Vascular Flashcards
Outline the major causes of ulcers
80 % of lower limb ulcers are of venous origin
Other common causes include arterial insufficiency and diabetic-related neuropathy
Rarely, they can also be caused by infection, trauma, vasculitis or malignancy (typically squamous cell carcinoma)
Describe venous ulcers
Shallow with irregular borders and a granulating base
Characteristically located over the medial malleolus
Prone to infection so can present with cellulitis
What causes venous ulcers?
Venous insufficiency
valvular incompetence or venous outflow obstruction
→ impaired venous return→ venous hypertension → “trapping” of white blood cells in capillaries and the formation of a fibrin cuff around the vessel
This hinders oxygen transportation into the tissue and causes release of inflammatory mediators
Risk factors for venous ulcers?
Increasing age
Pre-existing venous incompetence or history of VTE
Pregnancy
Obesity or physical inactivity
Severe leg injury or trauma
Key clinical features of venous ulcers?
Painful (particularly worse at the end of the day)
Often found in the gaiter region of the legs
Associated sxs of chronic venous disease will be present before they appear (e.g. aching, itching, or a bursting sensation)
What might you find on examination of a patient with a venous ulcer?
varicose veins with ankle or leg oedema
features associated with venous insufficiency:
- varicose eczema or thrombophlebitis
- haemosiderin skin staining
- lipodermatosclerosis (champagne bottle legs)
- atrophie blanche.
How can you investigate venous leg ulcers?
Clinical diagnosis
Duplex USS to diagnose underlying venous insufficiency
Ankle Brachial Pressure Index (ABPI) to assess for arterial component/ if compression bandaging is suitable
Swabs if suspected infection
Consider thrombophilia and vasculitic screening in young patients
How should you manage venous leg ulcers?
When would skin grafting be indicated?
Conservative:
leg elevation
exercise, weight loss and adequate nutrition
Mainstay of management:
multicomponent compression bandaging, changed once or twice a week (30-75% of venous leg ulcers will heal after 6 months)
ABPI must be measured as >0.6 before bandaging is applied
Dressings and emollients to maintain surrounding skin health
Abx if evidence of wound infection
Tx of any concurrent varicose veins with endovenous techniques or open surgery
If fail to heal after 12 weeks or >10cm2 skin grafting may be needed
Describe arterial ulcers
small deep lesions with well-defined borders and a necrotic base
commonly occur distally at sites of trauma and in pressure areas (e.g the heel)
Risk factors for arterial ulcers?
those of peripheral arterial disease:
smoking, diabetes mellitus, hypertension, hyperlipidaemia, increasing age, positive family history, and obesity and physical inactivity
Clinical features of arterial ulcers
(including PMH and associated signs)
Ulcer is often painful and develops over a long period with poor healing (little - no granulation tissue)
Preceding hx of intermittent claudication (pain when they walk) or critical limb ischaemia (pain at night)
Associated signs:
cold limbs, thickened nails, necrotic toes and hair loss
reduced or absent pulses
sensation maintained (unlike neuropathic ulcers)
Investigations for arterial ulcers?
Ankle Brachial Pressure Index (ABPI)
(>0.9 = normal; 0.9-0.8 = mild; 0.8-0.5 = moderate; <0.5 = severe)
Anatomical location investigated by examination and then imaging:
Duplex ultrasound
CT Angiography
Magnetic Resonance Angiogram (MRA)
Management of arterial ulcers?
(Conservative, Medical, Surgical)
Urgent referral for a vascular review
Conservative – smoking cessation, weight loss, and increased exercise ( supervised exercise programmes available)
Medical – cardiovascular risk factor modification - statin therapy, antiplatelet (aspirin or clopidogrel), and optimisation of blood pressure and glucose
Surgical – Angioplasty (with or without stenting) or bypass grafting (usually for more extensive disease).
Any non-healing ulcers despite a good blood supply may also be offered skin reconstruction with grafts.
Describe neuropathic ulcers.
What are the key risk factors?
painless ulcers that form on the pressure points on the limb (repeated trauma due to loss of protective sensation)
variable in size and depth, with a “punched out” appearance
Risk factors: anything that causes peripheral neuropathy!
- diabetes mellitus
- B12 deficiency
- compounded by foot deformity and concurrent peripheral vascular disease
Clinical features of neuropathic ulcers?
(in the hx and associated sxs)
Hx of peripheral neuropathy (often glove and stocking distribution)
Associated sxs:
painful neuropathy (burning/tingling in legs)
amyotrophic neuropathy (painful wasting of proximal quadriceps)
single nerve involvement (mononeuritis multiplex, such as CN III or median nerve)
Investigations for neuropathic ulcers?
Management?
Investigations:
Check blood glucose and serum B12
Swab if signs of infection
Xray if signs of deep infection (for osteomyelitis)
Use 10g monofilament or Ipswich touch test to assess extent of neuropathy
Management:
Flucloxacillin/debridement if infected
Referral to diabetic foot clinic and chiropodists
Therapeutic shoes
Improve blood glucose control
What is the name for a deformity causing the loss of the transverse arch?
A rocker-bottom sole
Any acutely painful limb that is cold and pale should be treated as acute limb ischaemia until proven otherwise, and is a surgical emergency.
What are the 6 Ps of acute limb ischaemia?
How should you investigate and manage?
Pain, Pallor, Pulselessness, Paresthesia, Perishingly cold, and Paralysis
Investigations:
Routine bloods, serum lactate, thrombophilia screen (if <50yrs without known risk factors) , group and save
ECG
Doppler at bedside
CT angiogram
Urgent vascular review
Management:
Treat as surgical emergency bc irreversible damage after 6 hours
Fluid resuscitate and start on IV heparin whilst deciding how to proceed
Risk factors for acute limb ischaemia?
atrial fibrillation
hypertension
smoking
diabetes mellitus
recent myocardial infarction
How to approach a suspected fracture in an acutely painful limb?
check for focal bony tenderness and inability to weight-bear
have a low-threshold for radiological imaging
Define AAA.
Give 5 potential causes
dilatation of the abdominal aorta greater than 3cm
atherosclerosis
trauma
infection
connective tissue disease (e.g. Marfan’s disease, Ehler’s Danlos, Loey Dietz)
inflammatory disease (e.g. Takayasu’s aortitis)
Risk factors for AAA? Key negative risk factor?
smoking
hypertension and hyperlipidaemia
family hx
male gender
increasing age
Diabetes is a negative risk factor!
How might a patient with an AAA present if they are symptomatic? (most are asymptomatic and can be found incidentally)
Pulsatile mass palpable on examination
Abdominal pain
Back or loin pain
Distal embolisation producing limb ischaemia
Aortoenteric fistula
Shock/syncope
Outline the AAA screening protocol in the UK
The national abdominal aortic aneurysm screening programme (NAAASP) offers a single abdominal USS for all men in their 65th year
Most men with a detected AAA will spend 3 to 5 years in surveillance prior to reaching the threshold for elective repair (must be > 55mm for direct referral to surgical team)
Differentials for symptomatic AAA?
Renal colic (most common)
diverticulitis
IBD/IBS
GI haemorrhage
Appendicitis
ovarian torsion/ rupture
splenic infarctions
Investigations and management for AAA?
Investigations:
USS to confirm diagnosis
If >5.5 cm then CT with contrast to determine suitability for endovascular procedures
Management:
Less than 5.5 cm:
Monitoring with Duplex USS
3.0 – 4.4cm: yearly ultrasound
4.5 – 5.4cm: 3-monthly ultrasound
Risk modification: smoking cessation, BP control, statin and aspirin therapy, WL (3% risk of cardiovascular mortality p.a)
Over 5.5cm:
Surgical intervention - open repair/endovascular repair
If unfit for surgery then only operate once 6cm
If over 6 inform DVLA and over 6.5 they shouldn’t drive
Who qualifies for surgical repair of AAA?
AAA >5.5cm in diameter, AAA expanding at >1cm/year, or a symptomatic AAA in a patient who is otherwise fit
Describe the 2 main approaches to surgical repair of an AAA
Open repair - midline laparotomy or long transverse incision, exposing the aorta, and clamping the aorta proximally and the iliac arteries distally, before the segment is then removed and replaced with a prosthetic graft
Endovascular repair - introducing a graft via the femoral arteries and fixing the stent across the aneurysm
Endovascular repair has improved short term outcomes but a higher rate of reintervention so often not used in younger patients
Major complication of endovascular repair of abdominal aneurysm (EVAR)?
endovascular leak - incomplete seal forms around the aneurysm so blood leaks around the graft
Major complications of AAA?
REAR
Rupture
Embolisation
Aortoduodenal fistula
Retroperitoneal leak
Rupture:
80% rupture posteriorly into the retroperitoneal space
20% rupture anteriorly into the peritoneal cavity ( very poor prognosis)
Around 50% patients present with the ‘classic triad’ of ruptured AAA. What is this?
flank or back pain, hypotension, and a pulsatile abdominal mass
Management of ruptured AAA?
Immediate high flow O2
IV access (2x large bore cannulae)
Urgent bloods (FBC, U&Es, clotting) with crossmatch for minimum 6U units
Careful tx of shock - raising BP may dislodge the clot so aim to keep BP≤100mmHg (permissive hypotension)
Transfer to the local vascular unit
unstable = require immediate transfer to theatre for open surgical repair
stable = CT angiogram to determine whether the aneurysm is suitable for endovascular repair
What is acute aortic syndrome?
a disruption of the layers of the arterial wall
split into 3 subgroups:
1. aortic dissection
2. penetrating aortic ulcer
3. intramural haematoma.
Define aortic dissection.
How can an aortic dissection progress?
A tear in the intimal layer of the aortic wall, causing blood to flow between and splitting apart the tunica intima and media
they can be acute (when diagnosed ≤14 days) or chronic (when diagnosed >14 days)
Distally , Proximally or Both
Anterograde dissections propagate towards the iliac arteries
Retrograde dissections propagate towards the aortic valve (can result in prolapse of the aortic valve, bleeding into the pericardium, and cardiac tamponade)
What is a penetrating aortic ulcer? How can it progress?
A penetrating aortic ulcer is an ulcer that penetrates the intima and progresses into the media of the artery
Can progress to intramural haematoma, aortic dissection, perforation, or aneurysm formation.
What is an intramural haematoma? How can it progress?
An intramural haematoma is a contained aortic wall haematoma with bleeding in the media. This can progress to aortic dissection, perforation or aneurysm formation.
How does the DeBakey classification group aortic dissections?
Anatomically
Type I – originates in the ascending aorta and propagates at least to the aortic arch
(typically seen in patients under 65yrs and carry the highest mortality)
Type II – confined to the ascending aorta
(classically in elderly patients with atherosclerotic disease and hypertension)
Type III – originates distal to the subclavian artery in the descending aorta
(Further subdivided into IIIa which extends distally to the diaphragm and IIIb which extends beyond the diaphragm into the abdominal aorta)
Risk factors for aortic dissection?
Male gender
Hypertension
Atherosclerotic disease
Connective tissue disorders (Marfan’s syndrome or Ehler’s-Danlos syndrome)
Bicuspid aortic valve
How do acute aortic syndromes present? (signs and symptoms)
Sxs:
tearing chest pain, classically radiating through to the back
Clinical signs:
tachycardia
hypotension
new aortic regurgitation murmur
signs of end-organ hypoperfusion (e.g. reduced urine output, paraplegia, lower limb ischaemia, abdominal pain or ALOC)
How should patients with aortic dissection be managed longer term?
lifelong antihypertensive therapy and surveillance imaging
Imaging would usually be at 1, 3, and 12 months post-discharge, with further scans at 6-12 month intervals thereafter depending on the size of the aorta.
Complications of acute aortic syndromes?
Aortic rupture
Aortic regurgitation
Cardiac tamponade
Myocardial ischaemia (coronary artery dissection)
Stroke or paraplegia (cerebral artery or spinal artery involvement)
How is carotid artery disease classified radiologically?
By the degree of stenosis (diameter reduction)
Mild
<50%
Moderate
50-69%
Severe
70-99%
Total Occlusion
100%
How does carotid artery disease present?
Asymptomatic
TIA
Stroke
What pathologies can be involved in carotid artery disease other than atherosclerosis?
Carotid Dissection – younger pt (<50yrs) with underlying connective tissue disease, event potentially precipitated by trauma/ sudden neck movement
Thrombotic Occlusion of Carotid Artery –can only be differentiated from atheromatous plaque on imaging
Fibromuscular Dysplasia – non-atheromatous stenotic angiopathy causing hypertrophy of the vessel wall, predominantly affecting young (<50yrs) females, more commonly affects renal arteries
Vasculitis –pts typically have systemic symptoms and other vessels may be affected
Name some non-cerebrovascular conditions that manifest neurologically like carotid artery disease
hypoglycaemia
Todd’s paresis
subdural haematoma
SOL
venous sinus thrombosis
post-ictal state
multiple sclerosis
What is a CEA? Who should be referred? Potential complications?
Carotid Endarterectomy- removing the atheroma and associated damaged intima
suitable pts should be operated on within the first 2 weeks following sx onset
All patients with an acute non-disabling stroke (or TIA) who have symptomatic carotid stenosis between 50 – 99% should be referred for assessment for CEA
Complications: ischaemic stroke and nerve damage to the hypoglossal, glossopharngeal, or vagus nerve
Stroke complications?
dysphagia
seizures or ongoing spasticity
bladder or bowel incontinence
depression, anxiety, or cognitive decline.
Define aneurysm. How may an aneurysm present?
persistent, abnormal dilatation of an artery to 1.5 times its normal diameter
Asymptomatic (found incidentally)
Symptomatic, but not ruptured
Symptomatic secondary to a rupture (stable or unstable)
What causes thoracic aortic aneurysms to develop?
(AABCTT)
Degradation of the tunica media causes the artery to lose structural integrity and dilate
Underlying pathologies:
(AABCTT)
Aortic dissection, aortic arteritis (e.g. Takayasu Arteritis)
Bicuspid aortic valve
Connective tissue diseases (e.g. Marfan’s syndrome or Ehlers-Danlos syndrome)
Trauma
Tertiary syphilis
