Duplex USS: Can be useful for detection + follow-up

97
Q

Briefly outline Management of Peripheral + Visceral Aneurysms

A

Watchful waiting + RF Reduction (Smoking, Anti-platelet + Statin therapy)

OR

Surgery (Open/ EV)

98
Q

Most commonly, Peripheral Aneurysms occur in the Popliteal, then the Femoral artery.

Popliteal Aneurysms have a high risk of Embolisation and/or Occlusion

How do Popliteal Aneurysms present?

A

Symptomatically;

  • Acute Limb Ischaemia
  • Less commonly, Intermittent Claudication

Compression symptoms on Popliteal Vein or Fibular nerve

99
Q

Outline Investigations for Popliteal Aneurysms

A

Initially: Duplex USS (rule out other causes of Popliteal Fossa swelling)

Further: CT/ MR Angiogram

100
Q

Outline Popliteal Aneurysm Management

A

Treat if;

  • Symptomatic
  • Asymptomatic but >2.5cm

In case of Thrombosis: if no patent tibial vessel, Embolectomy/ Thrombolysis before surgery

Surgery: EV or Open-Ligation or Resection w/ Bypass graft

101
Q

Femoral Artery Aneurysms are usually Pseudo-Aneurysms.

The 2 major causes are what?

A
  • Percutaneous Vascular Interventions

- Patent self-injecting (IV Drug users-> Groin)

102
Q

How do Femoral Artery Aneurysms present?

A

Symptoms from Thrombosis/ Rupture/Embolisation

Varying degrees of Claudication or Acute Limb Ischaemia, but often no symptoms other than groin swelling

103
Q

How are Femoral Artery Aneurysms investigated and treated?

A

Duplex USS, then CT/MR Angiography

Open Surgical repair

104
Q

In Visceral Arteries what Aneurysms are most common?

A

Splenic (most common-60%)
Hepatic (2nd most common-20%)
Renal

105
Q

List Splenic Artery Aneurysm RFs

A

Female, Multiparity
Portal HyperT
Pancreatitis/ Pancreatic Pseudocysts

106
Q

How do Splenic Artery Aneurysms present?

Ruptured vs unruptured

A

If symptomatic but unruptured;
- Vague Epigastric/ LUQ pain

If ruptured;

  • Severe abdo pain
  • Haemodynamic unstability
107
Q

How are Splenic Artery Aneurysms investigated and treated?

A

CT/ MR Angiography. USS may be used for monitoring (only in thinner pts)

If Stable, EV Repair (Embolisation/ Covered Stent Grafts)

If Unstable, consider Open Repair- Ligation + Bypass

108
Q

Percutaneous instrumentation is associated with 50% of Hepatic Artery Aneurysm cases

List 3 other causes

A

Trauma
Degenerative disease
Post-liver transplant (False Aneurysms form around vessel anastomoses)

109
Q

How may Hepatic Artery Aneurysms present?

A

Mostly Asymptomatic

If Symptomatic;

  • Vague RUQ/ Epigastric Pain
  • Jaundice
110
Q

How are Hepatic Artery Aneurysms investigated and treated?

A

CT/ MR Angiography

EV Repair, similar to Splenic Artery Aneurysms;

  • If Haemodynamically stable + Suitable anatomy
  • If not, consider Open repair
111
Q

How may Renal Artery Aneurysms present?

A

Often Asymptomatic, found incidentally

If Symptomatic;

  • Haematuria
  • Loin pain
  • Resistant HyperT
112
Q

How are Renal Artery Aneurysms investigated and treated?

A

CT/ MR Angiography

EV Repair;

  • Stent alone, if main renal artery affected
  • Coils + Covered stent graft, if Hilum affected

Rarely: Renal transplant

113
Q

Define Acute Limb Ischaemia

A

Sudden decease in limb perfusion, that threatens limb viability

(Arterial occlusion to a limb can lead to rapid ischaemia and poor functional outcomes within hours)

114
Q

List the 6P signs of Acute limb ischaemia

A
  • Pain, Pallor, Pulselessness
  • Parasthesia, Perishingly cold, Paralysis

(1st 3 most common)

115
Q

Describe the;

  • Prognosis
  • Sensory loss
  • Motor deficit
  • Arterial Doppler
  • Venous Doppler

Of Rutherford 1 (Viable) Acute Limb Ischaemia

A
  • No immediate threat
  • No sensory loss
  • No motor deficit
  • Audible arterial doppler
  • Audible venous doppler
116
Q

Describe the;

  • Prognosis
  • Sensory loss
  • Motor deficit
  • Arterial Doppler
  • Venous Doppler

Of Rutherford 2A (Marginally Threatened) Acute LI

A
  • Salvageable , if treated soon
  • Minimal/ no sensory loss
  • No motor deficit
  • Inaudible Arterial Doppler
  • Audible Venous Doppler
117
Q

Describe the;

  • Prognosis
  • Sensory loss
  • Motor deficit
  • Arterial Doppler
  • Venous Doppler

Of Rutherford 2B (Immediately Threatened) Acute LI

A
  • Salvageable, if immediately revascularised
  • More than toes, pain on rest
  • Mild/ Moderate motor deficit
  • Inaudible Arterial Doppler
  • Audible Venous Doppler
118
Q

Describe the;

  • Prognosis
  • Sensory loss
  • Motor deficit
  • Arterial Doppler
  • Venous Doppler

Of Rutherford 3 (Irreversible) Acute LI

A
  • Major tissue loss, permanent nerve damage
  • Major sensory loss
  • Major motor deficit, Paralysis
  • Inaudible Arterial Doppler
  • Inaudible Venous Doppler
119
Q

List Ddx for Acute LI

A
  • Critical LI
  • Acute DVT
  • Spinal cord/ Peripheral nerve compression
120
Q

List Acute LI Investigations

A
  • Routine Bloods, G+S, Serum lactate, Thrombophilia screen
  • ECG
  • USS Doppler, then CT Angiography
  • CT Arteriogram, if limb considered salvageable
    (Location, helps decide operative approach)
121
Q

Outline Initial Management for Acute Limb Ischaemia

A surgical emergency, permanent tissue damage within 6hrs

A

High flow O2, IV fluids

IV Heparin

122
Q

Outline Medical Management of Acute Limb Ischaemia

Who is it considered in?

A 
Prolonged Heparin course
Regular assessment (APTT, Clinical review)

Rutherford 1 and 2A

123
Q

When may Surgical Intervention be indicated for Acute LI treatment

A
  • No improvement after Conservative Management

- Rutherford 2B

124
Q

Outline Surgical Treatment for Acute Limb Ischaemia, before any irreversible damage occurs

A

Embolic cause: Embolectomy via Fogarty catheter
Thrombotic cause: Angioplasty

Both causes:

  • Local intra-arterial Thrombolysis
  • Bypass surgery
125
Q

Irreversible limb ischaemia needs Urgent Amputation/ Palliative care

Why do most post-op cases need a high level of care, usually at a High-Dependency Unit?

A

Ischaemia Re-perfusion Syndrome

126
Q

Outline Long Term Management of Acute Limb Ischaemia

A
  • Lifestyle changes
  • Anti-platelet agent or Anticoagulant
  • Treat any underlying cause (E.g AFib)

If Amputated;

  • OT + PT
  • Long term rehab
127
Q

Acute LI has a morality of 20%

A major complication is Re-perfusion injury. What can this sudden increase in capillary permeability lead to?

A
  • Compartment Syndrome

Substances released from damaged muscle cells;

  • K+ (->Hyperkalaemia)
  • H+ (-> Acidosis)
  • Myoglobin (-> Signifcant AKI)
128
Q

Chronic Limb Ischaemia is a peripheral arterial disease, resulting in symptomatic reduced blood supply to limbs.

What is it typically caused by?
Which parts of body are commonly affected?

A

Atherosclerosis (Rarely, Vasculitis)

Lower limbs (Upper limb and Gluteals can be affected)

129
Q

List RFs for Chronic Limb Ischaemia

A

Smoking, Obesity + Inactivity, DM
HyperT, Hyperlipidaemia
Increasing age, Fhx

130
Q

Chronic Limb Ischaemia presents differently, depending on the severity.

Outline the presentation of each stage, according to the Fontaine classification

A

Stage 1: Asymptomatic
Stage 2: Intermittent Claudication
Stage 3: Ischaemic rest pain
Stage 4: Ulceration and/or Gangrene

131
Q

Outline Buerger’s test and relate this to Buerger’s Angle

A

Pt lied supine, legs raised until pale then lowered until colour returns

Buerger’s angle;

  • Angle at which limb goes pale
  • Angle <20 degrees indicates severe ischaemia
132
Q

What is Leriche Syndrome

How does it present

A

A form of Peripheral Arterial Disease affecting Aortic Bifurcation

Buttock/ thigh pain, w/ ED

133
Q

What is Critical Limb Ischaemia

What are 3 ways it can be defined clinically?

A

The advanced form of Chronic Limb Ischaemia

  • ABPI <0.5
  • Presence of Ischaemic/ gangrene regions
  • Ischaemic rest pain for >2wks, needing opiates
134
Q

How may Critical Limb Ischaemia present O/E?

A
  • Pale + Cold
  • Weak/ Absent pulses

Thickened nails, Limb hair loss, Skin changes (Atrophy, Ulcer, Gangrene)

135
Q

List the 2 main ddx for Chronic Limb Ischaemia

A

Acute Limb Ischaemia

Spinal stenosis/ Neurogenic Claudication;

  • Back pain radiates down lateral leg
  • Symptoms relieved by sitting, rather than standing
136
Q

Outline Investigation for Chronic Limb Ischaemia

If <50 and no major RFs, Thrombophilia screen and Homocysteine levels checked

A
  • Basic Bloods, Lipid profile, HbA1c, Glucose
  • ECG
  • Doppler USS, then CT/MR Angiography
  • ABPI
137
Q

Most pts with Chronic Limb Ischaemia require CV Risk reduction

Outline Medical Management of Chronic Limb Ischaemia

A
  • Lifestyle changes
  • Statin + Anti-platelet
  • DM Control

If pt doesn’t have Critical Limb Ischaemia;
- Supervised exercise programme

138
Q

Outline Surgical management of Chronic Limb Ischaemia

Consider if RF modification and Supervised exercise fail to improve symptoms

A
  • Angioplasty w/ or w/o Stenting (Small discrete stenosis)
  • Bypass grafting (More extensive stenosis/ multiple segments)

Amputation considered if;
- Surgery unsuitable, w/ incurable symptoms or gangrene causing sepsis

139
Q

The 5-yr mortality in pts with Chronic Limb Ischaemia is around 50%

List complications of Chronic Limb Ischaemia

A

Sepsis
Acute-on-chronic ischaemia
Amputation
Reduced Mobility and QoL

140
Q

What is Acute Mesenteric Ishcaemia

A

Sudden decrease in bowel’s blood supply, resulting in bowel ischaemia

Leads to death, if not treated quickly

141
Q

List 4 common types of causes of Acute Mesenteric Ishcaemia

Rarer: Takayasu’s arteritis, Fibromuscular dysplasia, Thoracic Aorta Dissections

A

Thrombus-in-situ;
- AMAT, Acute Mesenteric Arterial Thrombosis

Embolism;
- AMAE, Acute Mesenteric Arterial Embolisation

Non-occlusive cause;
- NOMI, Non-Occlusive Mesenteric Ischaemia

Venous exclusion and congestion;
- MVT, Mesenteric Venous Thrombosis

142
Q

What proportion of Acute Mesenteric Ishcaemia cases are AMATs and AMAEs?

What are the underlying causes?

A

AMAT;

  • 25%
  • Atherosclerosis

AMAE;

  • 50%
  • TAA or Cardiac causes (Arrytmias, Prosthetic heart valve)
143
Q

What proportion of Acute Mesenteric Ishcaemia cases are NOMIs and MVTs?

What are the underlying causes?

A

NOMI;

  • 20%
  • Hypovolaemic, Cardiogenic Shock

MVT;

  • <10%
  • Coagulopathy, Malignancy, Autoimmune disorders
144
Q

The RFs for Acute Mesenteric Ischaemia depend on the underlying cause

List RFs for AMAEs, causing Acute Mesenteric Ischaemia

(Same as for Chronic Mesenteric Ischaemia, which is more common in Females and those >60)

A

Smoking
DM
HyperT, Hyperlipidaemia, Hypercholesterolaemia

145
Q

How may Acute Mesenteric Ischaemia present?

History, Exam

A

Constant generalised abdo pain
N+V (70% of causes)

O/E;

  • Non-specific tenderness
  • If late stage, signs of peritonism
146
Q

List Lab Test investigations for Acute Mesenteric Ischaemia

A

Urgent ABG: Assess acidosis + Serum lactate (Can be normal)

FBC, U&Es, LFTs, Amylase. G+S, Clotting screen

(Amylase rises in Mesenteric Ischaemia, Ectopic, Bowel Perforation, DKA)

147
Q

List Imaging investigations for Acute Mesenteric Ischaemia

A

CT w/ IV Contrast;

- Shows as Oedematous bowel-> Loss of bowel wall enhancement-> Pneumatosis

148
Q

Outline Initial Management of Acute Mesenteric Ischaemia

Surgical emergency

A
  • IV Fluids, Catheter, Fluid balance
  • Broad Abx (In case of Perforation or Bacterial Translocation)
  • Early ITU input
149
Q

Outline Definitve Management of Acute Mesenteric Ischaemia

Intervention depends on location, timing, severity

A

Excision of Necrotic/ Non-viable bowel;

  • If not suitable for re-vascularisation
  • Potential re-look laparotomy after 24-48hrs
  • High chance of Short Gut Syndrome

Re-vascularisation;

  • Removal of Thrombus/ Embolism via Radiological intervention
  • Angioplasty preferable, as Open surgery=risk of Aortic contamination
150
Q

List complications of Acute Mesenteric Ischaemia

What’s the mortality?

A

Bowel necrosis
Bowel perforation
If pts survive, may have Short Gut Syndrome

50-80%

151
Q

In Chronic Mesenteric Ischaemia, collateral blood supply means that at least 2 of Coeliac, SMA and IMA must be affected for pt to be symptomatic, most likely with at least 1 vessel occluded

How may Chronic Mesenteric Ischaemia present

(Exam findings often non specific)

A
  • Postprandial pain: (Usually 10mins to 4hrs after eating)

- Weight loss, N+V, Change in bowel habit

152
Q

Outline Investigations for Chronic Mesenteric Ischaemia

May be confounding signs of Anaemia

A

Routine Bloods, Ca, Mg, Lipids, Glucose, HbA1c

CT Angiography: Gold standard

153
Q

Initial management for Chronic Mesenteric Ischaemia is Conservative

Outline Surgical treatment if:

  • Severe/ Progressive disease
  • Debilitating symptoms (Inlcuding w loss, malabsorption)
A 
EV Procedures (More common):
- Mesenteric angioplasty w/ stenting

Open procedures: Endarterectomy or Bypass

154
Q

Hyperhidrosis: Sweating in excess of that required for regulation of body temp

This is via increased sympathetic stimulation from Thoracolumbar autonomic fibres.

Compare the 2 types of Hyperhidrosis

A

Primary;

  • No underlying cause
  • 33% of pts have Fhx

Secondary;
- Underlying condition or Medication

155
Q

List causes of Hyperhidrosis

A
  • Pregnancy/ Menopause
  • Anxiety
  • Infections (TB, HIV, Malaria)
  • Malignancy (Esp. Lymphoma)
  • Endocrine disorder
  • Medication (Antidepressants, Propranolol, Anti-AChEsterase)
156
Q

How may Primary Hyperhidrosis present?

How long must it be present for the diagnosis to be made

A
  • Focal sweating: Usually bilateral and symmetrical
  • Occurs at least x1/wk
  • Typical onset <25, Most start as a teen, improves with age
  • Usually stops during sleep

> 6mths

157
Q

How may Secondary Hyperhidrosis present?

A
  • Generalised sweating

- Mostly at night time

158
Q

Outline Investigations for Hyperhidrosis

Diagnosis often made through History and Exam

A

Bloods- FBC, CRP, U&E, Glucose, TFTs
CXR

All done as routine

159
Q

Outline non-surgical and non-medical management of Hyperhidrosis

A

Lifestyle advice;

  • Reduce Stress/ Anxiety, Spicy food
  • Absorbent underlayers, Loose clothes (natural fibre + leather shoes)

OTC Anti-perspirants (Al Chloride at night only can be trialled, but can cause painful red skin)

160
Q

Outline medical management of Hyperhidrosis

A

Propantheline;
- Only Anticholinergic agent licensed for use

Glycopyyrolate + Oxybutinin;

  • Can reduce sweating
  • Not readily available, often off-license
161
Q

Surgical management of Hyperhidrosis is reserved for pts with resistant symptoms that significantly affect QoL

What’s a side effect of surgical treatment

A

Many pts develop compensatory sweating in other locations

162
Q

List 3 surgical interventions for Hyperhidrosis

A

Iontophoresis
Botulinum toxin
ETS, Endoscopic Thoracic Sympathectomy

163
Q

Describe Iontophoresis and its use in treating Hyperhidrosis

A

Weak electrical current through area, via water soaked sponges

Only a short-term solution

(Likely works by a combo of Blocking sweat glands, Disrupting nerves, Making sweat more acidic)

164
Q

Describe Botulinum Toxin use in treating Hyperhidrosis

A

Injected into skin in very small doses to block nerve supply to sweat glands

Effects last 2-6mths, can be repeated

Only licensed for underarm use, not hands/feet as can cause weakness

165
Q

Describe ETS, Endoscopic Thoracic Sympathectomy and its use in treating Hyperhidrosis

A

Damage purposefully caused to Thoracic Sympathetic Ganglion supplying affected region

(Last resort, as risk of damage Nerves/ Lung parenchyma)

166
Q

What is Subclavian Steal Syndrome?

A

Rare condition causing syncope/ neurological deficits when blood supply to arm is increased via exercise

167
Q

Outline the pathophysiology of Subclavian Steal Syndrome

A

Proximal Stenosing Lesion/ Occlusion in Subclavian Artery

To compensate for increased O2 demand, blood drawn from collateral circulation, causing reversed blood flow in Ipsilateral Vertebral Artery

168
Q

Subclavian Steal Syndrome is 2:1 in Males:Females and 3:1 Left:Right

List causes of Subclavian Steal Syndrome

A

Atherosclerosis (commonly causes in Subclavian A)
Vasculitis, Thoracic Outlet Syndrome
Complications of Aortic Coarctation repair

169
Q

List RFs for Subclavian Steal Syndrome

A

Increasing age
DM, Smoking
HyperT, Hyperlipidaemia

170
Q

Outline Coronary-Subclavian Steal Syndrome

Which pts does it occur in?

A
  • Increased O2 demand in left arm steals blood from Internal Mammillary/ Thoracic Artery
  • leading to Cardiac Ischaemia

Pts who have had an IMA Graft (Internal Mammary Artery)

171
Q

How may Subclavian Steal Syndrome present?

A

Cerebral symptoms;

  • Vertigo, Visual loss, Diplopia, Syncope
  • Dysphagia, Dysarthria

Pts may present with Arm Claudication (Pain or Parasthesia) made worse by arm movement

172
Q

List investigations for Subclavian Steal Syndrome

A

Initial: Duplex USS

Definitive: CT Angiography or MRA

Routine CXR: Looks for External Subclavian Artery compression

173
Q

Risk scoring of Subclavian Steal Syndrome can be classed into 3 grades

Outline these

A

Pre-Subclavian Steal;
- Reduced Anterograde Vertebral flow

Intermittent Alternating Flow;

  • Antegrade flow in Diastolic phase
  • Retrograde flow in Systolic phase

Advanced Disease;
- Permanent Retrograde flow

174
Q

Outline Conservative Management of Subclavian Steal Syndrome

A

Statin + Anti-platelet therapy

Smoking, Weight, Optimising Glucose control

175
Q

Outline Surgical Management of Subclavian Steal Syndrome

A

EV or Bypass techniques;

  • Risks of Stroke or Brachial Plexus damage
  • Consider bypass for Long/ Distal occasions

Percutaneous Angioplasty +/- Stenting (Success rate >90%, higher rate of Re-stenosis)

176
Q

What is Thoracic Outlet Syndrome, TOS?

A

Set of symptoms due compression NV Bundle compression in Thoracic Outlet

(TO: Opening between Clavicle, Scapula, Rib 1)

177
Q

List RFs for Thoracic outlet syndrome, TOS

Subc Artery and Brachial Plexus pass Ant. to Anterior Scalene, BP can be compressed between Ant and Middle Scalenes

A
  • Trauma (Fracture)
  • Repetitive motion/ Athletes (Swim, Racquet sports, Bodybuilders)

Anatomical causes;

  • Scalene hypertrophy
  • Cervical Rib (C7 Rib, mostly asymptomatic)
  • Rib 1 abnormality
  • Costoclavicular ligament
178
Q

How may Thoracic outlet syndrome, TOS present in regards to HISTORY?

(Symptoms can be classed as Neurological, Venous, Arterial- nTOS, vTOS, aTOS)

A

Neurological;

  • Parasthesia, Muscle Weakness (Often Ulnar pattern, as lower fibres affected)
  • Muscle wasting, Pain radiating to Neck, Upper Back

Venous;

  • DVT, Extremity swelling (Paget-Schrötter Syndrome)
  • Prominent veins over shoulder

Arterial;

  • Claudication symptoms
  • Acute Limb Ischaemia
179
Q

How may Thoracic outlet syndrome, TOS present in regards to EXAMINATION?

A

Weakness/ Numbness
Swelling
Tenderness (often over Scalene muscles)
Signs of ischaemia

180
Q

List 3 Special tests for Thoracic Outlet Syndrome, TOS

A
  • Adson’s Manoeuvre
  • Roo’s test
  • Elvey’s test
181
Q

Outline Adson’s Manoeuvre

A

Palpate Ipsilateral radial pulse w/ arm abducted 30 at degrees

Ask pt to turn head towards Ipsilateral shoulder
Fully Abduct, Extend and Laterally Rotate shoulder

TOS suggested if Pulse decreased/ loss

182
Q

Outline Roo’s Test

A

Abduct + Externally Rotate Ipsilateral shoulder to 90 degrees, then bend elbow to 90 degrees

Ask pt to Open + Close hand slowly for 3mins

TOS suggested if: Symptoms worsen

183
Q

Outline Elvey’s test

A

Extend arm to 90 degrees, w/ Elbow Extended and Wrist Dorsiflexed

Tilt pt’s Ear to each shoulder

TOS Suggested if Radial Pulse lost/ Symptoms worsen

184
Q

Outline Initial Investigations for Thoracic Outlet Syndrome, TOS

A

Bloods- FBC, Coag,

CXR (>90% pts have a bony abnormality)

185
Q

Outline Further Investigations for Venous/ Arterial Thoracic Outlet Syndrome, vTOS/ aTOS

A

Venous + Arterial Duplex USS;
- With pt at rest and arm in stress positions to look for compression

CT/ MRI or Venogram

186
Q

Outline Further Investigations for Neurological Thoracic Outlet Syndrome, nTOS

A

Nerve Conduction studies;

  • Detection of decreased APs due to compression
  • Usually used to exclude Carpal/ Cubital Tunnel Sydromes, rather than nTOS diagnosis
187
Q

Outline General Further Investigations for Thoracic Outlet Syndrome, TOS

(Regardless of nTOS, vTOS or aTOS)

A

MRI to detect Cervical Ribs or Fibrous Bands

Urgent CT Angiogram, if signs of Ischaemia

188
Q

TOS treatment depends on type

Outline management of nTOS

A

PT for 6mths is 1st line:

  • Improves Neck + Shoulder mobility
  • Strengthens surrounding muscles, Relaxes Scalenes

Botulinum toxins: To relax Scalenes, Often w/ PT

189
Q

TOS treatment depends on type

Outline management of vTOS

A

Thrombolysis + Anti-Coagulation

Most cases need;

  • Surgery to decompress Thoracic Outlet
  • Venoplasty/ Venous reconstruction/ Venous stent
190
Q

TOS treatment depends on type

Outline management of aTOS

A

Most cases need correction of anatomical abnormalities

If Acute Limb Ischaemia, urgent vascular input as pt may need Embolectomy

191
Q

Elective surgery corrects symptoms in;

  • 90-95% of aTOS/ vTOS cases
  • 50-70% of nTOS cases

Outline TOS Surgical management

A

For Decompression procedures;

  • Supraclavicular/ Transaxillary approach
  • Can access 1st/ Cervical Rib

Restrictive bands can also be released

192
Q

List complications of TOS Surgery

A

Neurological/ Vascular damage

Haemo-/ Pneumo-/ Chylo- Thorax

193
Q

List TOS Complications

A

Permanent nerve damage

Aneurysmal dilation of Subclavian Artery -> Embolisation or Loss of Limb Function

194
Q

Describe the Prognosis of TOS

Variable in nTOS, much better in vTOS after surgery

A

Sometimes (especially in nTOS) symptoms can persists after PT and Surgery

Symptoms can recur from 1mth to 10yrs after surgery

195
Q

What is Deep Venous Insufficiency, DVI?

A

Chronic disease caused by DVT or Valvular Insufficiency

196
Q

What 2 conditions together are known as Chronic Venous Insufficiency

A 
Varicose vein (affects superficial veinous system)
Deep Venous Insufficiency
197
Q

DVI occurs due to failure of the venous system.

What are 3 things that characterise DVI

A

Valvular reflux
Venous HyperT
Obstruction

198
Q

Compare the 2 types of causes of DVI

A

Primary: Underlying defect to vein wall/ valve
( E.g Congenital and CT disorders)

Secondary: Defects due to damage
( E.g Trauma, Venous Outflow Obstruction, Post- thrombotic/ phlebitic disease)

199
Q

List RFs for DVI

A
  • Fhx, Female, Increasing age
  • Obesity, Smoking, Pregnancy
  • Long periods of standing
  • Previous DVT/ Phlebitis
200
Q

How may DVI present?

A

Chronic Lower limb swelling- Aching, Itchy, Painful
Venous Claudication: Bursting pain, Tightness on walking resolved by leg elevation

O/E;

  • Varicose eczema, Thrombophlebitis, Haemosiderin skin staining
  • Lipodermatosclerosis (Tapering legs above ankle, “Champagne bottle”)
  • Atrophie blanche (Local, round, white atrophic regions surrounded by dilated capillaries)
201
Q

Outline Investigations for DVI

A
  • Basic Bloods. ECHO if cardiac cause suspected
  • Foot pulses + ABPI to determine suitability for compression therapy
  • Doppler USS to assess: Stenosis, DVT/ Varicose Veins, Venous Reflux
  • MR Angiogram if: venous occlusion/ reflux
202
Q

Outline Conservative Management of DVI

A

Compression stockings + Analgesia

If pt has a Venous Ulcer, full compression treatment

203
Q

Outline Surgical Management of DVI

A

Less successful than Conservative

Little/ no benefit from Valvuloplasty

204
Q

Pts with Severe Post-Thrombotic Syndrome with an occluded Iliac Vein may be suitable for what novel procedure?

Describe this procedure

A

Venous Stenting

Puncturing Popliteal/ Femoral Vein in thigh, crossing occluded vein segment with a wire into the IVC.

Balloon then used to dilate Iliac Ven prior to Venous Stent placement

205
Q

Why is Venous Stenting only done for pts with the most severe symptoms despite maximal conservative therapy

A

Long-term outcomes are unknown, as its a novel intervention

206
Q

List common complications of DVI

A

Swelling, Recurrent cellulitis
Chronic pain, Ulceration

(Less common: DVT, Varicose veins, Secondary Lymphoedema)

207
Q

What are Varicose Veins

Often at Sapheno- Femoral -Popliteal junctions

A

Tortuous dilated vein segments associated with incompetence of the valves permitting blood to flow from Superficial-> Deep systems

208
Q

How does the presence of Varicose Veins affect the Superficial Venous System

A

Venous hypertension + Dilation

209
Q

99% of Varicose Veins are Primary Idiopathic

List Secondary causes

A
  • DVT
  • Ovarian or Pelvic masses (Fibroids, Pregnancy)
  • Arteriovenous malformations
210
Q

What percentage of women get Varicose Veins during/ after Pregnancy

A

40%

211
Q

List RFs for Varicose Veins

A

FPOP

Fhx, Prolonged standing
Obesity, Pregnancy

212
Q

How may Varicose Veins present?

A

Cosmetic issues, Aching, Itching

Later stages;

  • Skin changes, Ulceration, Thrombophlebitis
  • Bleeding (often post-trauma)

Venous Insufficiency signs: Ulceration, Varicose Eczema, Haemosiderin staining

213
Q

What is Saphenous Varix

Why is it commonly mistaken for a Femoral Hernia

A

Saphenous Vein dilation at Saphenofemoral junction

Both displays a cough impulse

214
Q

How is Saphena Varix best Investigated and Managed?

A

Duplex USS

High Saphenous Ligation

215
Q

What system is used to classify the manifestation of Varicose Veins

A

CEAP

Clinical features
aEtiology
Anatomical
Pathophysiology

216
Q

Outline Investigations for Varicose Veins

A

Gold standard: Duplex USS

Look for Deep venous incompetence, Occlusion, Stenosis

217
Q

Outline management of a pt with DVT and Varicose Veins

Blood flows Superficial to Deep veins

A

Can’t treat Superficial Incompetence, as venous blood has no route back

Pt offered non-surgical management

218
Q

Outline Non-invasive Management of Varicose Veins

A

Lifestyle changes (Avoid long standing, Weight, Increase exercise)

Compression stocking:
- if interventional treatment not suitable (as need to be worn lifelong)

If Venous Ulceration: 4-layer bandage

219
Q

What are 4 indications for Surgical treatment of Varicose Veins

A

Symptomatic Varicose Veins (Primary/ Recurring)

Lower-limb Skin Changes (Pigment, Eczema)

Superficial Vein Thrombosis w/ Venous Incompetence (SVT= Hard, Painful veins)

Venous Leg Ulcer (Skin break

220
Q

List 3 surgical treatment options for Varicose Veins

A

Foam Scleorotherapy

Thermal Ablation

Vein Ligation, Stripping and Avulsion

221
Q

Outline Vein Ligation, Stripping and Avulsion for VV treatment

A

Incison in Groin/ Popliteal fossa

Tying off + Stripping away the refluxing vein

222
Q

Outline Foam Sclerotherapy for VV treatment

A

Done under LA and USS Guidance to prevent foam entering Deep Venous system

Inject Sclerosing agent into Varicosed Veins-> inflammatory response that closes off the vein

223
Q

Outline Thermal Ablation for VV treatment

A

Heating vein from inside-> permanent damage, closing off the vein

Done w/ USS Guidance, under Local/ General Anaesthetic

224
Q

Many pts treated for Varicose Veins often need re-intervention surgery

List typical complications after surgery

A

Haemorrhage, Recurrence, Nerve damage (Saphenous, Sural)

Thrombophlebitis (Consider in Foam/Ablation ops)
DVT (Consider in EV procedures)

225
Q

What’s the usual cause of an Aorto-enteric Fistula?

A

AAA Repair

226
Q

When is Ischaemic rest pain most likely to show

A

At night, as legs elevated and reduced HR so less leg perfusion

(After time, they start sleeping in chairs)

227
Q

What percentage of men aged 65 have an abnormal Aorta and what percentage need surgery

A

1%

1 in 1000 (0.001%)

228
Q

What is the risk of a 5.5cm AAA rupturing?

This is equal to chance of open surgery killing the pt

A

10%

229
Q

Arterial stenosis/occlusion in which arteries can cause intermittent Claudication?

A

Superficial femoral artery

Popliteal artery

230
Q

Someone with Intermittent Claudication may be advised to walk through the pain as much as possible, because the condition may improve over the next 6mths.

How may this happen?

A

Development/opening of collateral vessels

Angio or Vasculogenesis??

231
Q

On elevation, blood leaves a pt’s leg and it becomes pale. On returning to normal, it becomes redder then the other leg.

Explain this

A
  • Severe ischaemia (from elevation)-> Local Vasodilator release
  • These increase the perfusion of the ischaemic foot when gravity acts on it again
232
Q

Outline Investigation for a DVT, including Well’s score interpretation (Not same as for PE)

A

Score ≤1: DVT Unlikely, do a D-Dimer
Score ≥2: DVT Likely, do a Doppler USS

  • Can also use Digital Subtraction or CT/MR Venogram
  • Digital Subtraction Venography is the Gold Standard but very invasive so rarely used
233
Q

Outline DVT Mx

A

DOAC OR LMWH OR Warfarin bridged w/ LMWH

1st line: DOAC for ≥3mths (6 if unprovoked)

  • ≥3-6mths if active cancer
  • Life long if recurrent

2nd: Percutaneous Mechanical Thrombectomy (Massive DVTs)

3rd: IVC Filter
- Reduces risk of PE, doesn’t treat DVT
- Used if Anticoagulation contra-indicated

Year 3 Surgery (7 decks)

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