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
Where does the pain localise to for different thoracic aortic aneurysms?
Ascending aorta- Anterior chest
Aortic arch - Neck
Descending aorta - Between the scapulae
Other associated sxs of thoracic aortic aneurysms?
Back pain – spinal compression by descending or thoracoabdominal aneurysm
Hoarse voice – from damage to the left recurrent laryngeal nerve in arch aneurysms
Distended neck veins – from SVC compression
Symptoms of heart failure – from involvement of the aortic valve
Dyspnoea or cough – tracheal or bronchial compression
Deep Venous Insufficiency is a chronic disease that can result in significant morbidity. It is commonly caused by either DVT or valvular insufficiency.
What are its causes?
Primary : there is an underlying defect to the vein wall or valvular component (includes congenital defects and connective tissue disorders)
Secondary : defects occur secondary to damage
including post-thrombotic disease, post-phlebitic disease, venous outflow obstruction, and trauma
Risk factors for DVI?
increasing age
female gender
pregnancy
previous DVT or phlebitis
obesity and smoking
Complications of DVI?
Common:
swelling, recurrent cellulitis, chronic pain and ulceration
More serious but less common:
DVT, secondary lymphoedema, and varicose veins.
What is a Marjolin ulcer?
rare type of cutaneous squamous cell carcinoma (SCC) developing at the site of severe or recurrent inflammation (such as in venous insufficiency)
Define hyperhidrosis. How can it be classified?
sweating in excess of that required for regulation of body temperature
Primary – no underlying cause, usually localised to specific areas, symmetrical distribution
Most cases start in teenage years and improve with time 1/3 have a positive family history
Secondary – associated with an underlying condition, generalised sweating or focal to specific areas
- Pregnancy or menopause
- Anxiety
- Infections (TB, HIV, or malaria)
- Malignancy (especially lymphoma)
- Endocrine disorders (hyperthyroidism, phaeochromocytoma, or carcinoid syndrome)
- Medication (e.g. anticholinesterases, antidepressants, or propranolol)
How should hyperhydrosis be investigated?
Diagnosis of primary hyperhidrosis is often made through history and examination
- focal sweating (bilateral and symmetrical) , occurring at least once a week, typical onset before 25yrs of age, should be present for >6months for diagnosis
Investigations to exclude secondary causes:
FBC, CRP, U&Es, TFTs
blood glucose
CXR
What is subclavian steal syndrome?
A rare condition causing syncope/ neurological deficits when the demand on blood supply to the affected arm is increased through exercise
Secondary to a proximal occlusion in the subclavian artery, typically on the left
In order to compensate for the increased oxygen demand in the arm, blood is drawn from the collateral circulation→reversed blood flow in the ipsilateral vertebral artery
Clinical features of SSS?
Cerebral symptoms in periods of increased arm activity:
vertigo
diplopia / visual loss
dysphagia
dysarthria
syncope
Arm claudication
Investigation of SSS?
duplex USS - can show the retrograde flow in the affected vertebral artery during exercise
Routine CXR - used to assess for any external compression on the subclavian artery
Definitive investigation is via CT angiography or MR angiography
Management of SSS?
Antiplatelet and statin therapy
Surgery: Percutaneous angioplasty ± stenting
Bypass for longer or distal occlusions
- carotid-subclavian bypass or axillo-axillary bypass
What is thoracic outlet syndrome? Major causes?
The clinical features that arise from compression of the neurovascular bundle (e.g. brachial plexus and subclavian a + v) within the thoracic outlet (space between clavicle and first rib)
Causes:
Hyperextension injuries
Repetitive stress injuries (e.g. work-related, particularly when working over the head)
External compressing factors (e.g. poor posture)
Anatomical abnormalities (e.g. anomalous cervical rib)
Hypertrophy of the scalene muscles
Clinical features of thoracic outlet obstruction?
dependent on neurological, arterial, or venous involvement
Neurological (MOST COMMON)- compression of brachial plexus can lead to parasthesia / motor weakness, often in ulnar distribution, may be muscle wasting
Arterial - claudication symptoms or acute limb ischaemia through either occlusion, distal embolisation, or aneurysm formation
Venous - DVT and extremity swelling (Paget-Schrötter syndrome); in untreated severe cases, there can be prominent veins over the shoulder due to collateralisation
What are varicose veins?
tortuous dilated segments of vein associated with valvular incompetence
> 3mm diameter
incompetent valves permit blood flow from the deep venous system to the superficial venous system (main examples are at the sapheno-femoral junction and sapheno-popliteal junction)
→ venous hypertension and dilatation of the superficial venous system
Causes of varicose veins?
Primary idiopathic : 98%
Secondary causes:
DVT
pelvic masses (e.g. pregnancy, uterine fibroids, and ovarian masses)
AV malformations
4 major risk factors for developing varicose veins?
Prolonged standing
Obesity
Pregnancy
Family history
Complications of untreated varicose veins?
aching / itching
skin changes
ulceration
thrombophlebitis
bleeding
What is a saphena varix?
dilatation of the saphenous vein at the saphenofemoral junction in the groin
displays a cough impulse so commonly mistaken for femoral hernia
Gold standard investigation for varicose veins?
duplex ultrasound (best done by a trained technician), assessing valve incompetence at the great/short saphenous veins and any perforators
How should you manage varicose veins with concurrent DVT?
you cannot treat their superficial incompetence, as the venous blood will have no route back- non surgical management
What is the NICE criteria for referral to vascular services for varicose veins?
Symptomatic primary or recurrent varicose veins
Lower‑limb skin changes e.g. pigmentation or eczema, thought to be caused by chronic venous insufficiency
Superficial vein thrombosis (characterised by the appearance of hard, painful veins) with suspected venous incompetence
A venous leg ulcer (a break in the skin below the knee that has not healed within 2 weeks)
Tx options for varicose veins?
Vein ligation, stripping, and avulsion – making an incision in the groin (or popliteal fossa) and identifying the responsible vein before tying it off and stripping it away
Foam sclerotherapy – injecting a sclerosing agent directly into the varicosed veins. This is done under ultrasound guidance with a local anaesthetic
Thermal ablation – heating the vein from inside (via radio-frequency or laser catheters), causing irreversible damage to the vein. This is done under ultrasound guidance and also may be performed under local (or general) anaesthetic.
What is acute limb ischaemia? What are the causes?
sudden decrease in limb perfusion that threatens the viability of the limb
Embolisation (source may be AF, post-MI mural-thrombus, AAA, or prosthetic heart valves)
Thrombus in situ
Trauma
What is the medical management of acute limb ischaemia?
What is the surgical management?
Why do patients require a high level of post-op care?
Prolonged course of heparin, suitable for those with Rutherford 1 or 2a
Surgical management is mandatory for those with Rutherford class 2b and above
Embolic cause:
Embolectomy via Fogarty catheter
Bypass surgery
Thrombotic cause:
Local intra-arterial thrombolysis
Angioplasty (combined with thrombolysis)
Bypass surgery
Risk of ischaemia reperfusion syndrome
Main risks of ALI?
Reperfusion injury
Compartment syndrome
AKI
What is required for definitive diagnosis of acute mesenteric ischaemia? What is the finding?
CT angiography scan with IV contrast
Arterial ischaemia will initially present on CT imaging as oedematous bowel ( ischaemia and vasodilatation) before progressing to a loss of bowel wall enhancement and then to pneumatosis
Management of acute mesenteric ischaemia?
Surgical emergency - urgent resuscitation required
IV fluids, catheter insertion, fluid balance chart
Broad spectrum abx to in case of faecal contamination (bowel perf)
Early ITU input due to significant acidosis and risk of multi-organ failure
Definitive management:
Excision of necrotic or non-viable bowel (if not suitable for revascularisation) - plan potential relook laparotomy in 24-48 hours
Revascularisation of the bowel - removal of thrombus or embolism, preferably through angioplasty (although open embolectomy possible)
Major complications of acute mesenteric ischaemia?
Mortality 50-80% even with tx
bowel necrosis and perforation
short gut syndrome in survivors - unable to absorb enough nutrients because there is not enough small intestine
What is chronic mesenteric ischaemia?
Ischaemia caused by reduced blood flow to the bowel that gradually deteriorates over time due to atherosclerotic plaques in the coealiac trunk, SMA and IMA
mostly in those >60yrs and is more common in female patients
Typically asymptomatic at rest and comes on when increased demand on blood supply e.g. after eating (like angina of the bowel)
Risk factors for chronic mesenteric ischaemia?
smoking, hypertension, diabetes mellitus, and hypercholesterolemia.
Classical symptoms associated with chronic mesenteric ischaemia?
Postprandial pain – 10mins-4hrs after eating
Weight loss – a combination of decreased calorie intake (sitaphobia) and malabsorption
Concurrent vascular co-morbidities, e.g. previous MI, stroke, or PVD
Examination findings are often non specific; evidence of malnutrition/cachexia, generalised abdominal tenderness, and abdominal bruits
Investigations for chronic mesenteric ischaemia?
Blood tests including FBC (anaemia) U&Es (malnutrition = electrolyte derangement) and lipid profile and blood glucose (CV risk)
CT angiography gold standard investigation
When is surgical intervention indicated in chronic mesenteric ischaemia? What are the options?
severe disease, progressive disease, or presence of debilitating symptoms (including signs of weight loss or malabsorption)
Endovascular procedures (more common) – consists of mesenteric angioplasty with stenting
Open procedures (less common) – either an endartectomy or a bypass procedure
always modify cardiovascular risk factors as well as surgery
Complications of chronic mesenteric ischaemia?
bowel infarction and malabsorption
What is chronic limb ischaemia? What might you find on examination? Risk factors?
a form of peripheral arterial disease that results in a symptomatic reduced blood supply to the limbs
typically caused by atherosclerosis (rarely vasculitis) and commonly affects the lower limbs
OE: limbs cool to touch, arterial ulcers, absent peripheral pulses, femoral bruits in advanced cases
Risk factors: smoking, diabetes, hypertension, hyperlipidaemia, increasing age, strong family history, and obesity or physical inactivity
Outline the Fontaine classification of chronic leg ischaemia
Stage I Asymptomatic
Stage II Intermittent claudication
Stage III Ischaemic rest pain
Stage IV Ulceration or gangrene, or both
What is Buerger’s test?
Test for chronic limb ischaemia
involves lying the patient supine and raising their legs until they go pale and then lowering them until the colour returns (or even becoming hyperaemic).
The angle at which limb goes pale is Buerger’s angle
- less than 20 degrees = severe ischaemia.
What is Leriche syndrome?
a form of peripheral arterial disease affecting the aortic bifurcation. It specifically presents with buttock or thigh pain and is associated with erectile dysfunction.
Critical Limb Threatening Ischaemia is the advanced form of chronic limb ischaemia.
It can be clinically defined in three ways:
Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia
Presence of ischaemic lesions or gangrene objectively attributable to the arterial occlusive disease
ABPI less than 0.5
Major differentials for limb ischaemia symptoms?
Spinal stenosis (‘neurogenic claudication’)
- pain from the back radiating down the lateral aspect of the leg (tensor fascia lata), often have symptoms on initial movement or symptoms that are relieved by sitting rather than standing
Acute limb ischaemia
Clinical features that are less than 14 days duration, often presenting within hours.
Rarer causes: popliteal artery entrapment syndrome, persistent sciatic artery, iliac endofibrosis, cystic adventitial disease, Buerger’s disease
Medical and surgical management of chronic limb ischaemia?
Medical:
Lifestyle advice (smoking cessation, regular exercise, weight reduction)
Statin therapy (atorvastatin 80mg OD)
Anti-platelet therapy (clopidogrel 75mg OD)
Optimise diabetes control
Surgical:
can be offered in suitable patients if (1) risk factor modification has been discussed; and (2) supervised exercise has failed to improve symptoms
If critical limb ischaemia- inpatients should be treated within 5 days, stable outpatients within 2 weeks
Options:
Angioplasty +/- stenting
Bypass grafting (diffuse disease or in younger patients)
Complications of chronic limb ischaemia?
sepsis (secondary to infected gangrene)
acute-on-chronic ischaemia
amputation
reduced mobility and quality of life
How are peripheral and visceral aneurysms best investigated?
CT angiography
Can use MR angiography for younger patients who require long term follow up bc reduced risk of kidney damage and radiation
What is the most common peripheral artery aneurysm?
How does it present?
How is it investigated and managed?
Popliteal artery aneurysm (70-80%)
High risk of embolisation and occlusion
Can be found incidentally on imaging
May present with acute limb ischaemia or compression symptoms (popliteal vein / peroneal nerve)
Investigation:
Duplex USS to rule out other causes of popliteal swelling e.g. Baker’s cysts/ lymphadenopathy
CT angiography - anatomical assessment of aneurysm and patency of distal vessels
Management:
symptomatic / asymptomatic but greater than 2.5cm = treatment
Endovascular/open repair
Femoral artery aneurysms are typically pseudoaneurysms, with the two major causes being:
Percutaneous vascular interventions
Patient self-injecting (typically intravenous drug users who inject into their groin)
How do pseudoaneurysms occur?
when there is a breach to the arterial wall, resulting in an accumulation of blood between the tunica media and tunica adventitia of the artery
typically occur following damage to the vessel wall, such as puncture following cardiac catheterisation or repeated injections to the vessel (from IVDU)
other causes include trauma, regional inflammation (e.g. splenic artery aneurysms secondary to acute pancreatitis) , or vasculitis
How do pseudoaneurysms present clinically?
Differentials?
tender pulsatile lump often over femoral artery
if infected, the area will be erythematous and tender; purulent discharge
herald bleed- early warning sign of massive delayed haemorrhage
Differentials with similar presentation:
true aneurysms
haematomas (especially after a procedure or trauma)
abscess (especially in an IVDU)
Gold standard investigation for pseudoaneurysm?
duplex ultrasound- turbulent forward and backward flow (termed “yin-yang sign”)
CT imaging if hard to see on USS
infected pseudo-aneurysm:
require urgent investigation and management as prone to rupture
routine bloods (FBC, CRP, U&Es, clotting)
blood cultures
pus MC&S (if discharging)
crossmatch due to risk of haemorrhage
management for larger or symptomatic pseudoaneurysms?
ultrasound-guided compression (painful, lasts 30 mins)
thrombin injection
infected pseudoaneurysms require surgical ligation
What medication should ALL patients with peripheral vascular disease be on?
clopidogrel (75mg) and atorvastatin (80mg)
When should severe PAD or critical limb ischaemia be treated by endovascular techniques?
short segment stenosis (e.g. < 10 cm), aortic iliac disease and high-risk patients
When should severe PAD or critical limb ischaemia be treated by open surgical techniques?
long segment lesions (> 10 cm), multifocal lesions, lesions of the common femoral artery and purely infrapopliteal disease
What drugs are licensed for tx of PAD?
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
How might coarctation of the aorta present?
How is it treated?
Aortic stenosis at the site of the ductus arteriosus insertion (remnant of DA acts as a fibrous constricting band around aorta)
Most common in boys and girls with Turners syndrome
May present with symptoms of arterial insufficiency e.g. syncope and claudication
Blood pressure mismatch may be seen
Radiofemoral delay
May see notching of ribs due to collateral flow through intercostal vessels
Treatment is either with angioplasty or surgical resection (the former is the most common)
Factors suggestive of thrombus as a cause for acute limb ischaemia?
pre-existing claudication with sudden deterioration
evidence of widespread vascular disease
reduced or absent pulses in contralateral limb
no obvious source for emboli
Factors suggestive of embolus as a cause for acute limb ischaemia?
sudden onset of painful leg (< 24 hour)
no history of claudication
no evidence of peripheral vascular disease (normal pulses in contralateral limb)
clinically obvious source of embolus (e.g. AF, recent MI)
evidence of proximal aneurysm (e.g. abdominal or popliteal)
What conservative management of PAD has proven beneficial?
Exercise training
patients are asked to exercise to the point of maximal pain tolerance and then rest, to try and increase collateral circulation
What may result in abnormally high ABPI readings?
vessel calcification- e.g. due to T2DM
Outline criteria for low risk and high risk of rupture in AAA
Low rupture risk
asymptomatic, aortic diameter < 5.5cm (i.e. small and medium aneurysms)
abdominal US surveillance and optimise cardiovascular risk factors (e.g. stop smoking)
High rupture risk
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
Which vessel is likely to be involved if the claudication causes buttock pain?
Iliac artery - iliac stenosis
Painful ulcers associated with a low ABPI are usually of what origin?
Arterial
What is Pyoderma gangrenosum?
Erythematous nodules or pustules which ulcerate
Associated with inflammatory bowel disease/RA
Can occur at stoma sites
Features of axillary/ brachial embolus?
50% of upper limb emboli will lodge in the brachial artery, 30% will lodge in the axillary artery
Sudden onset of symptoms: 6Ps
Sources are AF, mural thrombus
Cardiac arrhythmias may cause result in impaired consciousness in addition to the embolus
Features of Raynaud’s disease? Tx?
Idiopathic condition affecting young females
Usually affects hands > feet
Digits become: white →blue →red
Treatment is with calcium antagonists
What does ABPI tell us?
The ankle-brachial pressure index (ABPI) is the ratio of the systolic blood pressure in the lower leg to that in the arms
> 1.2: may indicate calcified, stiff arteries. This may be seen with advanced age or PAD
< 0.9: likely PAD. Values < 0.5 indicate severe disease which should be referred urgently
Why is ALI much more dangerous than chronic limb ischaemia?
No time to develop collaterals / undergo remodelling
3 key sxs of PAD?
Claudication, ischaemic rest pain, ulceration/gangrene
What should you ask in a hx about intermittent claudication?
Ask patients how far they can walk before they have to stop
Relative claudication distance - when pain starts
Absolute claudication distance - when they cannot carry on
Can be used to monitor disease progression
Describe the rest pain experienced in PAD
Worse at night/ when lying down
Felt in foot, improved when hanging foot out of bed ( takes pressure off of nerve)
Due to involvement of vasa nervosum- no blood supply to nerves surrounding blood vessels
3 main types of gangrene?
Dry- clear zone of demarcation eg black toes in frostbite
Wet - superadded infection, gooey, more likely in diabetes
Gas- clostridium perfringens
Most cases of PAD occur at the level of which artery?
superficial femoral artery
Key things to consider in management of PAD?
Consider if patients are on best medical therapy ( BMT) :
Anti platelets, statins and PPIs
DON’T use TED stockings in people with arterial insufficiency - you will make it worse
Use either angioplasty or bypass for definitive management
Post-op complications of varicose vein surgery?
Recurrence
Infection
Damage to nerves - sural (lateral) / saphenous (medial)
Scarring
Most common visceral artery aneurysm?
Splenic
