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
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
3
Q
Other than Radiculopathy, outline classes of Neurological causes of Acutely Painful Limb
A
Central- MS
Spinal- Disc hernia
Peripheral- Infective/ Traumatic
4
Q
Most Lower Limb Ulcers have Venous Origin (80%)
List 2 other common causes
A
Arterial insufficiency
Diabetic-related neuropathy
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
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
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
8
Q
List RFS for Venous Ulcers
A
Increasing age Pre-existing venous incompetence/ VTE history Pregnancy Obesity/ Inactivity Severe trauma
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
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
11
Q
Outline Conservative Venous Ulcer Management
A
Leg elevation, Improved exercise+Nutrition, W loss
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
13
Q
How should concurrent varicose veins be managed in venous ulcer treatment
A
Endovenous techniques or open surgery
14
Q
List RFs for Arterial Ulcers
Same as for Peripheral Arterial Disease
A
Smoking, Obesity, Inactivity, DM
HyperT, Hyperlipidaemia
Fhx
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)
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
17
Q
Outline Conservative management of Arterial ulcers
A
Lifestyle change- Smoking, Weight, Exercise
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
19
Q
Outline Surgical management of Arterial ulcers
A
Angioplasty (W/ or w/o Stenting)
OR
Bypass grafting (For more extensive)
20
Q
List RFs for Neuropathic Ulcers
A
Any condition causing Peripheral Neuropathy (Mostly, DM and B12 deficiency)
Foot deformity
Peripheral Vascular Disease
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
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)
23
Q
How are Neuropathic ulcers managed
A
Diabetic foot clinics- Blood Glucose, Diet, Exercise, CVD RFs managed
Regular Chiropody- Foot hygiene, correct footwear
24
Q
How does Charcot’s Foot present
A
Swelling
Deformity
Pain
Loss of function
25
List 4 types of Arterial Disease
Aortic Dissection
Thoracic Aortic Aneurysm
Abdo Aortic Aneurysm
Carotid Artery Disease
26
What are the 3 layers of an Arterial Wall?
Describe an Aortic Dissection
Tunica Intima, Media, Adventitia
Tear in Tunica Intima of Aortic wall, so blood flows in and splits apart the T. Intima and Media
27
Aortic Dissections peak between 50-70
Compare Acute and Chronic
List RFs
Acute: Diagnosed = 14 days
Chronic: Diagnosed >14 days
Male
CT Disorder (Marfan’s or Ehlers-Danlos)
HyperT, Atherosclerosis
Bicuspid Aortic Valve
28
Aortic Dissections can progress Proximally and/or Distally from initial tear.
Compare Anterograde and Retrograde Dissections
Anterograde: Propagate towards Iliac Arteries
Retrograde: Propagate towards Aortic Valve (at root of Aortic)
29
List complications of Retrograde Dissection
Aortic valve prolapse
Bleed into Pericardium
Cardiac tamponade
30
Aortic dissections are classified anatomically by two systems, DeBakey and Stanford.
Outline the Stanford Classification
(Into 2 groups)
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
31
Aortic dissections are classified anatomically by two systems, DeBakey and Stanford.
Outline the DeBakey Classification
(Groups dissections anatomically)
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
32
How does an Aortic Dissection present
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)
33
How will Pericarditis usually present
Pleuritic chest pain
ECG showing diffuse ST elevation
Possibly, Pericardial rub on Auscultation
34
How is an Aortic Dissection investigated
Bloods- FBC, LFT, U&E, Clotting, Crossmatch (≥4 units), ABG
```
CT Angiogram (Diagnose + Classify)
Transoesophgeal Echo can be useful, but operator dependent
```
35
Outline General Management for Aortic Dissections
| Specifics different for Type A and B
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)
36
Outline Type A Aortic Dissection management- Higher mortality
(Urgent transfer to Cardiothoracic centre + discussion with cardiac/ vascular surgeon)
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
37
Outline Uncomplicated Type B Aortic Dissection management
HTN management IV;
- B-blockers as 1st line (Labetalol)
- CCBs as 2nd line
38
Why is Endovascular Repair not recommended in treating Acute Type B Aortic Dissections
Risk of Retrograde Dissection
39
When is Surgical intervention indicated in Type B Aortic Dissecions
Rupture
Organ/ Limb Ischaemia
Uncontrollable Pain or HyperT
40
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?
Formation of an aneurysm
| Endovascular repair offers better survival chance
41
List complications of Aortic Dissection
(Depend on Site + Spread, Branches + Organs affected
Aortic Rupture/ Regurgitation
MI (Due to Coronary artery dissection)
Cardiac tamponade
Stroke/ Paraplegia (Spinal/ Cerebral Artery affected)
42
TAAs are less common than AAAs.
Which segments can be affected? Different segments affected= different symptoms
```
Ascending Aorta/ Aortic root (60%)
Aortic Arch (10%)
Descending Aorta (40%)
Thoraco-abdominal Aorta (10%(
```
43
TAAs develop due to degradation of which layer of the artery wall?
List the 2 main causes
Tunica Media
```
CT Disease (Marfan’s or Ehlers-Danlos)
Bicuspid Aortic Valve
```
(Other causes: Trauma, Aortic Dissection, Tertiary Syphilis, Aortic/ Takayasu’s Arteritis)
44
TAAs grow at a mean rate of 1-2mm/ year
List 3 groups in which they grow faster
Those with;
- Marfan’s
- Descending Aneurysms (vs Ascending)
- Dissected Aneurysms (vs non-dissected)
45
List RFs for TAA development
Fhx, Male, Increasing age
HTN, Atherosclerosis
Smoking, High BMI
46
TAAs are usually Asymptomatic and found incidentally.
List possible symptoms if Symptomatic
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
47
In TAA, Back Pain can be caused by Spinal Compression
What do Pain in Neck, Ant Chest, Between Scapulae suggest
Neck- Aortic Arch
Ant Chest- Ascending Aorta
Between Scapulae- Descending Aorta
48
TAAs are diagnosed through imaging, but what tests should an initial work-up include
Bloods, ECG, CXR
49
Outline Imaging and results of a TAA
CXR (not enough to diagnose):
- Wide mediastinal silhouette
- Enlarged Aortic knob
- Possibly, Tracheal deviation
- CT-Chest w/ Contrast: Preferred modality
- TOE
50
Outline Medical Management of TAAs
Statin + Antiplatelet therapy
| BP Control, Smoking cessation
51
Surgical Management/ Indication of TAAs is dependent on Location.
Outline for Ascending Aorta, Aortic Arch and Descending Aorta
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
52
Outline post-op monitoring for those treated for a TAA surgically
Outpatient CT/ MRI imaging, as development of a 2nd Aneurysm isn’t uncommon post-op
53
List AAA RFs
Is DM a RF?
Male, Increasing age, Fhx
Smoking, HyperT, Hyperlipidaemia
DM is not a RF, but is PROTECTIVE against AAA
54
How can an AAA present if symptomatic?
| Many are Asymptomatic, found incidentally/ on screening
Pain- Abdo/ Back/ Loin
Distal Embolisation-> Limb ischaemia
Aortoenteric Fistula
O/E;
- Abdo Pulsatile mass
- Rarely: Retroperitoneal Haemorrhage signs
55
Outline AAA screening in the UK, offered by NAAASP
Abdo USS for all Men aged 65
| Most men with AAA detected wait 3-5yrs in surveillance before qualifying for elective repair
56
How should an AAA be investigated
USS to confirm
| CT w/ Contrast: When 5.5cm in diameter
57
Outline Monitoring and Management of an AAA <5.5cm
| Surgery before 5.5.cm offers no survival benefit
Monitored via Duplex;
- 3 to 4.4cm: Yearly USS
- 4.5 to 5.4cm: 3-monthly USS
Smoking, Weight, Exercise
BP Control, Statin + Antiplatelet
58
An AAA of what diameter requires;
- the DVLA to be notified
- Not driving until repaired
>/= 6cm
>/= 6.5cm
59
List 3 AAA pt groups who surgery would be considered in
- Diameter >5.5.cm
- Expanding at >1cm/year
- Symptomatic AAA in a pt, otherwise fit
60
Describe Open and EV repair in AAA treatment
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
61
Compare outcomes of Open and EV AAA Repair
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)
62
Outline an important complication of EV AAA Repair
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
63
Other than Rupture, list complications of an AAA
Retroperitoneal leak
Embolisation
Aortoduodenal Fistula
64
List RFs for AAA Rupture
Symptoms: Pain, Shock/ Syncope, Vomit, Pulsatile mass, Tenderness
Increasing diameter
Smoking, HyperT
Female gender
65
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)
Peritoneal Cavity- 20%
Retroperitoneal- 80%
66
Outline AAA Rupture management
```
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
67
What is Carotid Artery Disease?
| Responsible for 10-15% of Ischaemic strokes, due to plaque rupture and/or thromboembolism
Atherosclerotic plaque in one/ both CCAs + ICAs-> Stenosis or Occlusion
68
Correlated Degree of Stenosis with Diameter Reduction
| Carotid Artery Disease
Mild Stenosis: <50% Reduction
Moderate: 50-69% Reduction
Severe: 70-99% Reduction
Total: 100%
69
List RFs for Carotid Artery Disease
Age (>65). Fhx
Smoking, HyperT, Hypercholesterolaemia
Obesity, DM, CVD history
70
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
TIA or Stroke
Carotid bruit in neck (<50% of cases)
May have Amaurosis Fugax
71
Atherosclerosis is the most common form of Carotid Artery Disease.
List 4 other pathologies that can be involved
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)
72
Outline Initial Investigations for Carotid Artery Disease
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
73
Outline Follow-up investigations for Carotid Artery Disease
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
74
Outline Acute Management of Carotid Artery Disease
| Thrombectomy: If confirmed ischaemic stroke + Proximal Ant Circulation on angiography
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
75
Outline Long Term Management of Carotid Artery Disease
| CVD RF reduction
- 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
76
Carotid Endarterectomy (CEAs) are now considered better than Stenting.
Who should be referred for assessment for a CEA
All pts with Acute TIA or Non-disabling stroke, who have symptomatic carotid stenosis between 50-99%
77
CEAs involve removing Atheroma and damaged T. Intima.
What are the main risks of CEA
Stroke, MI
Nerve damage to CN 9/ 10/ 12
Bleeding/ Infection
78
Whats a Pseudo-aneurysm
Blood gathers between T. Media and Adventitia, due to Arterial Wall breach
79
What typically causes Pseudo-aneurysms
Vasculitis, Regional Inflammation
Damage to vessel wall, e.g;
- Puncture after Cardiac Catheterisation
- Repeated injections to vessel
80
Where are Pseudo-aneurysm most common?
Femoral artery
| Can be at Radial artery, Carotid artery, Abdo/Thoracic Aorta
81
What can happen if a Pseudo-aneurysm gets infected
Pts can become Septic
| Increased chance of Rupture
82
How does an uninfected Pseudo-aneurysm present?
Pulsatile lump- Tender + Painful
May be Distal Arterial Occlusion, due to compression (check distal pulses)
83
How can an infected Pseudo-aneurysm present?
- Area will be Red + Tender
- Pt likely Septic (Fever, Tachycardia)
- Purulent material may discharge from any sinus opening
84
What do you do if a pt reports they had Bleeding from a Pseudo-aneurysm that has now stopped
Close monitoring + urgent management, as this may be a ‘Herald Bleed’ that could re-bleed at any time
85
Outline uninfected Pseudo-aneurysm investigations
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
86
Outline investigations, specific to infected Pseudo-aneurysm
Bloods
Blood culture
MC&S, if discharging
Cross-match sufficient amount of blood (High rupture risk)
87
List treatment options for Pseudo-aneurysms
Small ones can be left alone
Larger/ Symptomatic ones;
- USS-guided Thrombin injection
- USS-guided Compression
- EV Stenting
- Surgical repair/ Ligation
88
Describe USS-Guided Thrombin Injections
Pts can have follow-up imaging to ensure resolution
Thrombin injected directly into Pseudo-aneurysm lumen under US-Guidance
This forms a Thrombus within the Pseudo-aneurysm, so it can be closed off
89
Options of EV Stenting or Surgery depend on pt and location of Pseudo-aneurysm
Describe suitability of deploying EV Covered Stents
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
90
Describe use of Surgical repair/ Ligation in treating Pseudo-aneurysms
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
91
Outline management of an infected Pseudo-aneurysm
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
92
When using a Graft in treating a Pseudo-aneurysm, which graft types are more resistant to infection
Vein or Bovine grafts
93
Outline Complications following Surgical Ligation of a Pseudo-aneurysm
Small % of people will need Amputations
Mostly however, collateral supply will provide adequate blood flow distally
94
# Define an Aneurysm
Peripheral and Vascular Aneurysms can occur, but AAAs are most common
Persistent abnormal dilation of an artery >x1.5 its normal diameter
95
List RFs for Peripheral+Vascular Aneurysms
Trauma, Infection
CT/ Inflammatory Disease
Smoking
HyperT, Hyperlipidaemia
Fhx
96
Briefly, outline Investigations for Peripheral + Visceral Aneurysms
Usually, CT Angiography
MR Angiography: Good alternative, as less Radiation and Nephrotoxicity
Duplex USS: Can be useful for detection + follow-up
97
Briefly outline Management of Peripheral + Visceral Aneurysms
Watchful waiting + RF Reduction (Smoking, Anti-platelet + Statin therapy)
OR
Surgery (Open/ EV)
98
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?
Symptomatically;
- Acute Limb Ischaemia
- Less commonly, Intermittent Claudication
Compression symptoms on Popliteal Vein or Fibular nerve
99
Outline Investigations for Popliteal Aneurysms
Initially: Duplex USS (rule out other causes of Popliteal Fossa swelling)
Further: CT/ MR Angiogram
100
Outline Popliteal Aneurysm Management
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
Femoral Artery Aneurysms are usually Pseudo-Aneurysms.
The 2 major causes are what?
- Percutaneous Vascular Interventions
| - Patent self-injecting (IV Drug users-> Groin)
102
How do Femoral Artery Aneurysms present?
Symptoms from Thrombosis/ Rupture/Embolisation
Varying degrees of Claudication or Acute Limb Ischaemia, but often no symptoms other than groin swelling
103
How are Femoral Artery Aneurysms investigated and treated?
Duplex USS, then CT/MR Angiography
Open Surgical repair
104
In Visceral Arteries what Aneurysms are most common?
Splenic (most common-60%)
Hepatic (2nd most common-20%)
Renal
105
List Splenic Artery Aneurysm RFs
Female, Multiparity
Portal HyperT
Pancreatitis/ Pancreatic Pseudocysts
106
How do Splenic Artery Aneurysms present?
| Ruptured vs unruptured
If symptomatic but unruptured;
- Vague Epigastric/ LUQ pain
If ruptured;
- Severe abdo pain
- Haemodynamic unstability
107
How are Splenic Artery Aneurysms investigated and treated?
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
Percutaneous instrumentation is associated with 50% of Hepatic Artery Aneurysm cases
List 3 other causes
Trauma
Degenerative disease
Post-liver transplant (False Aneurysms form around vessel anastomoses)
109
How may Hepatic Artery Aneurysms present?
Mostly Asymptomatic
If Symptomatic;
- Vague RUQ/ Epigastric Pain
- Jaundice
110
How are Hepatic Artery Aneurysms investigated and treated?
CT/ MR Angiography
EV Repair, similar to Splenic Artery Aneurysms;
- If Haemodynamically stable + Suitable anatomy
- If not, consider Open repair
111
How may Renal Artery Aneurysms present?
Often Asymptomatic, found incidentally
If Symptomatic;
- Haematuria
- Loin pain
- Resistant HyperT
112
How are Renal Artery Aneurysms investigated and treated?
CT/ MR Angiography
EV Repair;
- Stent alone, if main renal artery affected
- Coils + Covered stent graft, if Hilum affected
Rarely: Renal transplant
113
Define Acute Limb Ischaemia
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
List the 6P signs of Acute limb ischaemia
- Pain, Pallor, Pulselessness
- Parasthesia, Perishingly cold, Paralysis
(1st 3 most common)
115
Describe the;
- Prognosis
- Sensory loss
- Motor deficit
- Arterial Doppler
- Venous Doppler
Of Rutherford 1 (Viable) Acute Limb Ischaemia
- No immediate threat
- No sensory loss
- No motor deficit
- Audible arterial doppler
- Audible venous doppler
116
Describe the;
- Prognosis
- Sensory loss
- Motor deficit
- Arterial Doppler
- Venous Doppler
Of Rutherford 2A (Marginally Threatened) Acute LI
- Salvageable , if treated soon
- Minimal/ no sensory loss
- No motor deficit
- Inaudible Arterial Doppler
- Audible Venous Doppler
117
Describe the;
- Prognosis
- Sensory loss
- Motor deficit
- Arterial Doppler
- Venous Doppler
Of Rutherford 2B (Immediately Threatened) Acute LI
- Salvageable, if immediately revascularised
- More than toes, pain on rest
- Mild/ Moderate motor deficit
- Inaudible Arterial Doppler
- Audible Venous Doppler
118
Describe the;
- Prognosis
- Sensory loss
- Motor deficit
- Arterial Doppler
- Venous Doppler
Of Rutherford 3 (Irreversible) Acute LI
- Major tissue loss, permanent nerve damage
- Major sensory loss
- Major motor deficit, Paralysis
- Inaudible Arterial Doppler
- Inaudible Venous Doppler
119
List Ddx for Acute LI
- Critical LI
- Acute DVT
- Spinal cord/ Peripheral nerve compression
120
List Acute LI Investigations
- 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
Outline Initial Management for Acute Limb Ischaemia
| A surgical emergency, permanent tissue damage within 6hrs
High flow O2, IV fluids
IV Heparin
122
Outline Medical Management of Acute Limb Ischaemia
Who is it considered in?
```
Prolonged Heparin course
Regular assessment (APTT, Clinical review)
```
Rutherford 1 and 2A
123
When may Surgical Intervention be indicated for Acute LI treatment
- No improvement after Conservative Management
| - Rutherford 2B
124
Outline Surgical Treatment for Acute Limb Ischaemia, before any irreversible damage occurs
Embolic cause: Embolectomy via Fogarty catheter
Thrombotic cause: Angioplasty
Both causes:
- Local intra-arterial Thrombolysis
- Bypass surgery
125
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?
Ischaemia Re-perfusion Syndrome
126
Outline Long Term Management of Acute Limb Ischaemia
- Lifestyle changes
- Anti-platelet agent or Anticoagulant
- Treat any underlying cause (E.g AFib)
If Amputated;
- OT + PT
- Long term rehab
127
Acute LI has a morality of 20%
A major complication is Re-perfusion injury. What can this sudden increase in capillary permeability lead to?
- Compartment Syndrome
Substances released from damaged muscle cells;
- K+ (->Hyperkalaemia)
- H+ (-> Acidosis)
- Myoglobin (-> Signifcant AKI)
128
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?
Atherosclerosis (Rarely, Vasculitis)
Lower limbs (Upper limb and Gluteals can be affected)
129
List RFs for Chronic Limb Ischaemia
Smoking, Obesity + Inactivity, DM
HyperT, Hyperlipidaemia
Increasing age, Fhx
130
Chronic Limb Ischaemia presents differently, depending on the severity.
Outline the presentation of each stage, according to the Fontaine classification
Stage 1: Asymptomatic
Stage 2: Intermittent Claudication
Stage 3: Ischaemic rest pain
Stage 4: Ulceration and/or Gangrene
131
Outline Buerger’s test and relate this to Buerger’s Angle
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
What is Leriche Syndrome
How does it present
A form of Peripheral Arterial Disease affecting Aortic Bifurcation
Buttock/ thigh pain, w/ ED
133
What is Critical Limb Ischaemia
What are 3 ways it can be defined clinically?
The advanced form of Chronic Limb Ischaemia
- ABPI <0.5
- Presence of Ischaemic/ gangrene regions
- Ischaemic rest pain for >2wks, needing opiates
134
How may Critical Limb Ischaemia present O/E?
- Pale + Cold
- Weak/ Absent pulses
Thickened nails, Limb hair loss, Skin changes (Atrophy, Ulcer, Gangrene)
135
List the 2 main ddx for Chronic Limb Ischaemia
Acute Limb Ischaemia
Spinal stenosis/ Neurogenic Claudication;
- Back pain radiates down lateral leg
- Symptoms relieved by sitting, rather than standing
136
Outline Investigation for Chronic Limb Ischaemia
| If <50 and no major RFs, Thrombophilia screen and Homocysteine levels checked
- Basic Bloods, Lipid profile, HbA1c, Glucose
- ECG
- Doppler USS, then CT/MR Angiography
- ABPI
137
Most pts with Chronic Limb Ischaemia require CV Risk reduction
Outline Medical Management of Chronic Limb Ischaemia
- Lifestyle changes
- Statin + Anti-platelet
- DM Control
If pt doesn’t have Critical Limb Ischaemia;
- Supervised exercise programme
138
Outline Surgical management of Chronic Limb Ischaemia
| Consider if RF modification and Supervised exercise fail to improve symptoms
- 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
The 5-yr mortality in pts with Chronic Limb Ischaemia is around 50%
List complications of Chronic Limb Ischaemia
Sepsis
Acute-on-chronic ischaemia
Amputation
Reduced Mobility and QoL
140
What is Acute Mesenteric Ishcaemia
Sudden decrease in bowel’s blood supply, resulting in bowel ischaemia
Leads to death, if not treated quickly
141
List 4 common types of causes of Acute Mesenteric Ishcaemia
| Rarer: Takayasu’s arteritis, Fibromuscular dysplasia, Thoracic Aorta Dissections
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
What proportion of Acute Mesenteric Ishcaemia cases are AMATs and AMAEs?
What are the underlying causes?
AMAT;
- 25%
- Atherosclerosis
AMAE;
- 50%
- TAA or Cardiac causes (Arrytmias, Prosthetic heart valve)
143
What proportion of Acute Mesenteric Ishcaemia cases are NOMIs and MVTs?
What are the underlying causes?
NOMI;
- 20%
- Hypovolaemic, Cardiogenic Shock
MVT;
- <10%
- Coagulopathy, Malignancy, Autoimmune disorders
144
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)
Smoking
DM
HyperT, Hyperlipidaemia, Hypercholesterolaemia
145
How may Acute Mesenteric Ischaemia present?
| History, Exam
Constant generalised abdo pain
N+V (70% of causes)
O/E;
- Non-specific tenderness
- If late stage, signs of peritonism
146
List Lab Test investigations for Acute Mesenteric Ischaemia
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
List Imaging investigations for Acute Mesenteric Ischaemia
CT w/ IV Contrast;
| - Shows as Oedematous bowel-> Loss of bowel wall enhancement-> Pneumatosis
148
Outline Initial Management of Acute Mesenteric Ischaemia
| Surgical emergency
- IV Fluids, Catheter, Fluid balance
- Broad Abx (In case of Perforation or Bacterial Translocation)
- Early ITU input
149
Outline Definitve Management of Acute Mesenteric Ischaemia
| Intervention depends on location, timing, severity
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
List complications of Acute Mesenteric Ischaemia
What’s the mortality?
Bowel necrosis
Bowel perforation
If pts survive, may have Short Gut Syndrome
50-80%
151
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)
- Postprandial pain: (Usually 10mins to 4hrs after eating)
| - Weight loss, N+V, Change in bowel habit
152
Outline Investigations for Chronic Mesenteric Ischaemia
| May be confounding signs of Anaemia
Routine Bloods, Ca, Mg, Lipids, Glucose, HbA1c
CT Angiography: Gold standard
153
Initial management for Chronic Mesenteric Ischaemia is Conservative
Outline Surgical treatment if:
- Severe/ Progressive disease
- Debilitating symptoms (Inlcuding w loss, malabsorption)
```
EV Procedures (More common):
- Mesenteric angioplasty w/ stenting
```
Open procedures: Endarterectomy or Bypass
154
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
Primary;
- No underlying cause
- 33% of pts have Fhx
Secondary;
- Underlying condition or Medication
155
List causes of Hyperhidrosis
- Pregnancy/ Menopause
- Anxiety
- Infections (TB, HIV, Malaria)
- Malignancy (Esp. Lymphoma)
- Endocrine disorder
- Medication (Antidepressants, Propranolol, Anti-AChEsterase)
156
How may Primary Hyperhidrosis present?
How long must it be present for the diagnosis to be made
- 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
How may Secondary Hyperhidrosis present?
- Generalised sweating
| - Mostly at night time
158
Outline Investigations for Hyperhidrosis
| Diagnosis often made through History and Exam
Bloods- FBC, CRP, U&E, Glucose, TFTs
CXR
All done as routine
159
Outline non-surgical and non-medical management of Hyperhidrosis
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
Outline medical management of Hyperhidrosis
Propantheline;
- Only Anticholinergic agent licensed for use
Glycopyyrolate + Oxybutinin;
- Can reduce sweating
- Not readily available, often off-license
161
Surgical management of Hyperhidrosis is reserved for pts with resistant symptoms that significantly affect QoL
What’s a side effect of surgical treatment
Many pts develop compensatory sweating in other locations
162
List 3 surgical interventions for Hyperhidrosis
Iontophoresis
Botulinum toxin
ETS, Endoscopic Thoracic Sympathectomy
163
Describe Iontophoresis and its use in treating Hyperhidrosis
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
Describe Botulinum Toxin use in treating Hyperhidrosis
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
Describe ETS, Endoscopic Thoracic Sympathectomy and its use in treating Hyperhidrosis
Damage purposefully caused to Thoracic Sympathetic Ganglion supplying affected region
(Last resort, as risk of damage Nerves/ Lung parenchyma)
166
What is Subclavian Steal Syndrome?
Rare condition causing syncope/ neurological deficits when blood supply to arm is increased via exercise
167
Outline the pathophysiology of Subclavian Steal Syndrome
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
Subclavian Steal Syndrome is 2:1 in Males:Females and 3:1 Left:Right
List causes of Subclavian Steal Syndrome
Atherosclerosis (commonly causes in Subclavian A)
Vasculitis, Thoracic Outlet Syndrome
Complications of Aortic Coarctation repair
169
List RFs for Subclavian Steal Syndrome
Increasing age
DM, Smoking
HyperT, Hyperlipidaemia
170
Outline Coronary-Subclavian Steal Syndrome
Which pts does it occur in?
- 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
How may Subclavian Steal Syndrome present?
Cerebral symptoms;
- Vertigo, Visual loss, Diplopia, Syncope
- Dysphagia, Dysarthria
Pts may present with Arm Claudication (Pain or Parasthesia) made worse by arm movement
172
List investigations for Subclavian Steal Syndrome
Initial: Duplex USS
Definitive: CT Angiography or MRA
Routine CXR: Looks for External Subclavian Artery compression
173
Risk scoring of Subclavian Steal Syndrome can be classed into 3 grades
Outline these
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
Outline Conservative Management of Subclavian Steal Syndrome
Statin + Anti-platelet therapy
| Smoking, Weight, Optimising Glucose control
175
Outline Surgical Management of Subclavian Steal Syndrome
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
What is Thoracic Outlet Syndrome, TOS?
Set of symptoms due compression NV Bundle compression in Thoracic Outlet
(TO: Opening between Clavicle, Scapula, Rib 1)
177
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
- 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
How may Thoracic outlet syndrome, TOS present in regards to HISTORY?
(Symptoms can be classed as Neurological, Venous, Arterial- nTOS, vTOS, aTOS)
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
How may Thoracic outlet syndrome, TOS present in regards to EXAMINATION?
Weakness/ Numbness
Swelling
Tenderness (often over Scalene muscles)
Signs of ischaemia
180
List 3 Special tests for Thoracic Outlet Syndrome, TOS
- Adson’s Manoeuvre
- Roo’s test
- Elvey’s test
181
Outline Adson’s Manoeuvre
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
Outline Roo’s Test
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
Outline Elvey’s test
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
Outline Initial Investigations for Thoracic Outlet Syndrome, TOS
Bloods- FBC, Coag,
| CXR (>90% pts have a bony abnormality)
185
Outline Further Investigations for Venous/ Arterial Thoracic Outlet Syndrome, vTOS/ aTOS
Venous + Arterial Duplex USS;
- With pt at rest and arm in stress positions to look for compression
CT/ MRI or Venogram
186
Outline Further Investigations for Neurological Thoracic Outlet Syndrome, nTOS
Nerve Conduction studies;
- Detection of decreased APs due to compression
- Usually used to exclude Carpal/ Cubital Tunnel Sydromes, rather than nTOS diagnosis
187
Outline General Further Investigations for Thoracic Outlet Syndrome, TOS
(Regardless of nTOS, vTOS or aTOS)
MRI to detect Cervical Ribs or Fibrous Bands
Urgent CT Angiogram, if signs of Ischaemia
188
TOS treatment depends on type
Outline management of nTOS
PT for 6mths is 1st line:
- Improves Neck + Shoulder mobility
- Strengthens surrounding muscles, Relaxes Scalenes
Botulinum toxins: To relax Scalenes, Often w/ PT
189
TOS treatment depends on type
Outline management of vTOS
Thrombolysis + Anti-Coagulation
Most cases need;
- Surgery to decompress Thoracic Outlet
- Venoplasty/ Venous reconstruction/ Venous stent
190
TOS treatment depends on type
Outline management of aTOS
Most cases need correction of anatomical abnormalities
If Acute Limb Ischaemia, urgent vascular input as pt may need Embolectomy
191
Elective surgery corrects symptoms in;
- 90-95% of aTOS/ vTOS cases
- 50-70% of nTOS cases
Outline TOS Surgical management
For Decompression procedures;
- Supraclavicular/ Transaxillary approach
- Can access 1st/ Cervical Rib
Restrictive bands can also be released
192
List complications of TOS Surgery
Neurological/ Vascular damage
Haemo-/ Pneumo-/ Chylo- Thorax
193
List TOS Complications
Permanent nerve damage
Aneurysmal dilation of Subclavian Artery -> Embolisation or Loss of Limb Function
194
Describe the Prognosis of TOS
| Variable in nTOS, much better in vTOS after surgery
Sometimes (especially in nTOS) symptoms can persists after PT and Surgery
Symptoms can recur from 1mth to 10yrs after surgery
195
What is Deep Venous Insufficiency, DVI?
Chronic disease caused by DVT or Valvular Insufficiency
196
What 2 conditions together are known as Chronic Venous Insufficiency
```
Varicose vein (affects superficial veinous system)
Deep Venous Insufficiency
```
197
DVI occurs due to failure of the venous system.
What are 3 things that characterise DVI
Valvular reflux
Venous HyperT
Obstruction
198
Compare the 2 types of causes of DVI
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
List RFs for DVI
- Fhx, Female, Increasing age
- Obesity, Smoking, Pregnancy
- Long periods of standing
- Previous DVT/ Phlebitis
200
How may DVI present?
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
Outline Investigations for DVI
- 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
Outline Conservative Management of DVI
Compression stockings + Analgesia
If pt has a Venous Ulcer, full compression treatment
203
Outline Surgical Management of DVI
Less successful than Conservative
Little/ no benefit from Valvuloplasty
204
Pts with Severe Post-Thrombotic Syndrome with an occluded Iliac Vein may be suitable for what novel procedure?
Describe this procedure
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
Why is Venous Stenting only done for pts with the most severe symptoms despite maximal conservative therapy
Long-term outcomes are unknown, as its a novel intervention
206
List common complications of DVI
Swelling, Recurrent cellulitis
Chronic pain, Ulceration
(Less common: DVT, Varicose veins, Secondary Lymphoedema)
207
What are Varicose Veins
| Often at Sapheno- Femoral -Popliteal junctions
Tortuous dilated vein segments associated with incompetence of the valves permitting blood to flow from Superficial-> Deep systems
208
How does the presence of Varicose Veins affect the Superficial Venous System
Venous hypertension + Dilation
209
99% of Varicose Veins are Primary Idiopathic
List Secondary causes
- DVT
- Ovarian or Pelvic masses (Fibroids, Pregnancy)
- Arteriovenous malformations
210
What percentage of women get Varicose Veins during/ after Pregnancy
40%
211
List RFs for Varicose Veins
FPOP
Fhx, Prolonged standing
Obesity, Pregnancy
212
How may Varicose Veins present?
Cosmetic issues, Aching, Itching
Later stages;
- Skin changes, Ulceration, Thrombophlebitis
- Bleeding (often post-trauma)
Venous Insufficiency signs: Ulceration, Varicose Eczema, Haemosiderin staining
213
What is Saphenous Varix
Why is it commonly mistaken for a Femoral Hernia
Saphenous Vein dilation at Saphenofemoral junction
Both displays a cough impulse
214
How is Saphena Varix best Investigated and Managed?
Duplex USS
High Saphenous Ligation
215
What system is used to classify the manifestation of Varicose Veins
CEAP
Clinical features
aEtiology
Anatomical
Pathophysiology
216
Outline Investigations for Varicose Veins
Gold standard: Duplex USS
Look for Deep venous incompetence, Occlusion, Stenosis
217
Outline management of a pt with DVT and Varicose Veins
| Blood flows Superficial to Deep veins
Can’t treat Superficial Incompetence, as venous blood has no route back
Pt offered non-surgical management
218
Outline Non-invasive Management of Varicose Veins
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
What are 4 indications for Surgical treatment of Varicose Veins
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
List 3 surgical treatment options for Varicose Veins
Foam Scleorotherapy
Thermal Ablation
Vein Ligation, Stripping and Avulsion
221
Outline Vein Ligation, Stripping and Avulsion for VV treatment
Incison in Groin/ Popliteal fossa
Tying off + Stripping away the refluxing vein
222
Outline Foam Sclerotherapy for VV treatment
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
Outline Thermal Ablation for VV treatment
Heating vein from inside-> permanent damage, closing off the vein
Done w/ USS Guidance, under Local/ General Anaesthetic
224
Many pts treated for Varicose Veins often need re-intervention surgery
List typical complications after surgery
Haemorrhage, Recurrence, Nerve damage (Saphenous, Sural)
Thrombophlebitis (Consider in Foam/Ablation ops)
DVT (Consider in EV procedures)
225
What’s the usual cause of an Aorto-enteric Fistula?
AAA Repair
226
When is Ischaemic rest pain most likely to show
At night, as legs elevated and reduced HR so less leg perfusion
(After time, they start sleeping in chairs)
227
What percentage of men aged 65 have an abnormal Aorta and what percentage need surgery
1%
1 in 1000 (0.001%)
228
What is the risk of a 5.5cm AAA rupturing?
This is equal to chance of open surgery killing the pt
10%
229
Arterial stenosis/occlusion in which arteries can cause intermittent Claudication?
Superficial femoral artery
| Popliteal artery
230
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?
Development/opening of collateral vessels
| Angio or Vasculogenesis??
231
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
- Severe ischaemia (from elevation)-> Local Vasodilator release
- These increase the perfusion of the ischaemic foot when gravity acts on it again
232
Outline Investigation for a DVT, including Well’s score interpretation (Not same as for PE)
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
Outline DVT Mx
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
