1
Q
What is Venous insufficiency? Potential causes?
A
The loss of a drop in pressure from stationary to mobile in the veins. This may be due to
- Venous valve incompetency
- Deep venous occlusion
- Calf muscle pump failure
- Immobility
- Depp/Superficial venous reflux
- Obesity
- Dependency
2
Q
What is the result of venous insufficiency?
A
Venous hypertension
- varicose veins
3
Q
What is Varicose veins?
A
A vein which has permanently lost its valvular efficiency and as a result of continuous dilation under pressure, in the course of time it becomes elongated, tortuous, pouched and thickened
4
Q
What are complications of great/small saphenous vein varices
A
Ischemic damage (hemosiderin deposition, skin thickening) on the ankle and the foot over time
5
Q
What is this an image off, explain their occurrence.
A
Lateral perforates may be damaged
Reticular veins exist in embryological development and then their role is taken over by the saphenous veins however this may not have occurred after the fact.
No real medical problem, may be of cosmetic concern for some
6
Q
Thigh reflux pattern of presentation
A
- Varicose veins in the lateral and pelvic areas due to incompetency in the anterior accessory (saphenous) thigh vein ( joins in the groin in the saphenofemoral junction
- Pelvic congestion syndrome.Pudendal Vein Reflux: seen in women in their 30’s)
- may be important as veins in the retroperitoneal area becoming incompetent’s
- Ovarian vein, vulva and vaginal veins
- can cause pain and heavy menstrual bleeding
- pain during intercourse
- feeling of bloating and discomfort
- can be associated with hemorrhoids
- may be important as veins in the retroperitoneal area becoming incompetent’s
7
Q
What is pelvic congestion syndrome?
symptoms?
A
- Pudendal Vein Reflux: seen in women in their 30’s - young pre-menopausal)
- may be important as veins in the retroperitoneal area becoming incompetent’s
- Ovarian vein, vulva and vaginal veins
- can cause pelvic pain, non-cyclical postural back pain
- heavy menstrual bleeding
- pain during intercourse
- feeling of bloating and discomfort
- can be associated with hemorrhoids
- may be important as veins in the retroperitoneal area becoming incompetent’s
8
Q
What is the treatment/managment for pelvic congestion?
A
- MR venography/ transvaginal US
- Endovascular therapy - more effective than surgery
9
Q
Give examples of complex patterns of reflux
A
- Combined deep and superficial reflux
- combined superficial reflux with deep obstruction
- Klippel-Trelaunay syndrome
- increased arterial flow to the vein → hypertrophy of the limb
- Park-Weber syndrome
- above the limb hypertrophy and AVMS
10
Q
What is the CEAP classification?
A
Classification of Varicose veins
- Clinical (C0-C6)
- 0 - no visible venous disease
- 1 - reticular veins and thread veins
- 2 - varicose veins
- 3 - oedema
- 4 - skin changes
- 5 - healed ulceration
- 6 - active ulceration
- Etiology (primary vs secondary)
- Anatomy (location eg. deep)
- Pathophysiology (reflux obstruction)
11
Q
What is the management for the C1 stage of the CEAP classification
Causes/Symptoms?
A
C1 - is reticular or thread veins
- Treatable: yes
- Cosmetic
- improves QoL
- Could be secondary to underlying superficial or deep venous pathology.
- Lateral cutaneous plexus often involved.
- Veins can be sizeable.
- Can be quite painful.
12
Q
What is the management for the C2 stage of the CEAP classification
Causes/Symptoms?
A
C2- is varicose veins
- elevation, exercise and weight loss
- compression stockings
- !not in pregnancy!
- endothermal ablation
- US-guided foam sclerotherapy
- Surgery
13
Q
What is the management for the C3 stage of the CEAP classification
Causes/Symptoms?
A
C3- Oedema
- not automatically treated on the NHS - needs to be referred
- compression
- and managing underlying damage/pathology
14
Q
What is the management for the C4 stage of the CEAP classification
Causes/Symptoms?
A
C4- Skin changes: Lipodermatosclerosis, pigmentation, haemosiderin deposition, eczema, atrophy blanche
- treat condition topically and treat underlying disease
- refer for assessment and treatment
- can also cause lose of motion
15
Q
What is the management for the C5 stage of the CEAP classification
Causes/Symptoms?
A
C5 - healed ulceration
- treatable on the NHS
- the healed site is where the increased venous pressure has caused ulceration
- could prevent ulcer recurrence
16
Q
What is the management for the C6 stage of the CEAP classification
Causes/Symptoms?
A
C6 - Active Ulceration
- mostly seen in elderly patients with reduced increased sedentary behavior
17
Q
What are the symptoms of Varicose veins
A
- Heaviness or tension
- Feeling of swelling
- Aching (W:53.8%)(M:32.5%)
- usually in the evening
- Restless legs (W:35.1% )(M:20%)
- Cramps (W:42%)(M:34%)
- Itching
- Tingling
18
Q
What are complications of Varicose veins
A
- Phlebitis - 20%
- Bleeding - 3%
- usually on people on anticoagulants → Elevation
- Skin changes - 25%
- Ulceration - 5-10%
19
Q
What points are important in a history to rule out varicose veins/ venous insufficiency?
A
- Symptoms
- Timing/ nocturnal etc
- Predisposing factors
- Alleviating factors
- Family history
- Cosmetic concerns
- Previous treatment
- Medical history
- Previous DVT
- Medical issues: Diabetes, anticoagulants
20
Q
What points are important on examination of a patient with suspected varicose veins or venous insufficiency?
A
- Inspection
- Site of varicosities
- Signs of venous hypertensive complications
- Eczema, oedema, ulceration
- Scars from previous surgery
- Muscle wasting. Immobility
- Palpate
- Arterial pulses (IMP)
- may use a doppler to hear pedal pulses
- Tenderness, lumpiness
- Arterial pulses (IMP)
- Control at saphenofemoral junction or saphenopopliteal junction (SFJ /SPJ)
- Supine vs standing
- Percussion–Tapping test
- finger on SFJ, lightly tap the varicose vein on one end - a thrill will be felt if there is continuity in this vein up to the SFJ due to insufficiency.
- Auscultation
- Trill or bruit over SFJ
- Auscultation for reflux using hand-held Doppler
21
Q
What investigation is carried out to check for varicose veins/ venous insufficiency?
A
Gold standard - Duplex US scan
- confirms or establishes source of reflux
- provides roadmap
- assesses the deep veins
- allows planning of treatment - guides treatment
22
Q
Explain Disconnection surgery for varicose veins
Procedure/ recovery
Complications
A
- High ties at groin.
- Usually combined with stripping.
- Traditional method
- Still valuable in some instances.
- Mainly under GA
- Recovery (1-2 wks)
- Complications
- Bleeding / Bruising
- Infection / Swelling
- Nerve Injury
- DVT
23
Q
What are the Endovenous therapies for varicose veins
A
Laser (EVLT) vs Radiofrequency Ablation (EVRFA)
This is the first line of intervention for confirmed varicose veins or truncal reflux
24
Q
Explain EVRFA (endovenous radiofrequency ablation) for varicose veins
Procedure/ recovery
Complications
A
- No Groin Incision
- uses a ultrasound guided venous catheter to gain access the vein, numb the vein lignocaine w/ adrenaline, separate vein from surrounding structures by using fluid , compress vein and heat the vein closing it as you go along
- Recovery (1-3 Days)
- (89% Normal activity in 24hrs)
- Complications: Rare
- Bleeding / Bruising
- Infection / Nerve Injury
- Swelling / Burns / DVT
- Results
- Success (85%-100%)
- 5yrs (85%)
25
Explain conventional Sclerotherpay
* Thread vein injection
* intradermal varicose veins
* conventionally used for isolated veins
26
Explain US-guided Foam injection Sclerotherapy
* NICE; offered if EVRFA or EVLT is unsuitable
* Foam injected under direct ultrasound guidance.
* slowly, never more than 12mls
* **Used for truncal veins.**
* Some limitations.
* Size of vein.
* Volume of foam (complications).
* Staged procedure.
* **Complications**
* Phlebitis
* Pigmentation
27
Explain Cyanoacrylate ebolisation
The use of glue through a catheter to embolize the vein
* avoids tumescence and avoids risk of foam embolization, non-thermal approacj.
28
Explain the Management of Venous Ulcers
Accurate assessment → Debridement and sensible dressing → compression therapy → treat the underlying problem
Underlying problems: venous problem, patient medical problems, look at social issues, mobility, nutrition
29
How would you assess a venous ulcer?
* look at exudate on dressing,
* assesses tissue- is it necrotic
* look at ulcer base
* granulating, sloughy, dry and fibrous?
* Ulcer Edge
* sloping, elevated, punched out, dry and fibrosed
* surrounding evidence of venous insufficiency
30
How would you assess if there is an arterial component to the venous issue?
* ABPI correlates well with angiography and symptoms.
* highest systolic pressure in the arm (brachial artery) versus the highest systolic pressure in the lower limb (interior posterior tibular)
* Normal ABI:
* 1.0 – 1.2(supine)
* Muscular augmentation
* Summation of pressure waves.
* 0.5 – 0.8 claudicants
* \<0.5 SCLI
* \<0.3 CLI
31
What types of Non-Adhesive dressings are there? examples (4)
Absorbent dressingsHydrocolloids, Alginates, foams
Impregnated dressings
Inadine, Silver, MMP inhibitors, Leptospermum honey (antimicrobial effect)
Specialist dressings
Negative suction, superabsorbent particles.
Biologic
Skin, dermal substitutes
32
Explain Compression therapy and its role in managing ulcers and venous insufficiency
Diminishes leg vein distension and stasis.
Cuts down on inflammation.
Diminishes oedema
Improves tissue perfusion and transfer.
Improves overall venous function.
? Improves venous pump function.
33
What types of Deep Venous disease is there?
Deep venous thrombosis
Pulmonary embolization
Venous infarction
Chronic sequelae
Post-thrombotic syndrome
Pulmonary hypertension
34
Explain the origin of a DVT
**Virchow’s triad:**
* **Changes to flow**
* Immobility
* Perioperative, paralysis.
* Extrinsic vessel compression.
* **Changes to blood coaguability**
* Thrombophilia, severe dehydration
* Malignancy, sepsis, Covid-19.
* Drugs such as COC
* **Changes to Vessel Wall**
* Deep vessel injection (eg IVDU)
* Trauma
35
How is a DVT Diagnosed?
Clinical features: History, Clinical features, Wells Score
D-dimer testing
Duplex US scanning
36
What are the vascular aspects of Covid-19
Significantly increased risk of thrombosis
Likely due to direct endothelial cell infection
Platelet aggregation and activation
Increased arterial and venous thrombosis
Increased risk of Stroke, critical limb and mesenteric ischaemia
Patients are prothrombotic.
Benefit in continuing statin therapy.
Digital manifestations of mild or asymptomatic Covid-19
Covid fingers or covid toes (chilblains)
37
What is the Preventative Management of a DVT
Prevent it by risk assessing a patient
* Perioperative prophylaxis
* Mechanical
* TEDs
* Active intermittent mechanical compression
* Early mobilization
* Coagualibility
* LMWH prophylaxis
* good hydration
* correct any risk factors (COC, smoking)
*
38
How do you manage an insitu DVT?
Anticoagulation
Heparin/LMWH
DOAC eg Rivaroxaban/ Apixiban.
Warfarin (monitoring required).
Compression hosiery
2 weeks minimum.
Longer if still symptomatic.
Ensure sufficient arterial supply and healthy enough skin.
39
Explain how thrombolysis works?
Catheter directed thrombolysis: in the iliofemoral vein only
* mechanical clot disruption/ aspiration
* Pharmacological lysis agents
* Alteplase (tissue plasminogen activator)
40
Explain the occurrence of Post-thrombotic syndrome?
* some patients can experience swelling, skin changes following a DVT
* 20-50% of patients experience this after a symptomatic DVT
* 5-10% suffer from severe PTS with features of advanced chronic venous insufficiency
* Can have severe impact on QoL
* can cause severe pain ulceration in young patients
41
Explain the pathophysiology of Post-thrombotic syndrome
* Obstruction at key points
* Reflux: loss of valvular integrity.
* Ambulatory venous hypertension.
* Triggering of inflammation: PAIN.
* Reduced calf perfusion with tissue hypoxia.
* Increased tissue permeability: Oedema
* Progressive pump dysfunction.
* * The quicker the clot resolution, the less collateral damage.
42
How does Venous Infarction present clinically?
* Pulses palpable initially
* Swelling (often severe)
* Tenderness (compartment syndrome)
* Discoloration/ cyanosis (Phlegmasia alba dolens/ Phlegmasia caerulea dolens)
43
How is Venous infarction medically managed/ treated
* MEDICAL EMERGENCY
* Elevation
* Fluid resuscitation
* Thrombolysis
* Consider emergency amputation
* 20% mortality.
44
Explain the pathophysiology of a Venous Infarct
* DVT is so extensive, venous return is not possible
* results in severe venous insufficiency, venous blockage associated with arterial insufficiency.
* Muscle is starved of blood, muscle starts to break down
* fluid seeps into the leg → increasing pressure → compartment syndrome
* still have pulses early on
45
Explain the occurrence of Upper Limb DVT
2-10% of all DVTs
* Secondary (lines, catheters, malignancy etc).
* Primary (vein being trapped under the first rib or surrounding muscle structures)
* Paget-Schroetter syndrome (effort thrombosis).
* Commoner in leaner, young, male patients.
* Repetitive overhead potion prior to presentation
* Commoner in athletes and overhead workers.
46
Define Ischaemia
Deficiency in supply of blood flow (perfusion) to the tissue bed
47
Define Absolute Ischaemia
Insufficient perfusion to continue normal cellular process that is **Limb-threatening**
This is critical ischaemia → Gangrene and rest pain
48
Define Relative Ischaemia
Insufficient perfusion to permit full function, which is okay at rest and is **Life Changing**
depends on needs →
asymptomatic, claudication
49
Define Acute Ischaemia
sudden occurrence of absolute ischaemia (6 P's)
* pulseless
* painful
* pale
* perishingly cold
* **Paraesthetic**
* **Paralysed**
50
Define Chronic Ischaemia
Established insufficient perfusion \>2 weeks
51
What is the pathway if there is a Neuroscensory deficit in the limb?
* → ask if the leg unsalvageable
* fixed discolouration or mottling, complete paralysis
* → if **_yes_** amputation or palliation
* → if **_no_** urgent CT and urgent revascularisation
52
What is the pathway if there isn't neurosensory deficit in a limb?
Image and aim for early revascularisation
53
What are causes of Acute Limb Ischaemia
* **Embolic** ( more common in the days of rheumatic fever)
* more common in chronic un-manged AF, endocarditis, proximal aneurysm
* **Thrombotic**
* Rupture of an atherosclerotic plaque
* **Aneurysm**
* Eg Popliteal artery thrombosis
* **Trauma**
* Fracture / Dislocation
* Knife, Gunshot wound
* IV drug use
* Iatrogenic
54
What is definitive management of Acute Limb-threatening Ischemia?
* intra-arterial thrombolysis
* surgical embolectomy
* angioplasty
* bypass surgery
* amputation: for patients with irreversible ischaemia
55
What is the initial treatment for Acute Limb-threatening Ischaemia
* _AtoE_
* _Heparin 5000 iu IV/ LMWH (Fragmin) s/c_
* _Analgesia: (IV opioids)_
* _Vascular review_
* Foot down
* Imaging
* Duplex
* Angiogram
* CTA/ MRA
* DSA
56
What is the treatment/ management for an Embolus?
Perform an embolectomy
Post embolectomy; find the cause
* Culture (possible endocariditis)
* Histology
* Image proximal arteries
* Echo: Bubble, TOE (transoesophageal)
* 24h tape
* Possible hypercoagulable condition
* _Anticoagulation post proccedure_
57
How would a patient with thrombotic disease present?
* May have a history of claudication
* May have missing contralateral pulses
* Risk factors for atherosclerosis
* Sinus rhythm
* Rarely presents hyper-acutely
58
How can thrombotic disease be managed?
* Thrombotic disease often involves underlying atherosclerosis
* Thrombolysis can clear an acute if it's done within the first 2 weeks and even better within the first week if presentation
* This clears the acute clot and leaves the atheromatous plaque which can then be stented via angioplasty
* if surgical intervention is needed it usually involves a bypass
59
How is limb ischaemia caused by trauma managed?
* Try and maintain flow with a shunt, fix bones or trauma sites then bypass any ischaemic regions
* May need to do a pre-emptive fasciotomy
* If there is a supracondylar fracture in children if t's pink but pulseless arm, doesn't always need a repair
* In IVDU and infection cases ligation is preferred rather than repair due to widespread infection
60
What is compartment syndrome and how does it present?
* when ischaemic muscle gets re-perfused leads to
* muscle oedema
* pressure in the compartment goes up
* causes microvascular compromise
* muscle necrosis
* intense pain - _especially to passive movement_
* paraesthesia in the feet
* pulselessness is a **_late_** sign
* requires fasciotomy → contact seniors
61
What are risk factors for Chronic Ischaemia
* Smoking
* Diabetes
* Hypercholesterolaemia
* Hypertension
Statin recommended for all patients
62
What is potential treatment for critical chronic ischaemia
* Angioplasty +/- stent often first option
* Long segment occlusion, vein conduit → Bypass
* Amputation if tissue loss advanced, low chance of revascularisation succeeding
* Palliation if frail and *compos mentis (*ie “in best interests”)
63
Explain what an angioplasty is
* Uses the Seldinger technique to gain trans-luminal access into the artery
* if there is an occlusion may need to pass the wire alongside the blockage (sub-intimally) then break back in to gain access to the artery
* developing technologies allows various different ways to gain access or break the plaques
* crossing devices
* debulking
* litho pasty
* Stent developments
* drug elution
* covered stents (if you're worried about the clot embolising)
64
What types of bypass surgery are there?
Following the anatomy of the patient
* Aorto-bifemoral
* Ileo-femoral
* Femoral above-knee popliteal
* Femoral below-knee Popliteal
* Femoral distal
* Popliteal pedal
_Extra-anatomical_
* femoral-femoral crossover - if the patient isn't fit enough to have abdominal surgery
* Axillo-bifemoral
65
What is the difference between vein and plastic grafts
* Vein
* Greater patency (85%, 80%, 70% for 1,3,5yrs)
* Less likely to become infected
* Not suitable if already used or removed for other surgery
* Plastic
* Increased thrombosis rates (70%, 35%, 25%)
* Increased risk of infection (any bacteraemia)
66
Define Aneurysm
permanent and irreversible localized dilation of a blood vessel to at least 50% more than its (expected) normal diameter
67
Define Ectasia
(permanent and irreversible localised) dilation of less than 150% of the normal (expected) diameter
68
Define Arteriomegaly
Diffuse arterial enlargement without discrete aneurysm formation
69
What is Subclavian Steal Syndrome?
a phenomenon causing retrograde flow in an ipsilateral vertebral artery due to stenosis or occlusion of the subclavian artery, proximal to the origin of the vertebral artery
* The most common cause is atherosclerosis and is most commonly seen on the left subclavian artery
70
What are risk factors for Subclavian Steal Syndrome?
* **Atherosclerosis**
* Takayasu arteritis,
* which is a form of large vessel granulomatous vasculitis, commonly seen in young or middle-aged women of Asian descent
* Subclavian artery compression in the thoracic outlet.
* This presentation usually presents in athletes like cricket bowlers and baseball pitchers, due to neuromuscular compression, as the subclavian artery crosses over the first rib.
* Presence of cervical rib,
* which is an extra rib that originates from the seventh cervical vertebra
* Following surgical repair of coarctation of the aorta
* Congenital abnormalities like right aortic arch
* Rare anatomical factors include aortic dissection, vertebral artery congenital malformations, and even external vertebral artery compression
71
Where are aneurysms most commonly seen?
* Infra-renal abdominal aorta forms \>90% if aneurysms
* Aortic arch
* Thoracic Aorta
* Supra-renal abdominal aorta
72
What is the Aetiology of aneurysms?
* Degenerative (non-specific)
* Familial
* M:F =2:1
* Smoking
* Vasculitic
* Connective Tissue abnormalities
* Caucasian
* Infection ‘Mycotic’
* Trauma
* Bicuspid valves (thoracic aortic aneurysm TAA)
* Aortopathies (for TAA, Marfan syndrome, Ehlers Danlos)
* Degenerative (non-specific)
* More likely to occur in Males 4:1
* _Diabetes reduces your risk of having an anneursym or rupture_
73
How do Aneurysms present?
* Majority are asymptomatic
* detected incidentally
* If they do have symptoms
* chest pain, back pain, haemodynamic instability in rupture
74
How are aneurysms diagnosed?
* Clinical Examination
* US imaging
* in asymptomatic individuals
* Cross-section imaging
75
What is the best management for a ruptured AAA
* prevention of rupture → elective treatment
* weight operative risks vs the risk of rupture
* LaPlace's law: maximum diameter is used as a txt criterion: \> 5.5 cm
* repair below that does not improve survival risk of surgery doesn't outweigh benefits of preventing the rupture
* **Open surgery (laparatomy) or Endovascuar Aortic Repair (EVAR)**
76
What screening is available for aneurysms?
* Only able to screen for Abdominal Aortic Aneurysms
* Ultrasound scan given
* with lifestyle modifications
* offered to men in their 65 years old
* not cost-effective in women or in other aneurysms
* if they are found to have one they are monitored yearly to check for growth referred to 3y vascular hospital once 5.5cm reached to consider txt
* possible benefit in screening women \>60yrs who are smokers
77
What are perioperative considerations to make for an Open repair of an aortic aneurysm?
* Very physically demanding on a patient
* cross-clamping of the aorta reduces blood flow to the legs during surgery
* long stay in hospital with high dependency post-surgery
* Long slow recovery period after
* a patient must be physically and mentally fit enough to take on the challenges of surgery and also have support around them
78
What are the complications of an Open Repair?
* graft infection
* aorto-enteric fistula
* autonomic dysfunction
* incisional hernia
* operative mortality of 5-8%
79
What are considerations and possible considerations to make for EVAR surgery
* Small groin incisions- less invasive
* can be done under regional/ local anaesthesia
* Stent-graft used causing possible
* migration
* potential for re-interventions
* endoleak blood flows around the stent into the sack
* → → → risk of rupture
* graft limb occlusion
Postoperatively
* need surveillance regularly CT scans
* increase risk of cancer
1-2% operative mortality
80
What does an open repair involve?
* Major laparotomy
* Aorto-iliac clamping
* Sutured Dacron graft
81
Future in managing and treating AAA?
* looking at the blood flow and turbulence with an aneurysm not only the aortic diameter to assess risk of rupture
* Looking at medical therapy to prevent the development and growth of AAA
* Metformin?
82
What is Claudication?
aching in the legs usually the calf that is precipitated by walking and is relieved by rest
* claudication pain is always reversible and is relieved by rest
* it tends to improve in time with exercise due to the opening of new collateral supply vessels and improved muscle function
* site of diseases is one level higher than the highest level of the affected muscle e.g *disease in the superficial femoral artery produces calf claudications*
83
What is the management of patients with claudication?
* most patients have associated vascular disease and investigation for occult coronary or cerebrovascular disease is mandatory
* should be commenced on an antiplatelet agent or statin
* smoking cessation and exercise encouraged
* investigated for Cauda Quina as osteoarthritis can result in intermittent claudication
84
How can Claudication present Neurologically?
* CAn be caused by Caudaa equina
* usually in elderly patients with an atypical history
* chronic back pain or back injury
* pain may be bilateral and in the distribution of S1-S3 dermatomes
* may be accompanied with paraesthesia in the feet and loss of ankle jerks
* all peripheral pulses palpable and leg well perfused
85
What investigations can be done to investigate Claudication?
* **FBC:** rule out polycythaemia
* **Blood glucose/ HbA1c:** diabetes
* **Lipids**: Hyperlipidaemia
* **ABI** (pre and post-exercise): an estimate of disease severity
* **ECG:** coronary artery disease
* **Angiography/ Duplex ultrasound:** precise location and extent of diseases, pre-procedure planning
* catheter angiography
* CT angiography
* MRA
86
What are treatments for an aortic transection
Dacron graft
87
What is a Stanford Type B Aortic dissection?
* This type of tear begins further down the aorta and further from the heart
* it extends from the descending aorta into the abdominal aorta but doesn't involve the first part of the aorta in the front of the chest
* can usually be treated with a stent-graft device inserted into the aorta
less common than type A and not as immediately life-threatening
88
What are the symptoms of an Aortic dissection?
* sudden severe, sharp pain in the chest and upper back
* described as tearing, stabbing or ripping pain
* Shortness of breath
* Fainting or dizziness
* Low BP; high suspicion when there's are 20mmHg between arms
* Rapid weak pulse
* Heavy sewating
* Confusion, vision loss, stroke symptoms
89
What are risk factors for developing an aortic dissection?
* Ongoing/ untreated Hypertension
* Atherosclerosis
* Aortic aneurysms
* Aortic valve disease
* congenital heart conditions, bicuspid aortic valve or Turner syndrome
* Connective tissue disorders: Marfan syndrome and Ehlers-Danlos Syndrome
90
What is extracranial arterial disease?
* a disorder characterised by atherosclerosis of the carotid or vertebral arteries resulting in cerebral, ocular or cerebellar ischaemic symptoms
* Cerebral: stroke, TIA
* Ocular: amaurosis figax
* Cerebellar: vertigo, ataxia, drop attacks
91
What is a TIA?
* a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia without infarction
* not lasting more than 24 hours
92
What are the risk factors for Extracranial arterial disease?
* Smoking
* HTN
* Cardiac disease
* Hyperlipidaemia
* Diabetes
* Obesity
93
What are the clinical features of Extracranial arterial disease?
* Cerebral (contralateral symptoms):
* motor: weakness, clumsiness, paralysis of a limb
* sensory: numbness, paraesthesia
* speech: receptive or expressive dysphagia
* Ocular: amaurosis figax
* transient loss of vision “vail coming down on visual field”
* Vertebrobasilar symptoms: vertigo, ataxia, dizziness, syncope, bilateral paraesthesia, visual hallucinations
* bruit may be heard over a carotid artery
94
What investigations should be carried out when patients present with symptoms of extracranial arterial disease?
* Duplex scanning
* Carotid angiography/ MRA (safer)
* CT or MRI can demonstrate the presence of an infarct
95
What is the management of a patient presenting with extra-cranial arterial disease?
Medical
* risk factor modification: smoking cessation, control BP, weight loss etc
* antiplatelet agent: aspirin or clopidogrel 75mg/day
* statins if evidence of vascular disease
* Anticoagulation in patients with cardiac embolic disease
Interventional
* Carotid endarterectomy (CEA) (+ maximum medical therapy)
* most benefits if performed within 2 weeks of the onset of symptoms
* Carotid artery stenting (CAS) (only in high-risk CEA patients)
* dual antiplatelet treatment showed be used during CAS
96
What is the preparation for patients undergoing IR procedures?
* Consent
* NBM
* Antibiotic prophylaxis?
* Coagulopathy?
* INR \<1.5, platelets \> 50-80,000 (N \>150,000)
* Monitoring
* Pulse oximetry, BP, ECG
* Oxygen
* IV sedation/analgesia
* Midazolam, fentanyl
* General anaesthesia
97
What are examples of embolic agents used for transarterial embolization? (temporary and permanent)
* Permanent
* Coils – fibred, microcoils, Nestor, Spirale, MReye
* PVA – 50-1000μ
* Microspheres
* Cyanoacrylate (‘glue’)
* Onyx
* Alcohol
* Temporary
* Gelatin sponge
98
What is grading used for renal trauma?
management of each one?
* **Grade I:** contusion/subcapsular hematoma, no parenchymal laceration
* conservative
* **Grade II:** laceration \< 1xm depth of renal cortex no urinary extraversion
* IR intervention
* **Grade III:** laceration \> 1 cm depth of the renal cortex, no urinary extravasation
* IR intervention
* **Grade IV:** Laceration extending through the renal cortex, medulla into collecting system minor renal artery or vein injury with contained hematoma
* nephrectomy
* **Grade V:** shattered kidney vascularized kidney, hilar avulsion
* nephrectomy
99
What is percutaneous ablation and give examples of these techniques?
heating/freezing of tumour through the skin on tumours to cill tumour
* PEI
* RFA
* Laser interstitial hyperthermia
* Cryotherapy
* Microwave
* Focussed US
100
What screening is available for AAA, what is the management of the outcome
Single Ultrasound at aged 65
* \< 3 cm: Normal → No further action
* 3 - 4.4 cm: Small aneurysm → Rescan every 12 months
* 4.5-5.4 cm: Medium aneurysm → Rescan every 3 months
* ≥5.5cm cm: Refer to vascular for probable intervention
101
What classifies as Low rupture risk AAA and how are they managed?
* asymptomatic, aortic diameter \< 5.5cm (i.e. small and medium aneurysms)
* abdominal US surveillance (on time-scales outlines above) and optimise cardiovascular risk factors (e.g. stop smoking)
102
What classifies as high rupture risk in a AAA and how is it managed?
* symptomatic, aortic diameter \>=5.5cm or rapidly enlarging (\>1cm/year)
* refer within 2 weeks to vascular surgery for probable intervention
* treat with elective endovascular repair (EVAR) or open repair if unsuitable. In EVAR a stent is placed into the abdominal aorta via the femoral artery to prevent blood from collecting in the aneurysm.
* A complication of EVAR is an _endo-leak,_ where the stent fails to exclude blood from the aneurysm, and usually presents without symptoms on routine follow-up.
103
What drugs outside of statins and clopidegrel are used in Peripheral artery disease and when are they indicated?
* naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life
* cilostazol: phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects - not recommended by NICE
304: Surgery
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